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Invasive Pneumococcal Disease, Recurrent Isolated, 1 OMIM

Description Recurrent invasive pneumococcal disease (IPD) is defined as 2 episodes of IPD occurring at least 1 month apart, whether caused by the same or different serotypes or strains (Ku et al., 2007). Recurrent IPD occurs in at least 2% of patients in most series, making IPD the most important known risk factor for subsequent IPD. Clinical Features Ku et al. (2007) described 2 otherwise healthy children with isolated recurrent IPD as the only clinical infectious manifestation of an inherited disorder in nuclear factor kappa-B (see 164011)-dependent immunity. ... Molecular Genetics In a 7-year-old boy born of unrelated Hungarian parents, Ku et al. (2007) found that recurrent invasive pneumococcal disease (IPD1; 610799) was related to compound heterozygosity for 2 mutations in the IRAK4 gene, located in the intron between exons 10 and 11: 1189-1G-T and 1188+520A-G (606883.0005). ... Autosomal recessive IRAK4 deficiency (607676) and X-linked recessive NEMO deficiencies (e.g., 300291, 300584) are primary immunodeficiencies that affect NF-kappa-B-mediated immunity and cause a relatively broad susceptibility to infections. The patients described by Ku et al. (2007) displayed none of the other known infectious phenotypes associated with these disorders.

IRAK4, MYD88, TLR4, MTA2, SUMF2

Irak-4 Deficiency GARD

IRAK-4 deficiency is a condition that affects the immune system ( primary immunodeficiency ). It causes recurring severe infections by a type of bacteria called pyogenic bacteria. Individuals with IRAK-4 deficiency seem to be particularly susceptible to infections caused by bacteria called Streptococcus pneumoniae . The deficiency is caused by mutations in the IRAK4 gene and is inherited in an autosomal recessive pattern. Treatment may include intravenous immunoglobulin therapy (IVIG), taking antibiotics before an infection develops, and vaccines.
Irak4 Deficiency OMIM

Description IRAK4 deficiency is an autosomal recessive primary immunodeficiency that impairs Toll (see TLR4; 603030)/IL1R (see IL1R1; 147810) immunity, except for the TLR3 (603029)- and TLR4-interferon-alpha (IFNA; 147660)/beta (IFNB; 147640) pathways (Ku et al., 2007). Clinical Features Haraguchi et al. (1998) described a 3-year-old female with interleukin-12 (see IL12B, 161561) deficiency associated with recurrent episodes of pneumococcal pneumonia with sepsis and other infections in the absence of fevers. ... They recommended testing for IRAK4 deficiency in patients with recurrent bacterial and fungal infections without sustained antibody response to immunization. Ku et al. (2007) tested TLR responses of whole blood and individual leukocyte subsets in 28 patients with IRAK4 deficiency and found that only the TLR3 agonist poly(I:C) could induce production of 11 non-IFN cytokines. ... Death occurred only in patients 8 years old and younger, and invasive disease occurred only in those 14 years old and younger. Ku et al. (2007) concluded that IRAK4-dependent TLRs and IL1Rs are vital for childhood immunity to pyogenic bacteria, particularly S. pneumoniae, but they are not essential for protective immunity to most infections.
Irak-4 Deficiency MedlinePlus

IRAK-4 deficiency is an inherited disorder of the immune system (primary immunodeficiency). This immunodeficiency leads to recurrent infections by a subset of bacteria known as pyogenic bacteria but not by other infectious agents. (Infection with pyogenic bacteria causes the production of pus.) The most common infections in IRAK-4 deficiency are caused by the Streptococcus pneumoniae , Staphylococcus aureus , and Pseudomonas aeruginosa bacteria. Most people with this condition have their first bacterial infection before age 2, and the infections can be life-threatening in infancy and childhood. Infections become less frequent with age. Most people with IRAK-4 deficiency have invasive bacterial infections, which can involve the blood (septicemia), the membrane covering the brain and spinal cord (meningitis), or the joints (leading to inflammation and arthritis).
Immunodeficiency Due To Interleukin-1 Receptor-Associated Kinase-4 Deficiency Orphanet

Interleukin-1 receptor-associated kinase-4 (IRAK-4) deficiency is an immunodeficiency associated with increased susceptibility to invasive infections caused by pyogenic bacteria. Epidemiology It has been described in less than 15 patients from eight families with onset occurring during childhood. Clinical description The most common recurrent infections in these patients were caused by Streptococcus pneumoniae or Staphylococcus aureus , leading to a range of clinical manifestations such as pneumonia, septic arthritis, cellulitis, osteomyelitis, otitis media, meningitis and sinusitis. In contrast, the patients appeared to be resistant to infection caused by most other bacteria, parasites and viruses but fungal infections have been reported. Although routine immunological evaluations generally gave normal results, the patients displayed reduced inflammatory responses and neutropenia during infectious episodes.

Invasive Pneumococcal Disease, Recurrent Isolated, 2 OMIM

Another form of this disorder (IPD1; 610799) is caused by mutation in the IRAK4 gene (606883). Clinical Features Ku et al. (2007) described a 4.5-year-old boy born to unrelated Belgian parents in whom recurrent invasive pneumococcal disease (IPD) as the only clinical infectious manifestation of an inherited disorder in nuclear factor kappa-B (see 164011)-dependent immunity. ... Molecular Genetics In the Belgian patient described by them, Ku et al. (2007) found a 518C-G transversion in exon 4 of the NEMO gene, predicted to result in an arg173-to-gly (R173G) mutation (300248.0023). ... Autosomal recessive IRAK4 deficiency (607676) and X-linked recessive NEMO deficiencies (e.g., 300291, 300584) are primary immunodeficiencies that affect NF-kappa-B-mediated immunity and cause a relatively broad susceptibility to infections. The patients described by Ku et al. (2007) displayed none of the other known infectious phenotypes associated with these disorders.

IKBKG

Hydrocele Testis Wikipedia

J Urol . 171 (3): 1271–3. doi : 10.1097/01.ju.0000112928.91319.fe . PMID 14767329 . ^ Ku u.a. 2001 KU, J. H.; KIM, M. E.; LEE, N.

FLT4, AKT1, PEX11B, GJC2, KLHL7, SOX18, PIGN, PIEZO1, ADAMTS3, VEGFC, RPL5, PTEN, PIK3CA, EZH2, MECOM, DIPK1A, CHIT1, TP63, VEGFA, EDN1, CYP4V2

Tan Syndrome Wikipedia

The lesions were excised with no recurrence during follow up. [1] References [ edit ] ^ a b c d e Aik Kah, Tan; Chui Yong, Ku; Annuar, Faridah Hanom (2011). "Neurothekeoma palpebrae in association with multiple superficial angiomyxomas: Tegumental Angiomyxoma- Neurothekeoma syndrome (TAN syndrome)" .

Adenomatoid Odontogenic Tumor Wikipedia

Two thirds of the cases are found in females. [5] References [ edit ] ^ Nigam S, Gupta SK, Chaturvedi KU (2005). "Adenomatoid odontogenic tumor - a rare cause of jaw swelling" .

MDM2, TP53, AMBN, H3P16, NSG1, MMRN1, FAM30A, TCEAL1, PCNA, KRAS, BCL2, CTNNB1, CDKN2A, CDKN1A, BMP4, BMP2, BGN, BGLAP, H3P10

Tropical Eosinophilia Wikipedia

The clearance of rapidly opsonised microfilariae from the bloodstream results in a hypersensitive immunological process and abnormal recruitment of eosinophils, as reflected by extremely high IgE levels of over 1000 kU/L. [7] [11] The typical patient is a young adult man from the Indian subcontinent. [9] Contents 1 Symptoms 2 Diagnosis 3 Treatment 4 References Symptoms [ edit ] A persistent or recurrent cough that gets aggravated at night, weakness, weight loss and a low fever raises the possible diagnosis of this disease. ... Others may cough up a little blood and may also have a wheeze. [2] Diagnosis [ edit ] The diagnostic criteria for tropical pulmonary eosinophilia [11] include: a history supportive of exposure to lymphatic filariasis ; a peripheral eosinophilia count greater than 3 × 10 9 /L); an elevated serum IgE levels (> 1000 kU/L); increased titers of antifilarial antibodies ; peripheral blood negative for microfilariae ; and a clinical response to diethylcarbamazine .

IL5, GATA3, RAG2, SHARPIN, TLR4, TLR2, MYD88, PTGDS, SERPINA1, SIGLEC8, GGTLC1, IL33, JAK2, IL25, MYDGF, HPGDS, POSTN, PTX3, FOXN1, P2RY6, STAT3, RNASE3, RNASE2, LOC102724197

Gastroblastoma Wikipedia

Mod Pathol doi: 10.1038/modpathol.2017.68 ^ Shin DH, Lee JH, Kang HJ, Choi KU, Kim JY, Park DY, Lee CH, Sol MY, Park JH, Kim HY, Montgomery E (2010) Novel epitheliomesenchymal biphasic stomach tumour (gastroblastoma) in a 9-year-old: morphological, ultrastructural and immunohistochemical findings.

Levator Ani Syndrome Wikipedia

PMID 18794003 . ^ a b Park DH, Yoon SG, Kim KU, et al. (May 2005). "Comparison study between electrogalvanic stimulation and local injection therapy in levator ani syndrome".

Proctalgia Fugax Wikipedia

Proctalgia fugax Specialty General surgery Proctalgia fugax , a variant of levator ani syndrome , is a severe, episodic pain in the regions of the rectum and anus . [1] It can be caused by cramping of the levator ani muscle, particularly in the pubococcygeal part . [2] Contents 1 Signs and symptoms 2 Prevention 3 Treatment 4 References 5 External links Signs and symptoms [ edit ] It most often occurs in the middle of the night [3] and lasts from seconds to minutes; [4] pain and aching lasting twenty minutes or longer would likely be diagnosed instead as levator ani syndrome . In a study published in 2007 involving 1809 patients, the attacks occurred in the daytime (33 percent) as well as at night (33 percent) and the average number of attacks was 13. Onset can be in childhood; however, in multiple studies the average age of onset was 45. Many studies showed that women are affected more commonly than men, [5] but this can be at least partly explained by men's reluctance to seek medical advice concerning rectal pain. [6] Data on the number of people afflicted vary, but prevalence may be as high as 8–18%. [4] [7] It is thought that only 17–20% of sufferers consult a physician, so obtaining accurate data on occurrence presents a challenge. [4] During an episode, the patient feels spasm-like, sometimes excruciating, pain in the rectum and/or anus , often misinterpreted as a need to defecate. To be diagnosed as proctalgia fugax, the pain must arise de novo (meaning the absence of clear cause).
Levator Syndrome GARD

Levator syndrome is characterized by sporadic pain in the rectum caused by spasm of a muscle near the anus (the levator ani muscle). The muscle spasm causes pain that typically is not related to defecation. The pain usually lasts less than 20 minutes. Pain may be brief and intense or a vague ache high in the rectum. It may occur spontaneously or with sitting and can waken a person from sleep. The pain may feel as if it would be relieved by the passage of gas or a bowel movement.

Afrophobia Wikipedia

S2CID 149746823 . v t e Anti-cultural, -national or -ethnic sentiment African Albanian American Arab Armenian Australian Austrian Azerbaijani British Buddhist Canadian Catalan Chechen Chilean Chinese Christian Croat Czech Dutch English Estonian European Filipino Finnish French Georgian German Greek Haitian Hazara Hindu Hispanic Hungarian Igbo Indian Indonesian Iranian Irish Israeli Italian Japanese Jewish Khmer Korean Kurdish Malay Manchu Mexican Middle Eastern Mongolian Montenegrin Muslim Pakistani Pashtun Polish Portuguese Quebec Romani Romanian Russian Scottish Serb Shia Slavic Somali Soviet Sufi Sunni Swede Tatar Thai Tibetan Turkish Ukrainian Venezuelan Vietnamese Western v t e White nationalism Foundations and related topics Alt-right Ableism Afrophobia Anti-autism Anti-communism Anti-Zionism Antisemitism Antiziganism Apartheid Aryan race Christian fundamentalism Christian Identity Christian nationalism Creativity Ethnic nationalism Eugenics Eurocentrism Europhilia Far-right Fourteen Words Ghost skin Hispanophobia Holocaust denial Homophobia Homosexual Agenda Identitarianism Islamophobia Kalergi Plan Kinism Ku Klux Klan National-anarchism Nazism Neo-Nazism Neo-Confederate Nordicism Race and intelligence Racism Right-wing terrorism Sinophobia Straight pride Transphobia White Australia policy White genocide conspiracy theory White Student Unions White identity White power skinhead White pride White separatism White supremacy Wotanism Zionist Occupation Government conspiracy theory Organizations Europe Blood & Honour Blue and White Front British National Party CasaPound Combat 18 Dutch Peoples-Union Front Comtois Golden Dawn Jobbik Kotlebists – People's Party Our Slovakia Les Identitaires National Action (UK) National Democratic Party of Germany National Front (UK) National Revival of Poland National Socialist Front National Socialist Movement of Denmark National Socialist Movement of Norway Nazi Party Nordic Resistance Movement Noua Dreaptă Party of the Swedes Russian National Unity Slavic Union Social-National Assembly Soldiers of Odin Sonnenkrieg Division Vigrid Voorpost Hundred-Handers (Group) North America 11th Hour Remnant Messenger American Freedom Party American Front American Nazi Party Atomwaffen Division Aryan Guard Aryan Nations Canadian Nationalist Party Combat 18 Council of Conservative Citizens Counter-Currents Publishing Groypers European-American Unity and Rights Organization Hammerskins Heritage Front Identity Evropa Ku Klux Klan Liberty Lobby National Alliance NAAWP National Citizens Alliance National Policy Institute National Vanguard Nationalist Movement Nationalist Party of Canada National Socialist Movement NSDAP/AO (1972) Proud Boys Rise Above Movement The Order Traditionalist Worker Party Redneck Shop White Aryan Resistance White Order of Thule Oceania Antipodean Resistance New Zealand National Front True Blue Crew United Patriots Front South Africa Afrikaner Weerstandsbeweging Afrikaner Volksfront Blanke Bevrydingsbeweging Conservative Party Kommandokorps South African National Front South African Party Media Music Blood & Honour National Socialist black metal Nazi punk Rock Against Communism Fashwave and Trumpwave Moon Man rap Print media American Renaissance Arktos Media The Aryan Alternative Candour National Vanguard The Occidental Quarterly Washington Summit Publishers Radio shows America First with Nicholas J.

Childhood Granulomatous Periorificial Dermatitis Wikipedia

. ^ a b c d e f g h i Kim, YJ; Shin, JW; Lee, JS; Park, YL; Whang, KU; Lee, SY (August 2011). "Childhood granulomatous periorificial dermatitis" .

Knobloch Syndrome Wikipedia

Genetics Home Reference . ^ Hull, S; Arno, G; Ku, CA; Ge, Z; Waseem, N; Chandra, A; Webster, AR; Robson, AG; Michaelides, M; Weleber, RG; Davagnanam, I; Chen, R; Holder, GE; Pennesi, ME; Moore, AT (2016).

COL18A1, ADAMTS18

Knobloch Syndrome GARD

Knobloch syndrome is characterized by severe vision problems and skull defects. The most common features include extreme nearsightedness (high myopia), recurrent retinal detachment , and occipital encephalocele . There are three types of Knobloch syndrome, which can be distinguished by the underlying genetic cause. Knobloch syndrome type I is caused by mutations in the COL18A1 gene. The genes associated with Knobloch syndrome type 2 and type 3 have not been identified; however, Knobloch syndrome type 3 has been linked to a specific region on chromosome 17, known as 17q11.2. Knobloch syndrome follows an autosomal recessive pattern of inheritance.
Knobloch Syndrome 1 OMIM

A number sign (#) is used with this entry because Knobloch syndrome-1 (KNO1) is caused by homozygous or compound heterozygous mutation in the COL18A1 gene (120328) on chromosome 21q22. Description Knobloch syndrome is an autosomal recessive developmental disorder primarily characterized by typical eye abnormalities, including high myopia, cataracts, dislocated lens, vitreoretinal degeneration, and retinal detachment, with occipital skull defects, which can range from occipital encephalocele to occult cutis aplasia (summary by Aldahmesh et al., 2011). Clinical Features Knobloch and Layer (1971) reported a family in which 5 of 10 sibs had high myopia, vitreoretinal degeneration with retinal detachment, and occipital encephalocele. One of the patients also had total anomalous pulmonary venous return (106700). All the affected sibs had normal intelligence (Pagon et al., 1978). The parents were unaffected and denied consanguinity.
Knobloch Syndrome Orphanet

A rare systemic disorder characterized by vitreoretinal and macular degeneration, as well as occipital encephalocele. Epidemiology The exact prevalence of Knobloch syndrome (KS) is unknown but less than 100 cases have been reported in the literature so far. Clinical description KS is characterized by early-onset severe myopia (usually becoming apparent in the first year of life), vitreoretinal degeneration with retinal detachment, macular abnormalities, and midline encephalocele (mainly in the occipital region). Predisposition to hydrocephalus is frequent. Ocular abnormalities vary and may include congenital cataract, iris abnormalities, and lens subluxation. Numerous extraocular abnormalities have been described: a single umbilical artery, pyloric stenosis, a flat nasal bridge, midface hypoplasia, bilateral epicanthic folds, abnormal lymphatic vessels in the lung, patent ductus arteriosus, cardiac dextroversion, generalized hyperextensibility of the joints, unusual palmar creases, and unilateral duplication of the renal collecting system.

Coxsackievirus-Induced Cardiomyopathy Wikipedia

Nature Medicine . 5 (3): 320–6. doi : 10.1038/6543 . PMID 10086389 . ^ Knowlton, KU (2008). "CVB infection and mechanisms of viral cardiomyopathy".

Accessory Auricle Wikipedia

Hodder Arnold. 2016-06-15. p. 969. ISBN 978-0-340-808-931 . ^ Ku, PK; Tong, MC; Yue, V (1998). "Polyotia- a rare external ear anomaly".

Melanocytoma Wikipedia

. ^ a b Mohmad, Zalilawati; Aik Kah, Tan; Chui Yong, Ku; Wan Abdul Halim, Wan Haslina; Kong Yong, Then (2011).

Surfer's Myelopathy Wikipedia

Retrieved 25 September 2016 . v t e Surfing Terminology Types Big wave Bellyboarding Bodyboarding Flowriding Kiteboarding Kneeboarding Lake surfing River surfing Shoulder surfing Skimboarding Standup paddleboarding Surf kayaking Tow-in Tube riding Windsurfing Women's surfing Surfers American Argentine Australian Brazilian British Filipino French Irish Maldivian New Zealand Peruvian Portuguese South African Environment Closeout Hawaiian scale Ocean surface wave Surf break Surfline Tidal bore Wave pool Equipment Surfboard Fins Wax Wax comb Foilboard Boardshorts Surfboard leash Locations By country Australia Brazil Canada Chile Ecuador India Indonesia Ireland Madeira New Zealand Peru South Africa Sri Lanka Taiwan Turkey United Kingdom Scotland United States Sites Banzai Pipeline Cyclops La Libertad Mavericks Puerto Escondido Ship Stern Bluff Teahupo'o Competitions Australian Boardriders Battle Australian Open of Surfing Rip Curl Pro Billabong Pipeline Masters Billabong Pro Jeffreys Bay Billabong Pro Teahupoo Billabong Pro Teahupoo 2008 Copa Movistar Duke Kahanamoku Invitational Surfing Championship East Coast Surfing Championships Hawaiian Pro Ku Ikaika Challenge Lion Foundation Surf League MEO Rip Curl Pro Portugal Noosa Festival of Surfing O'Neill Sebastian Inlet Pro O'Neill World Cup of Surfing Pipeline Bodysurfing Classic Quiksilver Big Wave Invitational Quiksilver Pro France Quiksilver Pro Gold Coast Red Bull Big Wave Africa Red Bull Cape Fear Rip Curl Pro Shark Island Challenge Smirnoff World Pro-Am Surfing Championships Stubbies Surfabout Surfest Triple Crown of Surfing US Open of Surfing World Surfing Championship World Surf League Organizations International Professional Surfers International Surfing Association International Surfing Day International Surfing Museum National Scholastic Surfing Association NYSurfFilmFestival Santa Cruz Surfing Museum SurfAid International Surfers Against Sewage Surfrider Foundation Surfing Australia Surfing South Africa The Moonshine Conspiracy Welsh Surfing Federation World Surf League Culture Art Fictional surfers Films Hair Music Shaka sign Hazards Shark attack Surfer's eye Surfer's ear Surfer's myelopathy Related topics Surf lifesaving v t e Medicine Specialties and subspecialties Surgery Cardiac surgery Cardiothoracic surgery Colorectal surgery Eye surgery General surgery Neurosurgery Oral and maxillofacial surgery Orthopedic surgery Hand surgery Otolaryngology ENT Pediatric surgery Plastic surgery Reproductive surgery Surgical oncology Transplant surgery Trauma surgery Urology Andrology Vascular surgery Internal medicine Allergy / Immunology Angiology Cardiology Endocrinology Gastroenterology Hepatology Geriatrics Hematology Hospital medicine Infectious disease Nephrology Oncology Pulmonology Rheumatology Obstetrics and gynaecology Gynaecology Gynecologic oncology Maternal–fetal medicine Obstetrics Reproductive endocrinology and infertility Urogynecology Diagnostic Radiology Interventional radiology Nuclear medicine Pathology Anatomical Clinical pathology Clinical chemistry Cytopathology Medical microbiology Transfusion medicine Other Addiction medicine Adolescent medicine Anesthesiology Dermatology Disaster medicine Diving medicine Emergency medicine Mass gathering medicine Family medicine General practice Hospital medicine Intensive care medicine Medical genetics Narcology Neurology Clinical neurophysiology Occupational medicine Ophthalmology Oral medicine Pain management Palliative care Pediatrics Neonatology Physical medicine and rehabilitation PM&R Preventive medicine Psychiatry Addiction psychiatry Radiation oncology Reproductive medicine Sexual medicine Sleep medicine Sports medicine Transplantation medicine Tropical medicine Travel medicine Venereology Medical education Medical school Bachelor of Medicine, Bachelor of Surgery Bachelor of Medical Sciences Master of Medicine Master of Surgery Doctor of Medicine Doctor of Osteopathic Medicine MD–PhD Related topics Alternative medicine Allied health Dentistry Podiatry Pharmacy Physiotherapy Molecular oncology Nanomedicine Personalized medicine Public health Rural health Therapy Traditional medicine Veterinary medicine Physician Chief physician History of medicine Book Category Commons Wikiproject Portal Outline This article about a medical condition affecting the circulatory system is a stub .

Innate Immune Defect Wikipedia

. ^ von Bernuth H, Picard C, Jin Z, Pankla R, Xiao H, Ku CL, et al. (August 2008). "Pyogenic bacterial infections in humans with MyD88 deficiency" .

Barakat Syndrome Wikipedia

PMID 18426329 . Further reading [ edit ] Gaynor KU, Grigorieva IV, Nesbit MA, et al.

GATA3, DGS2, QRSL1, HPT, DGCR2, PARP1, ZNF2, ZFPM2, GCM2, SLC18A2, SP1, STS, PTH, HSP90AA1, ESR1, COL11A2, ZNF72P

Hypoparathyroidism, Sensorineural Deafness, And Renal Disease OMIM

A number sign (#) is used with this entry because the phenotype of hypoparathyroidism, sensorineural deafness, and renal disease (HDR), also known as Barakat syndrome, is caused by haploinsufficiency of the GATA3 gene (131320) on chromosome 10p14. Clinical Features Barakat et al. (1977) reported steroid-resistant nephrosis with progressive renal failure and death at ages 5 and 8 years in 2 brothers who also had nerve deafness and hypoparathyroidism. At autopsy, the parathyroid glands were absent in 1 child and hypoplastic in the other. Barakat et al. (1977) also described male twins from another family with similar findings and death at age 3 years. At autopsy, their parathyroid glands were fibrotic and glomerular basement membranes were thickened.
Hypoparathyroidism-Sensorineural Deafness-Renal Disease Syndrome Orphanet

Hypoparathyroidism-sensorineural deafness-renal disease syndrome is a rare, clinically heterogeneous genetic disorder characterized by the triad of hypoparathyroidism (H), sensorineural deafness (D) and renal disease (R). Epidemiology The exact prevalence is unknown, but the syndrome is considered to be very rare. So far, about 180 individuals from different racial and ethnic groups have been reported in the worldwide medical literature. Patients of both sexes have been described. Clinical description HDR syndrome may present at any age with deafness, hypocalcemia, tetany and afebrile convulsions. Since prenatal ultrasonography is now a routine, congenital kidney and urinary tract anomalies could be the first presenting finding.
Barakat Syndrome GARD

Barakat syndrome , also known as HDR syndrome, is a rare, genetic syndrome characterized by h ypoparathyroidism , s ensorineural deafness , and r enal (kidney) disease . However, specific symptoms and severity can vary. About 65% of people with Barakat syndrome have all three of these features, while the others have various combinations of these features. Some people with Barakat syndrome have one or more of these as well as additional features. Hypoparathyroidism leads to low levels of calcium in the blood ( hypocalcemia ), which can cause symptoms such as muscle pain, muscle spasms, seizures, and rarely, cardiomyopathy. Hearing loss is the most consistent feature of Barakat syndrome. It is usually bilateral and can range from moderate to profound.

Stasis Papillomatosis Wikipedia

Lymphoedema may develop in many cases accompanied by acral thickening of the skin folds, hyperkeratosis and papillomatosis. [3] [5] References [ edit ] ^ a b c d e Schultz-Ehrenburg U, Niederauer HH, Tiedjen KU (May 1993). "Stasis papillomatosis.

Diabetes Mellitus, Noninsulin-Dependent OMIM

In a rat hepatoma cell line, inhibition of ATM with KU-55933, a selective ATM inhibitor, attenuated the phosphorylation and activation of AMP-activated protein kinase (see 602739) in response to metformin. ... Yee et al. (2012) commented on the GoDARTS and UKPDS paper and examined the inhibitory effect of KU-55933 on metformin in H4IIE cells and in HEK293 cells stably expressing OCT1. They demonstrated in both cases that KU-55933 inhibits metformin uptake via inhibition of OCT1 and that the attenuation of metformin-induced AMPK phosphorylation is a result of its inhibition of metformin uptake into the cells.

PPP1R3A, HNF4A, PAX4, AKT2, GCK, IRS1, KCNJ11, HNF1A, HNF1B, SLC2A4, NEUROD1, PDX1, SLC2A2, IRS2, WFS1, HMGA1, ABCC8, CDKAL1, INS, INSR, ENPP1, ADCY5, CAPN10, TCF7L2, PPARG, TGFB1, LIPC, BCL2, MAPK8IP1, HP, NOS3, PPARGC1A, HMOX1, LEPR, ICAM1, UCP2, LEP, SIRT1, ADIPOQ, EDNRA, EDN1, TNF, TNFRSF1A, NOS2, KL, CPT1A, SNAP25, ATP2A2, EDNRB, RETN, GCKR, SLC30A8, GLIS3, GCGR, FTO, GLP1R, PTPN1, JAZF1, KCNQ1, IGF2BP2, MTNR1B, THADA, HMG20A, NOTCH2, PROX1, KCNK16, GPD2, UBE2E2, AP3S2, MAEA, CMIP, PEPD, GRB14, CCND2, PLEKHA1, DGKD, ZFAND3, ITGA1, PSMD6, PAM, KSR2, NFATC2, CAT, SHBG, MIR375, SLC2A1, BRAF, SLC1A2, ST6GAL1, HHEX, JADE2, IL13RA1, MIR126, SOD2, VPS26A, GSTM1, MOK, GNB3, GCG, CNKSR2, AUTS2, IGF2, GP2, INPPL1, SREBF1, SOD1, FGF21, LPL, ZNF257, FBN1, USP48, PPARA, SCTR, EPC2, IAPP, FAM234A, KLF14, CYBA, RNF6, IDE, ETS1, GIPR, CASP3, TNFRSF1B, SFRP4, OGG1, ND1, ADAMTS9, GPX1, AR, NFKB1, MIR27A, EGFR, MIR192, PCSK2, COX2, PRKCB, MIR144, HBA1, TIMP1, C2CD4A, ATF3, SLC22A3, MIR221, TMEM18, C3, C2CD4B, MIR483, MIR222, MIR423, RELA, FAS, CISD2, CBS, HK1, ATP2A3, MIR130B, HLA-DRB5, MIR203A, MIR142, CCDC92, MIR140, MIR200A, MIR98, MIR204, PAX6, ECE1, MIR214, ITLN1, MIR10B, MIR30A, MIR377, MIR1260A, CDO1, RARRES2, CCR5, SMAD5, MAT1A, NUS1, MIR1249, MIR1296, MAPK8, MIR1226, MIR1306, MRAS, MIR1228, MIR744, MIR939, CD36, MIR885, MIR1307, MIR151A, GPT, RBP4, IGF1, ID1, MIR127, MIR215, HSD11B1, MIR205, HPX, MIR195, MTOR, MIR141, GIP, HIF1A, MIR181C, GH1, UCP3, SOCS3, MIR17HG, MIR125B1, MIR432, MIR92B, MIR628, MIR532, MIR487B, BCL2L11, CYP1A2, S100A6, IL6, MIR485, MIR409, MIRLET7D, CCL2, MIR339, MIR335, MIR1301, MIR33B, MIR1908, MIR3173, MIR4482, BCL2L1, MIR4516, MIR8061, MIR6741, PRKAA1, PCK1, PCSK1, NFE2L2, BHMT, MIR7704, PPARD, MIR1260B, NUCB2, NKX6-1, ADRA2A, SERPINF1, AKT1, ZC3HC1, AGER, SERPINE1, MIR6803, KCNU1, AVP, MIR2116, MAPK1, TMEM155, MMP9, CASP8, PTGS2, G6PC, NR3C1, GSK3B, IGF1R, CCN2, REG3A, PIK3R1, CALCA, MAPK3, MAFA, HMGCR, MMP3, NPPB, SERPINA12, CRTC2, PC, ABCG2, CD38, BECN1, BAX, MMP1, PRKCZ, PTGDS, PRKN, MADD, HTR2C, AGTR2, TRPC1, ARRB2, LNPEP, AOC3, TRPC6, DCX, DEFB1, SMAD4, MIF, DNMT1, SLC9A1, CARTPT, NOG, PLAT, PLN, MTNR1A, UGT1A1, NFE2L1, DNM1L, CYP2E1, PPP1R3C, FOXM1, UGT1A6, SRD5A1, NR1D1, NOS1, THBD, AGRP, GJA1, PRKCE, CYB5R4, MAPK9, TGFBR2, CCKAR, CDKN2B, MAPK14, ACOT2, CYTB, MKI67, CTF1, SCN1B, DAG1, F7, ANKRD23, COL3A1, OXCT1, FEM1B, SRC, CALM1, CYP11A1, HSD3B1, KLF11, MAP1LC3A, KCNMB1, ARX, NCOA6, HSD17B3, TSPAN8, PNPLA3, GPT2, CASP7, BAD, ABCC2, ASIP, CASP12, PHOX2A, EPAS1, ATP2A1, PPP2CA, AK1, GADD45GIP1, AANAT, ATP5F1B, SLC16A11, STAR, BEST1, MPST, MTR, ALDOB, PRKCI, CCHCR1, MC4R, LMNA, CRHR1, EIF3F, SDF2L1, HLA-DQB1, SLC12A3, ATF6, CDKN2B-AS1, CAMK1D, NEUROG3, CTNNB1, ALMS1, ARAP1, ATM, UMOD, CDC123, ANK1, GRK5, DUSP9, NOX4, ABO, CYP19A1, ARL15, ELN, SRR, TP53INP1, CASR, TM6SF2, PTPN22, KIF11, CUBN, MAP2K7, TMEM163, GPR55, SCGN, TFAP2B, AGMO, HMGA2, DNER, ALDH7A1, RBMS1, HECTD4, RFC2, LAMA1, AHR, PRPF31, SLC26A9, PROM1, CTBP1-DT, ARG1, UBE2Z, DGKB, POU5F1, AHI1, ZMIZ1, RP9, INS-IGF2, ZRANB3, COBLL1, FAF1, TCF19, PRC1, ACSL1, TH, ND5, PTPRD, RASGRP1, GLP2R, RBPJ, TUB, GATAD2A, BAZ1B, LINGO2, NRL, ALK, PBX4, SSR1, NDUFAF6, PRKAG2, CLIP2, WRN, POC5, DHDDS, OAS1, SNHG17, ABCA4, SGCD, SLC16A13, CAMTA1, CTRB1, ADGRL3, EHMT2, SPPL3, STUB1, CAMK2G, TRDN, MACF1, TSBP1, STX8, TTLL6, PTPRN2, CAMKK2, RREB1, TRPM1, BCL9, LIG4, ATXN1, CTBP1, SUGP1, ROM1, TPCN2, MPHOSPH9, MCM6, SH2B3, POMGNT1, MASP1, FBXW7, RBPJL, SGCG, LIMK1, PPP2R2C, PDE6B, CERKL, FAM161A, RBP3, HIVEP2, HLA-DRB9, HLA-DOB, PRIM2, GPR119, MAGEC3, ASCC2, HK2, PRPH2, PEX10, HLA-DRB1, HGSNAT, SSTR4, NPY, SUMO4, ARL6, MNX1, GUCA1B, LCN2, UNC5D, MOG, OSBPL7, PCSK9, TRNL1, NECTIN2, PRKAA2, RTN4RL1, TCF7, TTC8, MAK, PYY, CYB5D2, TTC39C, MAP6, DLEU7, MFAP1, CFAP77, RELN, MBNL1, RFLNA, EDARADD, RDH12, MCC, LINC02694, LINC01344, RPSAP52, PSMD9, PCARE, TNFRSF11B, NTRK2, PRKAB1, MMP2, PDE6G, NRG4, ST6GALNAC3, APOA5, LPA, CTTNBP2, NTRK3, LRMDA, PDE6A, ZSWIM3, LTA, HFE, PTH1R, PTH, PTGFRN, PCNT, REG1A, RHO, OSBPL1A, SLC5A2, ZNF513, SELE, CCDC149, C8orf37, CCNQ, PRRX1, PLCD1, IFNG, SLC5A1, IDH3B, IMPDH1, LINC01010, PLCB3, IL17A, IDH3A, IL18, SLC9B2, C17orf58, ND6, PPARGC1B, SELP, ZNF775, IL10, PLG, TRNQ, TRNS1, TRNS2, TRNK, SI, TRNH, TRNW, IL1RN, TRNF, IL4, IL1B, TRNE, IL1A, ST3GAL4, ST3GAL3, PPIL6, PDILT, CXCL8, ARL9, NEK2, ND4, REN, RP1, EYS, KCNQ3, PIK3CD, SPP1, HORMAD2, CHCHD6, RP2, PIK3CB, PIK3CA, NLRP3, MTHFR, SLCO4C1, SDHAF4, MSH3, RLBP1, KIF9-AS1, RGS13, RGS7, RGR, RFC1, NFKBIL1, RPGR, RPE65, MRPL12, CNDP1, CDHR1, COX3, REEP6, COX1, FFAR4, GPBAR1, SCD, ATXN7, ATXN2, SLC22A1, SAG, HNF1A-AS1, ZNF101, GOLGA6A, PON1, PIK3CG, TTLL8, CHMP4B, IL17REL, EHMT1, LINC01122, KCNQ1OT1, INTS8, RAB3GAP1, ENPP7P10, RALY, NLGN1, CPEB3, MGLL, MINDY1, SPATA7, CD59, CD81, UBAP2, ARHGAP15, CDK5, NUDT6, POLR3A, KIZ, CDKN2A, TRIOBP, SNRNP200, PALLD, ZHX3, LINC00844, ABCB9, ABCB10, CRB1, PRC1-AS1, BRS3, ARHGEF18, RPGRIP1L, ADAMTS9-AS2, LINC01426, CAD, UBE2E2-AS1, PROX1-AS1, CA4, OSER1-DT, SLC30A10, FBXL7, CEP68, ZZEF1, ANGPTL8, APOM, ARPIN-AP3S2, LMCD1-AS1, CNR1, ZBED3-AS1, ACKR3, MERTK, PDSS2, ATP8B2, DLEU1, LRFN2, RAMP2, CALCOCO2, CPA1, GPR158, TOPORS, STARD9, NAMPT, FRY, CRP, CRX, PITPNM2, CNGA1, CNGB1, GTF2I, NFAT5, PNPLA6, CETP, KLHL7, TEX14, ANKH, LINC00271, RAI1, HMGA2-AS1, CXCR6, PRPF8, SUMO2P17, CHUK, YKT6, ZGLP1, TXNIP, CLCNKB, C1GALT1, PRCD, ARL2BP, BLM, NR2E3, LOC102723407, AGT, AGTR1, LRP12, LINC02030, AHSG, PURG, LINC02484, ALB, LINC02841, PELO, AKR1B1, EXOC6, HPGDS, PALD1, FOXP1, CCND2-AS1, NSG1, LINC02576, SND1, LRP1B, FSCN3, ADRB3, ADIPOR1, ABCA1, ANKFY1, SNX7, PEX5L, GLRX5, HSD17B12, ASB3, ANGPTL4, ADA, ADRB2, ADARB1, SOST, IMPG2, GHRL, SCAPER, LINC01611, ADRA1A, ADRA2B, TBL2, ANPEP, RCBTB1, VPS33B, HNF4A-AS1, OSBPL3, SCAANT1, TXNL4B, PTPN23, MIR5094, ABI3BP, PINX1, SAMM50, FSCN2, BBS2, PRPF6, SRBD1, DIANPH, BDNF, DARS2, BGLAP, SBNO1, AMACR, LINC00824, ASCL2, LINC02010, APP, GIN1, APOA1, APOB, APOC3, HORMAD2-AS1, IFT172, APOE, CNTLN, APRT, POLDIP2, ETS1-AS1, PABPC4-AS1, LINC01339, TSBP1-AS1, C5orf67, ARL3, PKN2-AS1, GPSM1, TSPAN3, PCSK6, CST3, AGBL5, PABPC4, PEA15, EXT2, EYA2, OASL, FABP4, GDAP1L1, FABP2, OFD1, GCC1, ADIPOR2, NPRL3, IFT88, FGF23, FGF14, ZNF408, BEST3, MIR29A, ESR1, ALDH1A2, PRPF3, PIM3, NRXN1, NRXN3, PIEZO2, LRAT, LPAR2, XYLT1, PRPF4, APLN, KIF9, SEMA4A, SELENBP1, CLN8, MGAM, MTMR3, AKTIP, ZSCAN20, ZIC1, THSD4, TLR4, TULP1, TNKS2, ZNF34, GOT2, TP53, TNFAIP6, SLC2A10, FFAR1, UCP1, C16orf74, GPR42, TGFBR3, MLX, LINC02245, GSTP1, GSTT1, SPHKAP, MIR146A, FOXO1, GABPA, XRCC4, SCD5, CPED1, PCNX2, VWF, VSNL1, BICC1, GABRA4, USH2A, GABRG3, GAD1, GAD2, VEGFA, VDR, VCAM1, CLRN1, MED23, YTHDC2, DPP4, UBE3C, GTF2IRD1, DSPP, RHOBTB1, ACE, G6PC2, DECR1, MAGI2, DBP, SLC7A14, CLOCK, FCHSD2, ACE2, SINHCAF, USP3, CELSR1, RBM19, FGF19, MIR4435-2HG, RAPGEF5, GDF15, MTSS1, UVSSA, SFI1, CYP2C9, WSCD2, DEPDC5, TRIB3, DHX38, IFT140, SENP2, CYP21A2, KIAA1549, DOCK4, DARS1, MRPS35, BCHE, LIPE, AIMP2, RNF19A, LDLR, USF1, ARNTL, NOS1AP, AHSA1, GSTK1, PTEN, RBM45, RENBP, CTLA4, IGFBP1, CRK, GRAP2, DMD, GYS1, PON2, CCL5, POMC, IGFBP3, MME, STAT3, LGALS3, CYP2C19, SLCO6A1, LPIN1, F3, STAP2, APOA2, AQP7, FOXA2, SST, SLC17A5, MET, HMGB1, GPR151, NIDDM1, SELENOP, NIDDM2, GPRC6A, PCK2, GGT1, OR10A4, DIO2, HSPA5, GC, CYP3A4, LINC01672, MPO, GGTLC5P, SIRT6, TLR2, GLO1, ELMO1, BCL11A, MLXIPL, ARID4B, NRF1, P2RX7, MIR155, MSTN, CYP2B6, ACR, GGTLC3, MRGPRX1, ALDH2, PDR, GGT2, MRGPRX3, APOL1, HSPA1A, SIRT3, GPR166P, VN1R17P, OXER1, SLC2A11, FZD4, FNDC5, SNCA, MRGPRX4, MIR21, HSPA4, ABCG1, HSPA1B, LPAR3, CHI3L1, NR3C2, FGF2, CD14, ISL1, HAMP, LGR6, ARNT, ZBTB7C, CAV1, GGTLC4P, SGK1, PSEN1, NR1H4, CISD1, SELENOS, CD163, TMBIM4, VIP, CCN4, MFN2, ROCK1, IL22, GGTLC1, VIM, SLC22A2, SOD3, PLIN1, OGA, CNBP, PLA2G2A, SAT1, HAVCR1, FETUB, SFRP5, NAT2, EPO, IARS1, GLUL, LBP, MIR27B, STS, APOA4, ACACB, KNG1, MIR29B1, GAS6, IL15, CD44, HLA-DQA1, ATN1, FXN, CD68, ADM, MIR29B2, LOC102724197, MEFV, CRY2, HGF, FGF1, MTTP, DDIT3, ANGPTL3, BCL2A1, SIRT2, DKK1, INSRR, KCNJ4, IL33, FADS2, CASP1, IL6R, IL37, CCK, SORT1, TBC1D4, MT1A, HEBP1, PRL, MBL2, PARP1, GRK2, ARHGEF11, ROS1, TRPM5, PTX3, FADS1, PYCARD, IL2RA, KRT16, IL5, XPR1, IL2, BMP4, HIRA, LPAL2, FABP1, PADI4, CHDH, FANCD2, PTK2B, BRCA2, SOCS1, FN1, XBP1, SLC47A1, FOXC2, SLBP, PLA2G7, FGB, GHSR, DGAT1, LIPG, EPHB2, IGFBP2, MIR34A, ELANE, MT2A, HSPG2, SOAT1, DPPA3, SULT1E1, TPD52, SH2B1, HHIP, HDLBP, NR1I2, AZU1, MIR122, BTC, CPE, MAP4K4, PDHX, STAM2, NCAM1, ACP1, CMKLR1, NGF, NHS, PKD1, UTS2, MYH9, PGC, MTCO2P12, IFNL3, RAPGEF1, SORCS1, KIR3DL1, GPX3, KDR, P2RY12, TIMP3, SNAP23, FLVCR1, GRN, HDAC9, AMY2A, TNFSF14, COMT, RPL29, GPD1, PDE3B, RAPSN, DACT1, SPX, TRAF6, PVT1, CYP2D6, AKR1A1, KEAP1, MIR223, ALOX12, HDAC3, MARCHF1, ISG20, RNU1-1, ANGPT1, C1QTNF9, TNMD, GAS5, IL13, CXCL12, SPARC, ENO1, CCL16, GPR142, CXCL10, ENHO, STRA6, ST13, TFRC, NPC1, CACNA1E, STK11, STX1A, CCR2, PDK4, RUNX2, NRG1, ERBB2, S100A9, SQSTM1, C1QL3, BCAR1, CLPS, LRG1, TOMM40, GEM, ACACA, DDAH2, FKBP5, CISH, CDK4, LGR5, METRN, MUSK, CREB1, MIR17, FLAD1, TAS2R13, CD40LG, PSMA6, MIR143, SLC39A7, CLU, POU2F1, NR1H3, PTGES2, FOXP3, OLR1, PCNA, LRP5, GAPDH, SLC2A9, ABCB6, PRKCA, NR0B2, XRCC1, ENSA, CXCR4, F5, PLA2G10, NR4A1, PLA2G6, ABCG5, ACHE, FOXO3, FBRS, STAT5A, P2RX3, CACNA1D, FSD1, HPSE, NPPA, FGFR1, KLK3, ARSA, PRMT1, IGF2R, CHGA, KLF4, PPP1R3B, DHX40, ANXA1, PNPLA2, ELAVL2, ERP44, CIDEC, PRDM16, FBXO8, BMP7, VPS13C, STEAP4, NNMT, CCNL1, MCIDAS, HSPA2, APOD, KHDRBS1, APOH, DST, MIR30D, ADAM17, FCGR3B, FCGR3A, ISYNA1, POU2F3, OSM, MIR145, SMUG1, B2M, NR1H2, NTS, MIR152, TNFSF10, WNK1, UTS2R, TM7SF2, GGCT, WNT5B, TNFRSF12A, NUP62, DDAH1, COL18A1, CMA1, IMPACT, HEMGN, GFAP, TNFSF11, F2, SP6, F2R, OGN, FAAH, PDE5A, BTF3P11, IL18R1, PBX1, ERBB4, NBEAL2, SIRT4, TCF4, SIRT5, HCCS, ELOVL6, GTF2H1, TTR, CILP2, TEK, FSD1L, TERF1, TFAM, PHLPP1, BACE2, TRPV1, MIR182, G6PD, ESR2, VEGFC, TGFBI, GRB10, TGM2, BMP2, OPA1, PARL, LINC01194, SLC6A4, ENTPD1, PRKG1, CENPJ, DRD2, LOX, KCNJ1, DCTN4, MC3R, PPIG, TUBB4B, JAK2, JAK1, S100A8, CERS6, ITGAM, NOD1, SPRY2, RNR2, JPH3, ITGA2B, LAD1, TMEM154, LITAF, STK38, PTPN2, RPS6KB1, KLB, PLF, MBOAT4, UCN3, KCNMA1, ALOX5, KCNJ15, TIMM8A, SGSM3, BRD2, PLTP, CEACAM5, RRAD, PRTN3, KCNJ9, H6PD, RXRA, MUTYH, PSAT1, PROS1, IRAK1, ITGA2, ANGPTL2, PGR, AMD1P2, EBI3, LRP2, C1QTNF5, CREBRF, PPIA, ADCY3, PHOSPHO1, ABCB1, RAC1, LRP1, SFTPD, EGR1, CYP2J2, FOXD3, CAPN1, RN7SL263P, BMS1, COPA, RAD1, TFB1M, TMPRSS6, SERPINA1, C1QTNF1, AMD1, NTN1, C5AR2, CDK9, CD33, MMP8, CASQ1, METRNL, ALX4, CYP2C18, NPC1L1, TLR9, SCARB1, INTU, SELL, LARS2, CYBB, ARID1B, KLF7, MIR495, SLCO1B1, CX3CR1, DOK5, CYP2C8, CYP1A1, P2RY1, NCOA5, SLC27A4, MAGEE1, FST, GFPT2, DUSP12, LRPPRC, CDKN1B, CELA3A, RNLS, FAT1, FBN2, SLC52A2, FCGR2B, ATP6AP2, CDKN1C, PREX1, KMT2D, SEMA6A, KLHL42, CHRM3, MICA, CPT2, CDKN1A, CP, CRYZ, CDC42, COX4I1, NR1I3, FCN3, CTSD, FABP6, MIR486-1, COX8A, PDLIM5, PTPRU, CDK2, IVNS1ABP, ABCC5, POSTN, OGT, CSF2, HOTAIR, NISCH, AGXT2, BSG, P2RX2, DEFB103A, XYLT2, COL9A3, DYRK1A, MIR30C2, P2RX6, CIB1, EP300, RCAN1, FAM3A, MIR30C1, ABCG8, ATG7, MIR29C, SLC30A6, CAV3, EPHX2, ARID3A, CEBPB, GGA3, CEL, DNAJB3, MIR33A, MIR34C, MIR320A, CELA1, CAMP, CPB2, CALR, EGF, IL32, CAPN2, ADAM28, CES1, LILRB1, SLC25A20, CAPN3, SULF2, NOD2, HSPB3, EPOR, ARHGEF12, VASH1, ESRRA, TRIM72, SERPING1, ZNF410, COMP, MIR20B, PINK1, ICOSLG, CD5L, CHPT1, DAPK3, ABHD6, CYP17A1, CYP11B2, KLF5, MEG3, PDAP1, CYP3A5, SUCLA2, TXNRD2, CNDP2, ARHGAP22, TBC1D1, MEPE, KLRK1, SEMA3A, NPEPPS, AAA1, SPHK1, ATF7IP, PER2, DNASE1, FOXO6, SORBS1, TSC22D1, SARDH, NQO1, DHCR7, SOCS2, GDF11, P2RY2, NR4A3, SLAMF1, LDHA, LECT2, LGALS1, LIF, C1QTNF3, FAM3B, LMX1A, DUOX1, PVALB, ICOS, PTPRN, PTPN9, RMC1, CYP2R1, APLNR, AFP, AFM, KIF6, SMAD7, KCNIP1, ADORA1, MAPT, DUOX2, MBP, IL20, ADH1B, PLIN2, MDM2, MEF2A, NANS, FRMD3, TERF2IP, ALOX5AP, IL1R1, IL6ST, SLC39A1, IL12B, SDC2, SDC1, CXCL5, SRL, ALOX15, SPINK4, ITGAX, MSMO1, TSPAN31, S100B, COPD, SFXN1, GHS, RXRG, KCNJ6, DESI1, RRAS, PRRT2, DLL1, RORC, NPAS4, KISS1, KLK1, KRT18, PRSS55, PRKCD, LARP1BP2, HDAC7, PIK3C2G, TAAR1, NM, SLC25A3, PHB, ATP6V1H, PGF, PFKM, NOTCH1, NT5C3A, PEG3, NPHS1, BFAR, IL23A, ERFE, TRPM6, ACAT1, PDCD1, PWAR1, PCYT1A, OCA2, R3HDML, PCBD1, OPRM1, P2RX1, P2RX4, P2RX5, PAK1, ACLY, NFKBIA, PRKAR1A, POR, PRKAB2, MMP7, MMP12, MMP13, SRGN, PTPA, MMP14, MRC1, RNU6-392P, GPRC5B, GAL, MT1E, FITM2, MT1X, NF2, MTHFD1, METTL9, PLXNA2, SLC35G1, PLK1, GNPDA2, PLD1, PLCG1, PLAGL1, PLAG1, PLA2G1B, PKNOX1, PKLR, IKBKB, CHIT1, CRISPLD2, AZGP1, GSN, KLRC4-KLRK1, GSR, UGT2B15, TF, TERT, GATA6, SERPINA3, ANGPTL6, TERC, TXN2, VIPR1, UCHL1, TMEM132A, TAPBP, CFH, VLDLR, ERVK-18, C1QTNF12, HLA-DMA, ATP5PF, GAST, VTN, STX4, BID, GFER, STAT5B, TLR3, TRH, ACAD10, CRISP2, GLA, CEP55, CD2AP, CBLIF, P2RX5-TAX1BP3, MIR107, BCR, CIMT, GPR39, THBS1, TTN, GHR, FFAR2, TLE1, TKT, TXN, GCA, GPS2, KLF10, SESN2, GFPT1, ARID5B, GORASP2, MIR199A1, FGL1, SPINK1, AQP9, SOX4, SORD, SNRNP70, FKBP4, AOC2, ANXA6, SPZ1, HTN1, SLC30A1, APPL1, HTR2A, SLC16A1, TRPM7, ANGPT2, GPC5, SLC6A2, ST8SIA4, SLC2A5, ANKRD55, IGFALS, QRSL1, FHL1, MIR199A2, MIR20A, STAT4, LINC-ROR, PGR-AS1, SSTR5, WNT5A, MIR130A, ONECUT1, FLT1, SREBF2, NAT10, C4B_2, MYDGF, LOC107832851, DMAP1, LARP6, LY75-CD302, RASD1, RBM14-RBM4, LSR, NBAS, DEFB4B, MCS+9.7, HMGA1P8, LOC110806263, MMP26, RHOT1, CCL28, ALG1, METTL3, LIN7C, LINC00994, DIP, RPS10-NUDT3, GNG12-AS1, RAB14, WASHC1, CYRIB, VIM-AS1, NDUFA12, SLC50A1, NEIL3, LOC102723996, SIRT1-AS, THRIL, MIR1910, SLC38A2, ALL2, NLGN3, CASZ1, ENAH, ZFAND6, OPN1MW3, VPS35, EXOSC4, RNPC3, UGT1A10, UGT1A8, UGT1A7, ERRFI1, UGT1A5, UGT1A9, MIR3188, TEMPS, UGT1A4, BNC2, TRPM4, TET2, FBLIM1, SALRNA1, CBSL, LOC102723971, UGT1A3, TREM2, MIR3939, APPL2, MOCOS, ZC4H2, LGR4, DEFB103B, COMMD3-BMI1, MIR4756, USE1, ASAH2, ENOX1, BOP, CAMK2N1, SLC6A20, SLC52A1, CST12P, SAGE1, PLUT, WWOX, LRP1-AS, ADA2, MIR3666, IL17D, SHC3, CERNA3, HDL3, FXYD5, MIR4463, PERCC1, SOX6, UGGT2, ROBO4, DUSP26, SUCNR1, IGSF21, CISD3, TIMD4, TRIM47, KCTD1, MIF-AS1, TTC28-AS1, EXOC3L2, SLC9C1, UCN2, CYP4V2, WNT3A, GALP, SLC22A16, LY86-AS1, KRT90P, DSEL, HCCAT5, GORAB, BIRC8, AD7, RNU12, AQP11, H19, TXNRD3, SLC46A1, OPN4, PRDM6, CGB8, CGB5, MUC19, LINC00523, PGP, TRMT10A, ABCC11, BPIFA4P, HS6ST3, MMAB, PHF6, ZACN, SLC27A1, LINC-PINT, MALAT1, PPP1R1B, KAT8, CHKB-CPT1B, SLC41A2, HORMAD1, IMMP2L, LEKR1, SAMD12, MIXL1, GPR61, LINC01193, PWAR4, C7orf50, GLYR1, UBASH3B, ORAI1, PTPN5, GPIHBP1, MFSD9, HCAR2, ZNF469, ZBED3, ZGPAT, BRINP3, ZFP69, HSD17B13, ACTBL2, L3MBTL3, TIRAP, TAS2R12P, TAS1R3, NRK, CLDN19, SIK1, UPP2, PPM1K, SLC2A12, CBLL2, FAM3D, ACVR1C, DQX1, SGMS2, NLRP6, ARID2, PIFO, MLKL, TET3, PDIK1L, MTPN, LRGUK, ROMO1, OR2AG1, PIWIL4, SESN3, FGFBP3, GSC, MT1P3, HT, GPAT4, BEAN1, CD300LG, PTPRVP, SLC30A7, IL23R, FAM78B, CENPX, KLHDC7A, SGMS1, MED19, CADM2, ANGPTL5, DCD, THEM4, TADA1, AKNAD1, SLC41A1, OLIG1, SLC22A12, CASC2, ANKK1, OSBPL8, PTF1A, WDR72, NEGR1, HCG27, IL27, SPESP1, MARCHF8, FOLH1B, TPRG1L, LYPLAL1, UNC5B, TCHHL1, SKA1, MSI2, GGTA2P, JMJD1C, SLC39A12, TPPP2, SPIC, RFX6, SLC29A4, SETDB2, INHBE, MICC, MT1IP, CCAR2, MIR323B, MARK4, MIR146B, MIR202, SPTBN4, MIR496, MIR499A, MIER1, USP37, NPS, CHD8, POTEM, TSHZ3, ECSCR, HNP1, MIR424, MIR382, SLC25A19, EIF2AK4, IGAN1, NIF3L1, ELOVL5, BACH2, EXOC4, RNASEK, MIR378A, PLIN5, POTEKP, PGBP, UBL5, CXCL16, NEUROD4, POU5F1P3, CHCHD2P9, TNFSF12-TNFSF13, USP36, KMT5AP1, MUC5B, OPN1MW2, CPA6, HYMAI, CDK11A, SLC12A9, ARNTL2, CA10, SMARCAD1, OCTN3, CELF4, SPHK2, MIR708, C20orf181, MIR661, GOPC, PELI1, KIDINS220, POU5F1P4, CXADRP1, NCF1, CFAP97, WASH6P, XPO5, MIR590, MIR657, MIR593, PLEKHG5, MRS2, GJD2, ATP10A, SLC39A10, PROK2, MIR99A, TOMM5, MUL1, ASRGL1, MIR15A, MIR15B, MIR18A, MIR187, STN1, MIR200B, ADM2, PRR5L, BBS10, LIN28A, NLRX1, NEIL1, MIR206, TNFAIP8L2, MIR154, MOGAT2, MIR147A, MIR106B, MFRP, MED25, TLR10, NIPA2, MOB2, COLEC12, SETD7, ALPK1, TAS1R2, MIR125A, MIR128-1, TSEN2, MIR132, COASY, MIR210, IRX3, MIR95, MBOAT7, WDR13, MIR296, PDIA2, GORASP1, DCLRE1C, GMCL2, GMCL1, NFKBIZ, NSD1, MIR30E, FN3K, DMRTA1, MIR31, SLC17A9, UBE2O, FNDC4, GNPNAT1, RFX7, GRAMD2B, MIR217, LY6G6E, MIR219A1, KCTD15, MIR22, VKORC1, MIR23A, SLC30A5, MIR23B, BRD9, WNK4, MIR26B, FRTS1, ACD, SCLY, UTRN, LARS1, HACD3, IK, IGH, IGFBP5, IGFBP4, IFNA13, IFNA1, ICAM3, HTR4, HTR2B, HTC2, HSPD1, HSP90AA1, HSPB2, HSPB1, HSPA9, HSD11B2, HES1, HRC, HRAS, HOXA5, HNRNPK, HNRNPF, HNRNPA1, FOXA3, HMBS, IL3, IL4R, IL7, KCNJ10, L1CAM, KRT31, KRT19, KRT7, KPNA1, KIR3DL2, KIR2DS1, KEL, KCNN3, KCNN2, KCNK3, KCNJ3, CXCR1, KCND3, KCNC4, KCNB1, ITGB2, INSIG1, IMPA1, ILK, TNFRSF9, IL16, IL15RA, IL12A, HLF, HLA-DRA, HLA-DQB2, GDF1, GNAO1, GLRX, GLS, GCLC, GLB1, GK, GJA8, GJA4, GH2, GDNF, GDF2, OPN1MW, SFN, GCH1, GBP2, GATA4, GATA3, GAP43, GALNT2, GABRG2, GABPB1, FUT6, FUT2, NR5A1, GOLGB1, GPI, HLA-DQA2, HSD17B10, HLA-DPB1, HLA-DOA, HLA-DMB, HLA-A, CFHR2, HCRT, HBA2, HAS3, HARS1, HADH, HADHA, GZMB, GPM6A, GYG1, GTF3A, GSTA4, GSTA1, GRB2, FFAR3, GPR35, GPER1, GPR21, CXCR3, GPR1, LAMB3, LAMP1, LAMC2, CCN3, OAS3, NR4A2, NUCB1, NTRK1, YBX1, SLC11A2, NPY2R, NPR3, NPR2, NPR1, NPM1, NME1, P4HB, NGFR, NFYC, NFYB, NFYA, NFATC1, NEFL, NDUFS4, NAGLU, MYO5A, MYLK, MYL2, OMG, PAEP, MYF5, PDK2, PIN1, PIK3C3, PIK3C2A, SERPINE2, SERPINB6, PGM1, PFKFB3, PFKFB2, PFDN2, PER1, PECAM1, PDHB, PRDX1, PDGFRB, PDGFB, PDE4D, PDC, PDB1, PCOLCE, SERPINA5, PCDH8, PAWR, PAPPA, SERPINB2, MYH6, MYD88, LAMP2, SH2D1A, MAX, MAS1, MAOA, MAN2A1, MAN1A1, MAFD2, SMAD3, SMAD2, SMAD1, MXD1, LYZ, LY75, MC5R, LY9, LTF, LTBR, CYP4F3, LRP6, LPP, LOXL2, FADS3, LIPA, LCN1, STMN1, MB, SMCP, MUC1, MST1, MTRR, RNR1, ATP8, MT1L, MT1M, MT1JP, MT1H, MT1G, MT1F, MT1B, MSX2, MSH5, ADAM11, MSH2, MPI, ALDH6A1, KMT2A, MGST3, MGP, MGAT2, MFAP2, MAP3K5, MEF2C, ME1, FOS, FOLR2, FOLR1, CA5A, CCND3, CCKBR, CBR3, CBR1, RUNX3, RUNX1, CAV2, CAMK2A, CALCR, CACNB3, CACNA1C, CA2, CD4, VPS51, C5, CAPN5, C4B, C4A, TSPO, BRCA1, BPI, BNIP3, BMP6, BMI1, CD247, CD86, BLK, CGA, AP3S1, CKM, CKB, CIDEA, CHRNB4, CHRNA4, CHN2, CHM, CEACAM7, CEACAM3, CGB3, CFTR, CD34, CTSC, CENPA, CECR, CEBPA, CDX2, CDKN3, CDK6, CDH13, CDH2, CD48, ENTPD3, BLVRA, BGN, CLCN3, AIF1, AMY1C, AMY1B, AMY1A, BIN1, AMPD1, AMH, ALPP, ALPL, ALDH3B1, ALCAM, ALAS1, AIC, ANXA5, ADORA3, ADORA2B, ADH1C, ADD1, ADCYAP1, ACVR2B, ACTG2, ACTG1, ACTB, ACAA1, AAVS1, ANK2, APCS, CFB, ATIC, BCS1L, OPN1SW, HCN2, BCAT1, AVPR2, ATP5PO, ATP7A, ATP5MC1, ATP4A, ATP2B1, ATP12A, ATHS, BIRC2, SERPINC1, ARSL, ARR3, RND3, RHOA, AQP5, AQP2, FASLG, APOC4, APOC2, BIRC3, CLCN2, CLCN5, FOLH1, EFNB3, EPHA4, ENO2, MARK2, ELK3, ELAVL1, EIF4G1, EIF4EBP1, EIF4A2, EGR3, EGR2, CELSR2, EFNB2, EPHX1, LPAR1, TYMP, EBM, E2F1, DUSP6, DRD3, DPYS, DPYD, DPT, DNTT, DMP1, EPHB1, ERBB3, DLD, FASN, FMO3, FLNA, FLII, FHIT, FGFR4, FGF11, GPC4, FDXR, FCP1, FCGRT, FBP1, FAP, ERG, FABP5, FABP3, F2RL2, F2RL1, EXT1, EVC, ETV3, ETFA, ESRRG, ESRRB, FBL, DMBT1, SEPTIN1, CLK2, COL17A1, CS, CRMP1, CREM, CREBBP, CRABP2, CPT1B, COX10, COX7A1, COX5B, MAP3K8, CORT, COL9A2, CSHL1, COL9A1, COL8A1, COL6A3, COL4A5, COL4A2, COL2A1, COL1A1, CNTF, CNR2, CMM, CCR1, CSF3, CST2, DIAPH2, BRINP1, CFD, DES, DEFB4A, DEFA3, DEFA1, DDX3X, DDT, AKR1C2, DCN, DBI, DBH, CYP27B1, CTAA1, CYP27A1, CYP8B1, CYP7A1, CYP2A6, CYP1B1, CYB5A, CXADR, CUX1, CTSL, CTSH, CTRL, PKM, PLA2G4A, PLEK, RBM14, SPTLC1, AGPAT1, PROCR, HYOU1, CARM1, UNC13B, CAP1, TIMM44, FAM3C, IFI30, LYPLA1, SPON1, SLC19A2, SPON2, NSA2, PEMT, ATP8A1, DLC1, CITED2, KLF2, WARS2, TCIRG1, SIGMAR1, FSTL3, SLC35A1, OLFM4, OLIG2, CCL27, BTN2A1, ADAMTS13, ESM1, LIAS, METAP2, EHD1, MALT1, FGL2, NMU, CD300C, CYP46A1, PPP1R13L, NPC2, CPLX1, WASF3, STARD10, SLC17A3, CAPN9, EBP, CD226, CTCF, IGF2BP3, IGF2BP1, USP16, ZMPSTE24, FLOT1, TREH, AIM2, GDF3, CXCL14, STXBP5L, GAL3ST1, ADAMTS2, ATG5, AKAP6, CHST3, FHL5, HOMER1, EIF2AK3, ITM2B, KIF20B, NCR1, TJP2, PEX16, TMPRSS11D, TGFBRAP1, ADGRG1, PIWIL1, ITGB1BP1, MSC, LARGE1, HACD1, SOX13, WTAP, TRIM13, MAFB, NUTF2, MPHOSPH10, TSHZ1, RBM6, HIPK3, PREB, AKT3, SCO2, KCNE2, THRAP3, EXOG, RNF10, NCOR1, SGSM2, HEPH, IP6K1, TOX, HDAC4, SART3, ECE2, AQR, EIF5B, LPIN2, NCOR2, PTPRT, MAP4K5, SLC16A7, DHDH, MCTS1, RGCC, SLC27A6, REM1, TRBV7-8, IGHD1-14, SLCO1B3, PCLO, MCAT, EIF3K, PDLIM3, SESN1, KLF15, SIT1, SERP1, IL17B, DISC1, DKK4, SIGLEC7, ACAD8, GREM1, BSCL2, PCOLCE2, CNNM1, DBNL, TBK1, HSPB8, MBL3P, CSAD, WAC, BPIFA1, TLR7, DNAJC27, IGF2-AS, GP6, IPO11, HSPA14, IRAK4, SLC35B3, G0S2, MYLIP, SLC40A1, TBX21, ERO1A, SLC2A8, SLC39A3, RHOD, PADI1, GPR132, HOOK2, CD274, CTNNA3, NUPR1, MYCBP, CHEK2, FAIM2, PSD3, SYNE1, TTC28, COBL, ARC, SIK2, FBXO28, SYT11, TBC1D9, CAND2, KDM1A, NT5C2, DICER1, RAB18, SACM1L, SBNO2, CARD8, MLXIP, COG2, ACOT7, MGAT4A, SLCO2B1, PTGDR2, AKAP13, CRTC1, NCS1, KLHL3, PANX1, PITPNC1, KIFBP, ATRNL1, TENM4, TKFC, PART1, MGAT4C, ARIH1, KLK5, TAFA5, SLC39A6, LY96, ZFPM2, BACE1, ZMYND8, DAPK2, FAM215A, SEC14L2, PES1, BRD4, TRAM1, NPTXR, TRS-AGA2-3, MLYCD, SLC33A1, ZBED1, SERPINF2, XCL1, SLC2A3, SLC1A7, SLC1A5, SKP2, SKIL, SIX3, SHC1, SRSF5, SELPLG, SDHA, CX3CL1, CCL22, SLC6A8, CCL20, CCL11, CCL8, CCL7, CCL4, CCL3, SCO1, SCN8A, SCN7A, SCN2A, SAA2, SLC5A5, SLC8A1, S100A12, SRI, TADA2A, TACR3, TAC3, TAC1, SYT4, SYT1, STXBP3, STX5, STIM1, STC1, SSTR2, SRD5A2, SLC9A3, SPRR2A, SPG7, SOX5, SOX2, SORL1, SIGLEC1, SMPD1, SLPI, SLCO1A2, SLC18A2, SLC10A2, SAA1, S100A4, TAL1, DNAJC3, PTMAP4, PTMA, PTGER3, PTBP1, PTAFR, PSMD3, PSMD2, PSMB6, PSMA7, PSG2, TMPRSS15, EIF2AK2, PTPN6, MAPK7, PRKD1, PPP1R2, POU3F1, POU2F2, PODXL, SEPTIN5, PNLIP, PMM2, PML, PMAIP1, PTPN4, PTPN11, RYR2, REG1B, RTN1, CLIP1, RPS19, RPS6KA3, RPS6KA2, RPN2, RPE, RORB, RNH1, RIT2, REV3L, REL, PTPRB, RCN2, RARB, RANGAP1, RAG1, RAB27A, RAB5B, RAB4A, PYGB, PTPRS, PTPRF, PTPRC, TAF1, TCP1, HTR3B, API5, ADAM19, MBTPS1, TNFRSF25, PAGE1, VAMP4, VAMP8, HSD17B6, JRK, KHSRP, DENR, PIAS1, CST7, TNFRSF14, DGKZ, IRS4, DOC2B, DYRK3, LOH19CR1, BRAP, PICALM, ZNF239, SLC14A2, AAAS, FOSL1, TNFSF12, RAB11A, MAFK, NOL3, PCSK7, HGS, MTMR7, USP2, USP14, PAPSS2, RPL14, CCRL2, TAF1C, F2RL3, KALRN, TRPA1, RIPK2, EIF2B5, ZPR1, FUBP1, PER3, TMEM11, BANF1, GALR2, TNFRSF11A, DLK1, TNFRSF18, SIGLEC5, ECB2, HBFQTL2, PRDX2, TLL1, HSP90B1, NR2C2, TPO, TPM4, TPM1, TOP2A, TOP1, TNFAIP3, NR2E1, TLR5, TLR1, TLE3, TRPM2, TJP1, TIMP2, TIAM1, THBS4, THBS2, TGFB2, TGFA, TFPI, TFAP2A, TERF2, TEP1, TRAF3, TST, TFEB, NSD2, LAP, PRRC2A, MANF, SLMAP, ZNF236, ZFP36, SF1, YWHAG, YY1, XDH, XBP1P1, WARS1, TNFRSF4, VPREB1, VEGFB, VDAC1, UPK2, UGT1A, UGCG, SCGB1A1, UBE2B, TYROBP, TYK2, TXNRD1, LINC02605

Type 2 Diabetes Mayo Clinic

Overview Type 2 diabetes is a condition that happens because of a problem in the way the body regulates and uses sugar as a fuel. That sugar also is called glucose. This long-term condition results in too much sugar circulating in the blood. Eventually, high blood sugar levels can lead to disorders of the circulatory, nervous and immune systems. In type 2 diabetes, there are primarily two problems. The pancreas does not produce enough insulin — a hormone that regulates the movement of sugar into the cells. And cells respond poorly to insulin and take in less sugar. Type 2 diabetes used to be known as adult-onset diabetes, but both type 1 and type 2 diabetes can begin during childhood and adulthood.
Type 2 Diabetes MedlinePlus

Type 2 diabetes is a disorder characterized by abnormally high blood sugar levels. In this form of diabetes, the body stops using and making insulin properly. Insulin is a hormone produced in the pancreas that helps regulate blood sugar levels. Specifically, insulin controls how much glucose (a type of sugar) is passed from the blood into cells, where it is used as an energy source. When blood sugar levels are high (such as after a meal), the pancreas releases insulin to move the excess glucose into cells, which reduces the amount of glucose in the blood.
Type 2 Diabetes Wikipedia

Type of diabetes mellitus with high blood sugar and insulin resistance Type 2 diabetes Other names Diabetes mellitus type 2; adult-onset diabetes; [1] noninsulin-dependent diabetes mellitus (NIDDM) Universal blue circle symbol for diabetes [2] Pronunciation / d aɪ ə b iː t ə s / Specialty Endocrinology Symptoms Increased thirst , frequent urination , unexplained weight loss , increased hunger [3] Complications Hyperosmolar hyperglycemic state , diabetic ketoacidosis , heart disease , strokes , diabetic retinopathy , kidney failure , amputations [1] [4] [5] Usual onset Middle or older age [6] Duration Long term [6] Causes Obesity , lack of exercise, genetics [1] [6] Diagnostic method Blood test [3] Prevention Maintaining normal weight, exercising , eating properly [1] Treatment Dietary changes , metformin , insulin, bariatric surgery [1] [7] [8] [9] Prognosis 10 year shorter life expectancy [10] Frequency 392 million (2015) [11] Type 2 diabetes ( T2D ), formerly known as adult-onset diabetes , is a form of diabetes that is characterized by high blood sugar , insulin resistance , and relative lack of insulin . [6] Common symptoms include increased thirst , frequent urination , and unexplained weight loss . [3] Symptoms may also include increased hunger , feeling tired, and sores that do not heal. [3] Often symptoms come on slowly. [6] Long-term complications from high blood sugar include heart disease , strokes , diabetic retinopathy which can result in blindness , kidney failure , and poor blood flow in the limbs which may lead to amputations . [1] The sudden onset of hyperosmolar hyperglycemic state may occur; however, ketoacidosis is uncommon. [4] [5] Type 2 diabetes primarily occurs as a result of obesity and lack of exercise. [1] Some people are more genetically at risk than others. [6] Type 2 diabetes makes up about 90% of cases of diabetes , with the other 10% due primarily to type 1 diabetes and gestational diabetes . [1] In type 1 diabetes there is a lower total level of insulin to control blood glucose, due to an autoimmune induced loss of insulin-producing beta cells in the pancreas . [12] [13] Diagnosis of diabetes is by blood tests such as fasting plasma glucose , oral glucose tolerance test , or glycated hemoglobin (A1C). [3] Type 2 diabetes is largely preventable by staying a normal weight, exercising regularly, and eating properly. [1] Treatment involves exercise and dietary changes . [1] If blood sugar levels are not adequately lowered, the medication metformin is typically recommended. [7] [14] Many people may eventually also require insulin injections. [9] In those on insulin, routinely checking blood sugar levels is advised; however, this may not be needed in those taking pills. [15] Bariatric surgery often improves diabetes in those who are obese. [8] [16] Rates of type 2 diabetes have increased markedly since 1960 in parallel with obesity. [17] As of 2015 there were approximately 392 million people diagnosed with the disease compared to around 30 million in 1985. [11] [18] Typically it begins in middle or older age, [6] although rates of type 2 diabetes are increasing in young people. [19] [20] Type 2 diabetes is associated with a ten-year-shorter life expectancy. [10] Diabetes was one of the first diseases described. [21] The importance of insulin in the disease was determined in the 1920s. [22] Contents 1 Signs and symptoms 1.1 Complications 2 Causes 2.1 Lifestyle 2.2 Genetics 2.3 Medical conditions 3 Pathophysiology 4 Diagnosis 5 Screening 6 Prevention 7 Management 7.1 Lifestyle 7.2 Medications 7.2.1 Blood sugar control 7.2.2 Blood pressure lowering 7.2.3 Other 7.3 Surgery 8 Epidemiology 9 History 10 References 11 External links Signs and symptoms Overview of the most significant symptoms of diabetes. The classic symptoms of diabetes are frequent urination ( polyuria ), increased thirst ( polydipsia ), increased hunger ( polyphagia ), and weight loss . [23] Other symptoms that are commonly present at diagnosis include a history of blurred vision , itchiness , peripheral neuropathy , recurrent vaginal infections , and fatigue . [13] Other symptoms may include loss of taste . [24] Many people, however, have no symptoms during the first few years and are diagnosed on routine testing. [13] A small number of people with type 2 diabetes can develop a hyperosmolar hyperglycemic state (a condition of very high blood sugar associated with a decreased level of consciousness and low blood pressure ). [13] Complications Main article: Complications of diabetes Type 2 diabetes is typically a chronic disease associated with a ten-year-shorter life expectancy. [10] This is partly due to a number of complications with which it is associated, including: two to four times the risk of cardiovascular disease , including ischemic heart disease and stroke ; a 20-fold increase in lower limb amputations , and increased rates of hospitalizations . [10] In the developed world, and increasingly elsewhere, type 2 diabetes is the largest cause of nontraumatic blindness and kidney failure . [25] It has also been associated with an increased risk of cognitive dysfunction and dementia through disease processes such as Alzheimer's disease and vascular dementia . [26] Other complications include hyperpigmentation of skin ( acanthosis nigricans ), sexual dysfunction , and frequent infections. [23] There is also an association between type 2 diabetes and mild hearing loss. [27] Causes The development of type 2 diabetes is caused by a combination of lifestyle and genetic factors. [25] [28] While some of these factors are under personal control, such as diet and obesity , other factors are not, such as increasing age, female gender, and genetics. [10] Obesity is more common in women than men in many parts of Africa. [29] The nutritional status of a mother during fetal development may also play a role, with one proposed mechanism being that of DNA methylation . [30] The intestinal bacteria Prevotella copri and Bacteroides vulgatus have been connected with type 2 diabetes. [31] Lifestyle Main article: Lifestyle causes of type 2 diabetes Lifestyle factors are important to the development of type 2 diabetes, including obesity and being overweight (defined by a body mass index of greater than 25), lack of physical activity, poor diet, stress , and urbanization . [10] [32] Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of cases in Pima Indians and Pacific Islanders. [13] Among those who are not obese, a high waist–hip ratio is often present. [13] Smoking appears to increase the risk of type 2 diabetes. [33] A lack of sleep has also been linked to type 2 diabetes. [34] Laboratory studies have linked short-term sleep deprivations to changes in glucose metabolism, nervous system activity, or hormonal factors that may lead to diabetes. [34] Dietary factors also influence the risk of developing type 2 diabetes. Consumption of sugar-sweetened drinks in excess is associated with an increased risk. [35] [36] The type of fats in the diet are important, with saturated fats and trans fatty acids increasing the risk, and polyunsaturated and monounsaturated fat decreasing the risk. [28] Eating a lot of white rice appears to play a role in increasing risk. [37] A lack of exercise is believed to cause 7% of cases. [38] Persistent organic pollutants may also play a role. [39] Genetics Main article: Genetic causes of type 2 diabetes Most cases of diabetes involve many genes , with each being a small contributor to an increased probability of becoming a type 2 diabetic. [10] The proportion of diabetes that is inherited is estimated at 72%. [40] More than 36 genes and 80 single nucleotide polymorphisms (SNPs) had been found that contribute to the risk of type 2 diabetes. [41] [42] All of these genes together still only account for 10% of the total heritable component of the disease. [41] The TCF7L2 allele , for example, increases the risk of developing diabetes by 1.5 times and is the greatest risk of the common genetic variants. [13] Most of the genes linked to diabetes are involved in pancreatic beta cell functions. [13] There are a number of rare cases of diabetes that arise due to an abnormality in a single gene (known as monogenic forms of diabetes or "other specific types of diabetes" ). [10] [13] These include maturity onset diabetes of the young (MODY), Donohue syndrome , and Rabson–Mendenhall syndrome , among others. [10] Maturity onset diabetes of the young constitute 1–5% of all cases of diabetes in young people. [43] Medical conditions There are a number of medications and other health problems that can predispose to diabetes. [44] Some of the medications include: glucocorticoids , thiazides , beta blockers , atypical antipsychotics , [45] and statins . [46] Those who have previously had gestational diabetes are at a higher risk of developing type 2 diabetes. [23] Other health problems that are associated include: acromegaly , Cushing's syndrome , hyperthyroidism , pheochromocytoma , and certain cancers such as glucagonomas . [44] Individuals with cancer may be at a higher risk of mortality if they also have diabetes. [47] Testosterone deficiency is also associated with type 2 diabetes. [48] [49] Eating disorders may also interact with type 2 diabetes, with bulimia nervosa increasing the risk and anorexia nervosa decreasing it. [50] Pathophysiology Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance . [13] Insulin resistance, which is the inability of cells to respond adequately to normal levels of insulin, occurs primarily within the muscles, liver , and fat tissue. [51] In the liver, insulin normally suppresses glucose release. However, in the setting of insulin resistance, the liver inappropriately releases glucose into the blood. [10] The proportion of insulin resistance versus beta cell dysfunction differs among individuals, with some having primarily insulin resistance and only a minor defect in insulin secretion and others with slight insulin resistance and primarily a lack of insulin secretion. [13] Other potentially important mechanisms associated with type 2 diabetes and insulin resistance include: increased breakdown of lipids within fat cells , resistance to and lack of incretin , high glucagon levels in the blood, increased retention of salt and water by the kidneys, and inappropriate regulation of metabolism by the central nervous system . [10] However, not all people with insulin resistance develop diabetes since an impairment of insulin secretion by pancreatic beta cells is also required. [13] In the early stages of insulin resistance, the mass of beta cells expands, increasing the output of insulin to compensate for the insulin insensitivity. [52] But when type 2 diabetes has become manifest, a type 2 diabetic will have lost about half of their beta cells. [52] Fatty acids in the beta cells activate FOXO1 , resulting in apopotosis of the beta cells. [52] Diagnosis WHO diabetes diagnostic criteria [53] [54] edit Condition 2-hour glucose Fasting glucose HbA 1c Unit mmol/L mg/dL mmol/L mg/dL mmol/mol DCCT % Normal < 7.8 < 140 < 6.1 < 110 < 42 < 6.0 Impaired fasting glycaemia < 7.8 < 140 6.1–7.0 110–125 42–46 6.0–6.4 Impaired glucose tolerance ≥ 7.8 ≥ 140 < 7.0 < 126 42–46 6.0–6.4 Diabetes mellitus ≥ 11.1 ≥ 200 ≥ 7.0 ≥ 126 ≥ 48 ≥ 6.5 The World Health Organization definition of diabetes (both type 1 and type 2) is for a single raised glucose reading with symptoms, otherwise raised values on two occasions, of either: [55] fasting plasma glucose ≥ 7.0 mmol/l (126 mg/dl) or with a glucose tolerance test , two hours after the oral dose a plasma glucose ≥ 11.1 mmol/l (200 mg/dl) A random blood sugar of greater than 11.1 mmol/l (200 mg/dl) in association with typical symptoms [23] or a glycated hemoglobin (HbA 1c ) of ≥ 48 mmol/mol (≥ 6.5 DCCT %) is another method of diagnosing diabetes. [10] In 2009 an International Expert Committee that included representatives of the American Diabetes Association (ADA), the International Diabetes Federation (IDF), and the European Association for the Study of Diabetes (EASD) recommended that a threshold of ≥ 48 mmol/mol (≥ 6.5 DCCT %) should be used to diagnose diabetes. [56] This recommendation was adopted by the American Diabetes Association in 2010. [57] Positive tests should be repeated unless the person presents with typical symptoms and blood sugars >11.1 mmol/l (>200 mg/dl). [56] ADA diabetes diagnostic criteria in 2015 [58] edit Diabetes mellitus Prediabetes HbA 1c ≥6.5% 5.7-6.4% Fasting glucose ≥126 mg/dL 100-125 mg/dL 2h glucose ≥200 mg/dL 140-199 mg/dL Random glucose with classic symptoms ≥200 mg/dL Not available Threshold for diagnosis of diabetes is based on the relationship between results of glucose tolerance tests, fasting glucose or HbA 1c and complications such as retinal problems . [10] A fasting or random blood sugar is preferred over the glucose tolerance test, as they are more convenient for people. [10] HbA 1c has the advantages that fasting is not required and results are more stable but has the disadvantage that the test is more costly than measurement of blood glucose. [59] It is estimated that 20% of people with diabetes in the United States do not realize that they have the disease. [10] Type 2 diabetes is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency. [60] This is in contrast to type 1 diabetes in which there is an absolute insulin deficiency due to destruction of islet cells in the pancreas and gestational diabetes that is a new onset of high blood sugars associated with pregnancy. [13] Type 1 and type 2 diabetes can typically be distinguished based on the presenting circumstances. [56] If the diagnosis is in doubt antibody testing may be useful to confirm type 1 diabetes and C-peptide levels may be useful to confirm type 2 diabetes, [61] with C-peptide levels normal or high in type 2 diabetes, but low in type 1 diabetes. [62] Screening No major organization recommends universal screening for diabetes as there is no evidence that such a program improve outcomes. [63] [64] Screening is recommended by the United States Preventive Services Task Force (USPSTF) in adults without symptoms whose blood pressure is greater than 135/80 mmHg. [65] For those whose blood pressure is less, the evidence is insufficient to recommend for or against screening. [65] There is no evidence that it changes the risk of death in this group of people. [64] They also recommend screening among those who are overweight and between the ages of 40 and 70. [66] The World Health Organization recommends testing those groups at high risk [63] and in 2014 the USPSTF is considering a similar recommendation. [67] High-risk groups in the United States include: those over 45 years old; those with a first degree relative with diabetes; some ethnic groups, including Hispanics, African-Americans, and Native-Americans; a history of gestational diabetes ; polycystic ovary syndrome ; excess weight; and conditions associated with metabolic syndrome . [23] The American Diabetes Association recommends screening those who have a BMI over 25 (in people of Asian descent screening is recommended for a BMI over 23). [68] Prevention Main article: Prevention of type 2 diabetes Onset of type 2 diabetes can be delayed or prevented through proper nutrition and regular exercise. [69] [70] Intensive lifestyle measures may reduce the risk by over half. [25] [71] The benefit of exercise occurs regardless of the person's initial weight or subsequent weight loss. [72] High levels of physical activity reduce the risk of diabetes by about 28%. [73] Evidence for the benefit of dietary changes alone, however, is limited, [74] with some evidence for a diet high in green leafy vegetables [75] and some for limiting the intake of sugary drinks. [76] There is an association between higher intake of sugar-sweetened fruit juice and diabetes, but no evidence of an association with 100% fruit juice. [77] A 2019 review found evidence of benefit from dietary fiber . [78] In those with impaired glucose tolerance , diet and exercise either alone or in combination with metformin or acarbose may decrease the risk of developing diabetes. [25] [79] Lifestyle interventions are more effective than metformin. [25] A 2017 review found that, long term, lifestyle changes decreased the risk by 28%, while medication does not reduce risk after withdrawal. [80] While low vitamin D levels are associated with an increased risk of diabetes, correcting the levels by supplementing vitamin D3 does not improve that risk. [81] Management Further information: Diabetes management Management of type 2 diabetes focuses on lifestyle interventions, lowering other cardiovascular risk factors, and maintaining blood glucose levels in the normal range. [25] Self-monitoring of blood glucose for people with newly diagnosed type 2 diabetes may be used in combination with education, [82] although the benefit of self-monitoring in those not using multi-dose insulin is questionable. [25] In those who do not want to measure blood levels, measuring urine levels may be done. [82] Managing other cardiovascular risk factors, such as hypertension , high cholesterol , and microalbuminuria , improves a person's life expectancy. [25] Decreasing the systolic blood pressure to less than 140 mmHg is associated with a lower risk of death and better outcomes. [83] Intensive blood pressure management (less than 130/80 mmHg) as opposed to standard blood pressure management (less than 140-160 mmHg systolic to 85–100 mmHg diastolic) results in a slight decrease in stroke risk but no effect on overall risk of death. [84] Intensive blood sugar lowering (HbA 1c <6%) as opposed to standard blood sugar lowering (HbA 1c of 7–7.9%) does not appear to change mortality. [85] [86] The goal of treatment is typically an HbA 1c of 7 to 8% or a fasting glucose of less than 7.2 mmol/L (130 mg/dl); however these goals may be changed after professional clinical consultation, taking into account particular risks of hypoglycemia and life expectancy. [68] [87] [88] Hypoglycemia is associated with adverse outcomes in older people with type 2 diabetes. [89] Despite guidelines recommending that intensive blood sugar control be based on balancing immediate harms with long-term benefits, many people – for example people with a life expectancy of less than nine years who will not benefit, are over-treated . [90] It is recommended that all people with type 2 diabetes get regular eye examinations . [13] There is weak evidence suggesting that treating gum disease by scaling and root planing may result in a small short-term improvement in blood sugar levels for people with diabetes. [91] There is no evidence to suggest that this improvement in blood sugar levels is maintained longer than four months. [91] There is also not enough evidence to determine if medications to treat gum disease are effective at lowering blood sugar levels. [91] Lifestyle A proper diet and exercise are the foundations of diabetic care, [23] with a greater amount of exercise yielding better results. [92] Exercise improves blood sugar control, decreases body fat content and decreases blood lipid levels, and these effects are evident even without weight loss. [93] Aerobic exercise leads to a decrease in HbA 1c and improved insulin sensitivity. [94] Resistance training is also useful and the combination of both types of exercise may be most effective. [94] A diabetic diet which includes calorie restriction to promote weight loss is generally recommended. [95] [58] Other recommendations include emphasizing intake of fruits, vegetables, reduced saturated fat and low-fat dairy products, and with a macronutrient intake tailored to the individual, to distribute calories and carbohydrates throughout the day. [58] [96] Several diets may be effective such as the Dietary Approaches to Stop Hypertension (DASH), Mediterranean diet , low-fat diet , or monitored carbohydrate diets such as a low carbohydrate diet . [58] [97] [98] Viscous fiber supplements may be useful in those with diabetes. [99] Vegetarian diets in general have been related to lower diabetes risk, but do not offer advantages compared with diets which allow moderate amounts of animal products. [100] There is not enough evidence to suggest that cinnamon improves blood sugar levels in people with type 2 diabetes. [101] Culturally appropriate education may help people with type 2 diabetes control their blood sugar levels, for up to 24 months. [102] If changes in lifestyle in those with mild diabetes has not resulted in improved blood sugars within six weeks, medications should then be considered. [23] There is not enough evidence to determine if lifestyle interventions affect mortality in those who already have DM2. [71] As of 2015 [update] , there is insufficient data to recommend nonnutritive sweeteners, but note they may help reduce caloric intake. [103] Medications Metformin 500mg tablets. Blood sugar control See also: Anti-diabetic medication There are several classes of anti-diabetic medications available.

Galactose Epimerase Deficiency Wikipedia

PMC 1717903 . PMID 10086948 . ^ Park HD, Park KU, Kim JQ, Shin CH, Yang SW, Lee DH, Song YH, Song J (November 2005).

GALE, GALK1, GALT