GCK


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GCK

A gene on chromosome 7p15.3-p15.1 that encodes a glucokinase (hexokinase) that phosphorylates glucose yielding glucose-6-phosphate, the first usual step in glucose metabolism.

Molecular biology
GCK mutations are linked to type-2 diabetes, maturity-onset diabetes of the young, type 2 (MODY2) and persistent hyperinsulinemic hypoglycaemia of infancy (PHHI).
References in periodicals archive ?
Expression levels of Enpp1, Gck, Pck1, Fas, Igfbp-1, and Apoe transcripts in the liver of rats in the cycle of fasting and refeeding.
The igfbp-1 and gck gene expressions are regulated by nutritional status or the glucose levels.
For TPACK-G (See Table 2), two statistically significant differences identified were GK (F = 11.97, p < .001) and GCK (F = 3.18, p < .05).
Together with Gck, GLUT2 forms the glucose sensor that facilitates the entrance of glucose into the cell.
The individuals with autosomal dominant mutations in GCK gene on chromosome 7p originally displayed an abnormal glucose sensing with stable mild hyperglycemia in maturity onset diabetes of the young T2DM (MODY) [75,76], which occurs at an age onset of 25 years or younger [77,78].
We also consistently observed markedly decreased expression and activity of Pepck, Gck, G6pase, and Glut2, all enzymes that control gluconeogenic flux in the liver of TCDF-treated mice.
Despite a median 48.6 years of follow-up of 99 patients with GCK MODY, also known as MODY 2, the prevalence and severity of retinopathy, nephropathy, peripheral neuropathy, cardiovascular disease, and peripheral vascular disease weren't significantly different from those of controls (JAMA 2014;311:279-86).
And we think that if they do, it might be because they later go on to develop type 2 diabetes; for instance, if they become obese and have a genetic predisposition in addition to having their GCK mutation," Dr.
[9.] YC Chan, HT Fung, CK Lee, SH Tsui, HK Ngan, MY Sy ML Tse, CW Kam, GCK Wong, HK Tong, ACH Lit, TW Wong, FL Lau.
Berberine regulated Gck, G6pc, Pck1 and Srebp1c expression and activated AMP-activated protein kinase in primary rat hepatCytes.
Glycogen use and release are dependent on 6-phosphoric acid enzymatic synthesis and hydrolysis, and these reactions are catalysed by glucokinase (GCK) andglucose-6-phosphatase (G6Pase).
The eGFRs by GCK and GCKR genotypes were substantially in the same trend to this analysis, with the marginally significant decreasing effect of PPARD T-842CT/C + C/C on eGFR, suggesting the influence of GCK and GCKR polymorphisms on human renal functions (Table 3).