(1) The Ala54 and Thr54 allele frequencies in Chinese were 0.71 and 0.29 respectively; (2) The FABP2-Ala54Thr variation was neither associated with fasting and post-challenged plasma glucose levels nor with NIDDM; (3) This variation was neither associated with fasting lipid profile nor with obesity; (4) The IGT subjects with genotype Thr54(+) (Thr54 homozygotes and heterozygotes) had lower fasting, 2-hour and total C-peptide levels and smaller AUC representing lesser C-peptide secretion after glucose challenge than those with genotype Thr54(-) (Ala54 homozygotes) (P = 0.04, 0.03, 0.01 and 0.01 respectively).
(a) To study whether there was an increased prevalence of glucose intolerance in the parents of probands with Type 1 diabetes and (b) to look for any possible link between the glucose intolerance in the parents with HLA-DQB1 alleles transmitted in excess to the Type 1 diabetes offspring.
4) Direct genetic analysis is effective in rarer forms of glucose intolerance (MODY, mitochondrial mutations, etc.) but encounters serious difficulties with typical late-onset NIDDM.
Glucose intolerance did not worsen in CD14 KO mice grafted with bone marrow stem cells from high fat-fed WT mice when compared with recipient KO mice grafted with cells from CD14 KO donor mice.
Impaired glucose tolerance and impaired insulin secretion have been reported in families with PAX6 mutations and it is suggested that they result from defective proinsulin processing due to lack of prohormone convertase 1/3, encoded by PCSK1.
Glucose intolerance and insulin resistance of Lrictor(KO) mice could be fully rescued by hepatic expression of activated Akt2 or dominant negative FoxO1.
Glucose intolerance and insulin resistance of Lrictor(KO) mice could be fully rescued by hepatic expression of activated Akt2 or dominant negative FoxO1.
Glucose intolerance was partially prevented by <i>L. kefiri</i> treatment (GTT) and local inflammation (TNFα; IL1β; IL6 and INFγ) was completely inhibited in EAT.<i>L. kefiri</i> supplementation generated an impact on gut microbiota composition, changing <i>Bacteroidetes</i> and <i>Firmicutes</i> profiles.
Glucose intolerance was partially prevented by <i>L. kefiri</i> treatment (GTT) and local inflammation (TNFα; IL1β; IL6 and INFγ) was completely inhibited in EAT.<i>L. kefiri</i> supplementation generated an impact on gut microbiota composition, changing <i>Bacteroidetes</i> and <i>Firmicutes</i> profiles.
Glucose intolerance was partially prevented by <i>L. kefiri</i> treatment (GTT) and local inflammation (TNFα; IL1β; IL6 and INFγ) was completely inhibited in EAT.<i>L. kefiri</i> supplementation generated an impact on gut microbiota composition, changing <i>Bacteroidetes</i> and <i>Firmicutes</i> profiles.
Impaired Glucose Tolerance and Reduced Plasma Insulin Precede Decreased AKT Phosphorylation and GLUT3 Translocation in the Hippocampus of Old 3xTg-AD Mice.
FEV(1), FVC and BMI presented a significant linear correlation with plasma glucose value at 120 min at OGTT and were significantly lower in both CF-IGT and CFRD versus the CF-NGT group, whereas no differences were found between the CF-IGT and CFRD groups.
PAX6 is also involved in the development of the endocrine pancreas, and reported to be a genetic factor common to aniridia and glucose intolerance, although the latter is usually mild.
ARNT expression is reduced in diabetic human islets and beta cell-specific ARNT knockout mice show the impaired glucose tolerance and abnormal insulin secretion that are characteristic of type 2 diabetes.
UCP3 protein content was significantly lower in prediabetic IGT subjects and in diabetic patients compared with healthy controls (39.0 +/- 28.5, 47.2 +/- 24.7, and 72.0 +/- 23.7 arbitrary units, respectively; P < 0.05), whereas the levels of the mitochondrial protein complex I-V were similar between groups.