We demonstrate dominant cosegregation of diabetes and aniridia with a deletion distal to PAX6, which is clinically distinct from the mild glucose intolerance previously reported with PAX6 coding mutations.
Presence of impaired glucose tolerance coupled with kidney disease in the proband and one parent was also highly predictive for HNF1B mutations (OR=11.11, 95%CI:1.13-109.36).
There was a weak relationship between the iAUC<sub>0-240 min</sub> for GIP and GLP-1 in the combined (r = 0.23, P = 0.015) and in the IGT (r = 0.34, P = 0.01), but not in the NGT (r = 0.15, P = 0.14) group.
Vildagliptin suppressed an inappropriate glucagon response to an oral glucose challenge in patients with T2DM, to a mixed meal challenge in patients with T2DM and type 1 diabetes mellitus, and to a mixed meal challenge in subjects with IGT and IFG.
The increment of postprandial GLP-1 and insulinsecretion may have a role in normalizing postprandial glycaemia and slowing the establishment of glucose intolerance.
Drug-induced activation of this inhibitory designer receptor almost completely shut off glucagon secretion in vivo, resulting in significantly impaired insulin secretion, hyperglycemia, and glucose intolerance.
Our results indicate that high-glucose load leads to glucose intolerance with insulin resistance through impairment of GLP-1 secretion, increase of blood glucose levels via activating TLR4 and increasing levels of IL-6 and TNF-α in mice.
Obese mice exhibited fasting hyperglycemia, hyperinsulinemia, and impaired glucose tolerance, as well as decreased serum levels of adiponectin and increased levels of leptin, resistin, and insulin-like growth factor 1.
Obese mice exhibited fasting hyperglycemia, hyperinsulinemia, and impaired glucose tolerance, as well as decreased serum levels of adiponectin and increased levels of leptin, resistin, and insulin-like growth factor 1.
Our results indicate that high-glucose load leads to glucose intolerance with insulin resistance through impairment of GLP-1 secretion, increase of blood glucose levels via activating TLR4 and increasing levels of IL-6 and TNF-α in mice.
We found that the serum ADMA and C-reactive protein levels were significantly increased in IGT and diabetic patients, whereas the levels of lipoprotein A and adiponectin were decreased, especially in diabetic patients with obesity.
Our results indicate that high-glucose load leads to glucose intolerance with insulin resistance through impairment of GLP-1 secretion, increase of blood glucose levels via activating TLR4 and increasing levels of IL-6 and TNF-α in mice.
Increased visceral fat may be caused by up-regulated PPARγ (peroxisome proliferator-activated receptor gamma) and RXRα/β (retinoid X receptors) in liver and adipose tissue, and glucose intolerance is observed in F1 adult females prenatally supplemented with BC, while F1 males do not exhibit these symptoms.
Outcomes were also assessed in patients with diabetes and/or hyperglycemia (impaired glucose tolerance [IGT] and diabetes population [IGT-diabetes population]) and all patients included in the 3 studies (intention-to-treat [ITT] population).
Improvement of reduced grooming behavior and normalization in reduced plasma insulin levels were seen only in 5M+2M Tg2576 mice while in 10M+2M Tg2576 mice oral galactose induced metabolic exacerbation at the level of plasma insulin, GLP-1 homeostasis and glucose intolerance, and additionally increased hippocampal sAβ1-42 level, decreased IR expression and increased GSK-3β activity.
Our findings may have implications for the microvascular complications associated with T2DM.<b>NEW & NOTEWORTHY</b> Higher concentrations of serum factors, specifically Interleukin-6 and its soluble receptor found in individuals with type 2 diabetes (T2DM) appear to impair endothelial cell capillary-like network formation compared with those present in serum from individuals with impaired glucose tolerance and normal glucose tolerance.
Our results indicate that high-glucose load leads to glucose intolerance with insulin resistance through impairment of GLP-1 secretion, increase of blood glucose levels via activating TLR4 and increasing levels of IL-6 and TNF-α in mice.
Aging is associated with reductions in fasting GLP-1 and GIP, and glucose-stimulated GLP-1, which may predispose to the development of glucose intolerance and type 2 diabetes.
We found that heat-killed <i>S. thermophilus</i> treatment reduced fasting blood glucose levels and alleviated glucose intolerance and total cholesterol in diabetic ZDF rats.Additionally, heat-killed <i>S. thermophilus</i> increased the interleukin 10 while reducing the levels of lipopolysaccharide, interleukin 6, and tumor necrosis factor-α in diabetic ZDF rats.The heat-killed <i>S. thermophilus</i> treatment can normalize the structure of the intestinal and colon mucosal layer of diabetic rats.