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Hypothalamic insulin signaling is required for inhibition of glucose production
The results reveal a new site of action of insulin on glucose production and suggest that hypothalamic insulin resistance can contribute to hyperglycemia in type 2 diabetes mellitus. Expand
Lower blood glucose, hyperglucagonemia, and pancreatic α cell hyperplasia in glucagon receptor knockout mice
The data indicate that glucagon is essential for maintenance of normal glycemia and postnatal regulation of islet and α and δ cell numbers and the lean phenotype of Gcgr−/− mice suggests glucagon action may be involved in the regulation of whole body composition. Expand
Inhibition of GAPDH activity by poly(ADP-ribose) polymerase activates three major pathways of hyperglycemic damage in endothelial cells.
In this report, we show that hyperglycemia-induced overproduction of superoxide by the mitochondrial electron transport chain activates the three major pathways of hyperglycemic damage found inExpand
Hyperglycemia-induced mitochondrial superoxide overproduction activates the hexosamine pathway and induces plasminogen activator inhibitor-1 expression by increasing Sp1 glycosylation.
Hyperglycemia-induced mitochondrial superoxide overproduction increases hexosamine synthesis and O-glycosylation of Sp1, which activates expression of genes that contribute to the pathogenesis of diabetic complications. Expand
Inhibition of hypothalamic carnitine palmitoyltransferase-1 decreases food intake and glucose production
Results indicated that changes in the rate of lipid oxidation in selective hypothalamic neurons signaled nutrient availability to the hypothalamus, which in turn modulated the exogenous and endogenous inputs of nutrients into the circulation. Expand
Hypothalamic KATP channels control hepatic glucose production
It is shown that activation of ATP-sensitive potassium (KATP) channels in the mediobasal hypothalamus is sufficient to lower blood glucose levels through inhibition of hepatic gluconeogenesis, and that any alteration within this central nervous system/liver circuit can contribute to diabetic hyperglycaemia. Expand
Central administration of oleic acid inhibits glucose production and food intake.
It is reported that intracerebroventricular administration of the long-chain fatty acid oleic acid markedly inhibits glucose production and food intake and limits further delivery of nutrients to the circulation. Expand
Mechanisms of fatty acid-induced inhibition of glucose uptake.
It is concluded that fatty acids caused a dose-dependent inhibition of insulin-stimulated glucose uptake (by decreasing glycogen synthesis and CHO oxidation) and that FFA and/or glycerol increased insulin-suppressed hepatic glucose output and thus caused insulin resistance at the peripheral and the hepatic level. Expand
Endogenous glucose production is inhibited by the adipose-derived protein Acrp30.
Results indicate that an acute increase in circulating Acrp30 levels lowers hepatic glucose production without affecting peripheral glucose uptake, and a moderate rise in circulating levels of the adipose-derived protein Acp30 inhibits both the expression of hepatic gluconeogenic enzymes and the rate of endogenous glucose production. Expand
SirT1 gain of function increases energy efficiency and prevents diabetes in mice.
SirT1 gain of function primes the organism for metabolic adaptation to insulin resistance, increasing hepatic insulin sensitivity and decreasing whole-body energy requirements, which have important implications for Sirtuin-based therapies in humans. Expand