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Contribution of oxidative metabolism and glycolysis to ATP production in hypertrophied hearts.
A reduced contribution of fatty acid oxidation to energy production in hypertrophied rat hearts is accompanied by a compensatory increase in glycolysis during low work conditions.
Energy Metabolism in the Hypertrophied Heart
In response to a prolonged pressure- or volume-overload, alterations occur in myocardial fatty acid, glucose, and glycogen metabolism. Oxidation of long chain fatty acids has been found to be reduced
Dichloroacetate improves postischemic function of hypertrophied rat hearts.
5-Aminoimidazole-4-carboxamide 1-beta -D-ribofuranoside (AICAR) stimulates myocardial glycogenolysis by allosteric mechanisms.
The data are consistent with allosteric activation of GP by ZMP being responsible for the glycogenolysis caused by AICAR in the intact rat heart.
Single-dose dexamethasone induces whole-body insulin resistance and alters both cardiac fatty acid and carbohydrate metabolism.
The data provide evidence that in a setting of insulin resistance, an increase in LPL could facilitate increased delivery of fatty acid to the heart, leading to excessive triglyceride storage, and could be explained by the enhanced LPL mRNA expression following DEX.
Heterogeneity of gut capillary transit times and impaired gut oxygen extraction in endotoxemic pigs.
The hypothesis that endotoxin increases the heterogeneity of gut capillary transit times and impairs oxygen extraction is tested and may be an important cause of impaired oxygen extraction.
Bcl-2 and Bcl-xL Suppress Glucose Signaling in Pancreatic β-Cells
This work suggests that prosurvival Bcl proteins normally dampen the β-cell response to glucose and thus reveals these core apoptosis proteins as integrators of cell death and physiology in pancreatic β-cells.
Distinct Early Signaling Events Resulting From the Expression of the PRKAG2 R302Q Mutant of AMPK Contribute to Increased Myocardial Glycogen
These findings are the first to highlight temporal differences in the effects of the PRKAG2 R302Q mutation on cardiac metabolic signaling events and suggest that expression of γ2R302Q induces AMPK activation and the eventual increase in glycogen content.