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dihydroxyacetone/obesity

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Effects of pyruvate and dihydroxyacetone consumption on the growth and metabolic state of obese Zucker rats.

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Female obese Zucker rats (aged 6 wk) were randomly assigned to one of two control or one of three experimental-diet groups. Experimental diets contained 6% pyruvate (Pyr). 6% dihydroxyacetone (Dha), or 3% each pyruvate and dihydroxyacetone (Pyr-Dha). Control-group 1 was fed a normal diet ad libitum

Effect of pyruvate and dihydroxyacetone on metabolism and aerobic endurance capacity.

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Pyruvate and dihydroxyacetone are three carbon compounds that when infused directly into the blood or taken orally produce strong metabolic effects. When chronically fed to animals as part of their diet, pyruvate plus dihydroxyacetone reduce the rate of weight gain and body fat content during

Body composition, energy utilization, and nitrogen metabolism with a severely restricted diet supplemented with dihydroxyacetone and pyruvate.

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To determine the effect of dietary modification on energy utilization during severely restrictive hypocaloric feeding, we measured body composition, energy deficit, and nitrogen metabolism in 13 obese women housed in a metabolic ward consuming a 2.1-MJ diet for 21 d with the three-carbon compounds

Detection of molecular paths associated with insulitis and type 1 diabetes in non-obese diabetic mouse.

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Recent clinical evidence suggests important role of lipid and amino acid metabolism in early pre-autoimmune stages of type 1 diabetes pathogenesis. We study the molecular paths associated with the incidence of insulitis and type 1 diabetes in the Non-Obese Diabetic (NOD) mouse model using available
OBJECTIVE We sought to test the hypothesis that increasing postprandial hepatic glycogen synthesis rate would decrease food intake and growth rate in obese Zucker rats. METHODS Supplements of glutamine, with and without dihydroxyacetone (DHA), which have previously been shown to stimulate hepatic

The application of microcalorimetry to the assessment of metabolic efficiency in isolated rat hepatocytes.

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1. Heat output by suspensions of isolated rat hepatocytes was determined by using a modified batch-type microcalorimeter. 2. The ratio of O(2) uptake (determined polarographically) to heat output was used to assess the metabolic efficiency of isolated hepatocytes. 3. Cells from starved or fed rats

Taurine increases glucose sensitivity of UCP2-overexpressing beta-cells by ameliorating mitochondrial metabolism.

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A low-taurine diet during fetal or early postnatal life causes abnormal pancreatic beta-cell development. Tissue and plasma taurine concentrations can also be low in diabetic patients. We examined the effect of taurine on impaired glucose responses in diabetic rat beta-cells adenovirally

Overexpression of short heterodimer partner recovers impaired glucose-stimulated insulin secretion of pancreatic beta-cells overexpressing UCP2.

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The short heterodimer partner (SHP) (NR0B2) is an orphan nuclear receptor whose function in pancreatic beta-cells is unclear. Mitochondrial uncoupling protein (UCP2) in beta-cells is upregulated in obesity-related diabetes, causing impaired glucose-stimulated insulin secretion (GSIS). We

Recent advances in the synthesis of rare sugars using DHAP-dependent aldolases.

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The occurrence rates of non-communicable diseases like obesity, diabetes and hyperlipidemia have increased remarkably due to excessive consumption of a high-energy diet. Rare sugars therefore have become increasingly attractive owing to their unique nutritional properties. In the past two decades,
OBJECTIVE To investigate the efficacy of the 3-carbon compounds pyruvate and dihydroxyacetone (PD) in inhibiting reaccumulation of body weight and fat with refeeding after weight loss. METHODS Longitudinal, in Clinical Research Center. After weight loss induced by hypoenergetic diet (1.3 MJ/d) for 3

Green tea catechins: inhibitors of glycerol-3-phosphate dehydrogenase.

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Green tea catechins, especially (-)-epigallocatechin-3-gallate (EGCG), are known to regulate obesity and fat accumulation. We performed a kinetic analysis in a cell-free system to determine the mode of inhibition of glycerol-3-phosphate dehydrogenase (GPDH; EC 1.1.1.8) by EGCG. GPDH catalyzes the

Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?

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The metabolic syndrome (MetS) is manifested by a lipid triad which includes elevated serum triglycerides, small LDL particles, and low high-density lipoprotein (HDL) cholesterol, by central obesity (central adiposity), insulin resistance, glucose intolerance and elevated blood pressure, and it is

Fructose and carbonyl metabolites as endogenous toxins.

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Dietary fructose consumption is one of the environmental factors contributing to the development of obesity and a fatty liver (hepatic steatosis). A two-hit hypothesis has been proposed for progression of hepatic steatosis to the more serious non-alcoholic steatosis (NASH), with the first hit being

Insulin secretion by isolated perfused rat and mouse pancreas.

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A method for isolation and perfusion of a pancreas preparation consisting of pancreas, stomach, proximal duodenum, and spleen is described. Basic characteristics of regulation of insulin secretion from the perfused pancreas isolated from rats, albino mice, obese mice (ob/ob), and black mice were

Structure of glycerol-3-phosphate dehydrogenase, an essential monotopic membrane enzyme involved in respiration and metabolism.

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Sn-glycerol-3-phosphate dehydrogenase (GlpD) is an essential membrane enzyme, functioning at the central junction of respiration, glycolysis, and phospholipid biosynthesis. Its critical role is indicated by the multitiered regulatory mechanisms that stringently controls its expression and function.
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