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Regulation of pathways of glucose metabolism in the kidney. The activity of the pentose phosphate pathway, glycolytic route and the regulation of phosphofructokinase in the kidney of lean and genetically obese (ob/ob) mice; comparison with effects of diabetes.

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The activities of enzymes of the glycolytic route, the pentose phosphate pathway and NADPH-linked enzymes have been measured in the kidneys of genetically obese (ob/ob) mice and their lean litter mates. The renal content of glucose 6-phosphate (G6P), fructose 6-phosphate (F6P), fructose

Aspects of the regulation of hepatic phosphoribosyl pyrophosphate formation in the obese (ob/ob) mouse: relationship to the pentose phosphate pathway.

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The content of phosphoribosyl pyrophosphate (PPRibP) and of intermediates involved in its synthesis has been measured in the livers of obese (ob/ob) mice 2 months and 3-4 months of age, a period of dynamic growth and marked hepatic hypertrophy and hyperplasia, and comparison made with the values

Activated glucose-6-phosphate dehydrogenase is associated with insulin resistance by upregulating pentose and pentosidine in diet-induced obesity of rats.

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Recent studies have shown that glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme for the pentose phosphate pathway, was involved in insulin resistance via reduced nicotinamide adenine dinucleotide phosphate, while the roles of pentose were not examined. In the present study, the

Circadian feeding drive of metabolic activity in adipose tissue and not hyperphagia triggers overweight in mice: is there a role of the pentose-phosphate pathway?

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High-fat (HF) diets trigger an increase in adipose tissue and body weight (BW) and disordered eating behavior. Our study deals with the hypothesis that circadian distribution of energy intake is more relevant for BW dynamics than diet composition. Four-week-old mice were exposed for 8 wk to a HF

[The pentose cycle in obese subjects].

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The effects of triiodothyronine on some metabolic parameters of obese individuals. Blood C-14-glucose replacement rate, respiratory C-14-O-2, the pentose cycle, the biological half-life of T-3 and the concentration of T-3 in adipose tissue.

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New insight on obesity and adipose-derived stem cells using comprehensive metabolomics.

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Obesity affects the functional capability of adipose-derived stem cells (ASCs) and their effective use in regenerative medicine through mechanisms that are still poorly understood. In the present study we used a multiplatform [LC/MS, GC/MS and capillary electrophoresis/MS (CE/MS)], metabolomics,

A simple method to monitor hepatic gluconeogenesis and triglyceride synthesis following oral sugar tolerance test in obese adolescents.

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Hepatic energy metabolism is a key element in many metabolic diseases. Hepatic anaplerosis provides carbons for gluconeogenesis (GNG) and triglyceride (TG) synthesis. We aimed to optimize a protocol that measures hepatic anaplerotic contribution for GNG, TG synthesis, and hepatic pentose phosphate

Evidence that the 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD1) is regulated by pentose pathway flux. Studies in rat adipocytes and microsomes.

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11 beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1) catalyzes the interconversion of biologically inactive 11 keto derivatives (cortisone, 11-dehydrocorticosterone) to active glucocorticoids (cortisol, corticosterone) in fat, liver, and other tissues. It is located in the intraluminal

Adaptive responses of enzymes of carbohydrate and lipid metabolism to dietary alteration in genetically obese Zucker rats (fa/fa).

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1. Measurements have been made of the activities of enzymes of the glycolytic route, the pentose phosphate pathway, the tricarboxylic acid cycle and lipogenesis in liver and adipose tissue from genetically obese (fa/fa) rats and their lean litter mates (fa/ --). The effect of food restriction for a

Diet and the role of 11beta-hydroxysteroid dehydrogenase-1 on obesity.

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11beta-Hydroxysteroid dehydrogenase-1 (11beta-HSD-1) is a key regulatory enzyme in glucocorticoid metabolism, specifically in regulating intracellular concentrations of cortisol, the primary glucocorticoid. While the excessive level of circulating cortisol in Cushing's disease is of adrenal origin,

Glucose handling by hepatocytes from obese Zucker rats.

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Hepatocytes isolated from obese Zucker rats showed a significantly higher rate of both [U-14C]glucose and [U-14C]lactate incorporation into [14C]lipid than those from their lean counterparts. This was associated with a marked increase in the lipogenic rate measured by the incorporation of 3H2O into

Effects of laparoscopic Roux-en-Y gastric bypass on glucose-6 phosphate dehydrogenase activity in obese type 2 diabetics.

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BACKGROUND Glucose-6-phosphate dehydrogenase (G6PD) is the rate-limiting enzyme of the pentose phosphate pathway that provides the majority of NADPH required for lipid biosynthesis. G6PD overexpression has been implicated in insulin resistance, hyperlipidemia, and increased oxidative stress in

Metabolism of glucose in the small intestine of lean and obese (ob/ob) mice.

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The possibility of alterations in the metabolism of glucose in the small intestine of C57BL/6J (ob/ob) obese-diabetic mice has been investigated. Glucose metabolism was assessed by direct measurement in vitro, and by assaying the activities of glycolytic and pentose phosphate pathway enzymes. The

Effects of exercise and of food restriction on the development of spontaneous obesity in rats.

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The effects of exercise and of food restriction on Zucker obese and lean rats were studied. Zucker obese rats pair-fed to lean littermates gained more body fat on the same intake indicating greater efficiency of diet utilization. Exercise significantly reduced the fat pad weights and body fat

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