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glucose 6 phosphate dehydrogenase/obésité
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Enzymatic adaptations by cultured adipocytes of human infants and children: effect of obese serum on the activities of lactate-, malate-, and glucose-6-phosphate dehydrogenases.
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To determine whether there are any biochemical characteristics which distinguish human adipose cells from human skin fibroblasts, assays of lactate dehydrogenase with pyruvate as substrate (LDH-P), malate dehydrogenase (MDH), and glucose-6-phosphate dehydrogenase (G6PDH) were done on both cell types
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
Mononuclear leukocytes from obese patients with type II diabetes have reduced activity of hexokinase, 6-phosphofructokinase and glucose-6-phosphate dehydrogenase.
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In the present study we measured the activity of some cytosolic enzymes involved in intracellular glucose metabolism in mononuclear leukocytes from 77 obese subjects of which 39 were nondiabetic and 38 had newly-diagnosed untreated type II diabetes mellitus. 28 subjects (19 nondiabetic and 18
[Roles of glucose-6-phosphate dehydrogenase in obesity induced by high fat diet].
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OBJECTIVE
To explore the roles of glucose-6-phosphate dehydrogenase (G6PD) and its downstream NADPH oxidase (NOX) in obesity induced by high fat diet.
METHODS
40 male Wistar rats were randomly divided into a high fat diet group (30 rats) and a control group (10 rats) fed with rat chow. After six
Dietary induction of hepatic glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and malic enzyme in lean and obese female Zucker rats.
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Responses of the hepatic lipogenic enzymes, glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), and malic enzyme (ME) to starvation refeeding and diet shifting were determined in lean and obese female Zucker rats. Rats were either fed nonpurified diet, starved 48 hr,
Effects of dehydroepiandrosterone on obesity and glucose-6-phosphate dehydrogenase activity in the lethal yellow mouse (strain 129/Sv-Ay/Aw).
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We investigated the anti-obesity effects of the adrenal androgen, dehydroepiandrosterone (DHEA), on genetically predisposed obese lethal yellow mice (Ay/Aw). Secondly, we tested the hypothesis that DHEA promotes its anti-obesity effects by decreasing the activity of glucose-6-phosphate dehydrogenase
Glucose-6-Phosphate Dehydrogenase Deficiency Improves Insulin Resistance With Reduced Adipose Tissue Inflammation in Obesity.
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Glucose-6-phosphate dehydrogenase (G6PD), a rate-limiting enzyme of the pentose phosphate pathway, plays important roles in redox regulation and de novo lipogenesis. It was recently demonstrated that aberrant upregulation of G6PD in obese adipose tissue mediates insulin resistance as a result of
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
Overexpression of glucose-6-phosphate dehydrogenase is associated with lipid dysregulation and insulin resistance in obesity.
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Glucose-6-phosphate dehydrogenase (G6PD) produces cellular NADPH, which is required for the biosynthesis of fatty acids and cholesterol. Although G6PD is required for lipogenesis, it is poorly understood whether G6PD in adipocytes is involved in energy homeostasis, such as lipid and glucose
Superoxide production by NAD(P)H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and aorta before the development of cardiac dysfunction. The role of glucose-6-phosphate dehydrogenase-derived NADPH.
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Increased oxidative stress is a known cause of cardiac dysfunction in animals and patients with diabetes, but the sources of reactive oxygen species [e.g., superoxide anion (O(2)(-))] and the mechanisms underlying O(2)(-) production in diabetic hearts are not clearly understood. Our aim was to
The role of glucose-6-phosphate dehydrogenase in adipose tissue inflammation in obesity.
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Obesity is closely associated with metabolic diseases including type 2 diabetes. One hallmark characteristics of obesity is chronic inflammation that is coordinately controlled by complex signaling networks in adipose tissues. Compelling evidence indicates that reactive oxygen species (ROS) and its
[Influence of reducing diets on the glucose-6-phosphate dehydrogenase activity of the fatty tissue in patients with metabolic-alimentary obesity].
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The glucose-6-phosphate-dehydrogenase activity by the fatty tissue in patients with alimentary adiposity was studied. A well-marked fall of the activity by comparison with controls, especially in patients with hyperlipidemia, was revealed. Following treatment of the patients with reduction diets
Effect of hormones on fatty acid release and glucose-6-phosphate dehydrogenase activity in human adipose tissue in relation to obesity.
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A possible interrelation between glucose-6-phosphate dehydrogenase and dehydroepiandrosterone in obesity.
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[Glucose-6-phosphate dehydrogenase activity in the adipose tissue of patients with metabolic-alimentary obesity].
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