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Stranica 1 iz 93 rezultatima
Reduction of hepatic glucocorticoid receptor and hexose-6-phosphate dehydrogenase expression ameliorates diet-induced obesity and insulin resistance in mice.
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Intracellular glucocorticoid (GC) receptor (GR) function determines tissue sensitivity to GCs and strongly affects the development of type 2 diabetes and obesity. 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) mediates intracellular steroid exposure to mouse liver GR by prereceptor
The R453Q and D151A polymorphisms of hexose-6-phosphate dehydrogenase gene (H6PD) influence the polycystic ovary syndrome (PCOS) and obesity.
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Hexose-6-phosphate dehydrogenase (H6PDH) influences 11β-hydroxysteroid dehydrogenase activity, a key enzyme in the peripheral metabolism of cortisol that modulates insulin sensitivity in adipose tissue. To study the associations of R453Q and D151A polymorphisms in the H6PDH gene (H6PD) with
[Biochemical bases of hexose metabolism in children and heredity in the molecular biology of diabetes, obesity, atherosclerosis, infarction, cancer. Correlations].
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Fasting-mediated alteration studies in insulin action on lipolysis and lipogenesis in obese women.
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The effects of fasting on insulin-induced antilipolysis and lipogenesis were investigated in vitro in isolated human fat cells of 11 obese females. Glycerol release and lipogenesis were determined simultaneously in the same test tube and related to methylglucose transport and specific insulin
L-Fucose ameliorates high-fat diet-induced obesity and hepatic steatosis in mice.
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Gastric emptying of hexose sugars: role of osmolality, molecular structure and the CCK₁ receptor.
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BACKGROUND
It is widely reported that hexose sugars slow gastric emptying (GE) via osmoreceptor stimulation but this remains uncertain. We evaluated the effects of a panel of hexoses of differing molecular structure, assessing the effects of osmolality, intra-individual reproducibility and the role
Decreased responsiveness of gluconeogenesis to the modulation by sulfonylureas in hepatocytes isolated from obese (fa/fa) Zucker rats.
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The influence of the hypoglycemic agent glipizide (0-100 microM) on the rate of gluconeogenesis from lactate, as well as on the levels of fructose 2,6-bisphosphate, has been investigated in hepatocytes isolated from genetically obese (fa/fa) Zucker rats and from their corresponding lean (Fa/-)
Increased glycogen synthase kinase-3β and hexose-6-phosphate dehydrogenase expression in adipose tissue may contribute to glucocorticoid-induced mouse visceral adiposity.
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Increased adiposity in visceral depots is a crucial feature associated with glucocorticoid (GC) excess. The action of GCs in a target tissue is regulated by GC receptor (GR) and 11ß-hydroxysteroid dehydrogenase type 1 (11ß-HSD1) coupled with hexose-6-phosphate dehydrogenase (H6pdh). Glycogen
Lack of adipose-specific hexose-6-phosphate dehydrogenase causes inactivation of adipose glucocorticoids and improves metabolic phenotype in mice.
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Excessive glucocorticoid (GC) production in adipose tissue promotes the development of visceral obesity and metabolic syndrome. 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) is critical for controlling intracellular GC production, and this process is tightly regulated by hexose-6-phosphate
Sucrose access differentially modifies 11beta-hydroxysteroid dehydrogenase-1 and hexose-6-phosphate dehydrogenase message in liver and adipose tissue in rats.
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11Beta-hydroxysteroid dehydrogenase-1 (11beta-HSD-1) plays a key role in the regulation of intracellular glucocorticoid concentrations. Increased message and/or activity of adipose 11beta-HSD-1 are characteristics of human and animal models of obesity. Hexose-6-phosphate dehydrogenase (H6PDH) is
Preadipocyte 11beta-hydroxysteroid dehydrogenase type 1 is a keto-reductase and contributes to diet-induced visceral obesity in vivo.
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Glucocorticoid excess promotes visceral obesity and cardiovascular disease. Similar features are found in the highly prevalent metabolic syndrome in the absence of high levels of systemic cortisol. Although elevated activity of the glucocorticoid-amplifying enzyme 11beta-hydroxysteroid dehydrogenase
Modification of microsomal 11beta-HSD1 activity by cytosolic compounds: glutathione and hexose phosphoesters.
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11beta-Hydroxysteroid dehydrogenase1(11beta-HSD1) can serve either as an oxo-reductase or dehydrogenase determined by the redox state in the endoplasmic reticulum (ER). This bidirectional enzyme governs paracrine glucocorticoid production. Recent in vitro studies have underscored the key role of
Carbohydrate handling in exercising muscle of obese Zucker rats.
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OBJECTIVE
To determine the differential substrate utilization of substrates by exercising muscle and in the fatigued state in lean and obese rats.
METHODS
The rats were treadmill-exercised until fatigued, when their oxygen consumption increased by 1.85 x factor. Blood and hind leg tissue (muscle and
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,
Characterization of Metabolomic Profile Associated with Metabolic Improvement after Bariatric Surgery in Subjects with Morbid Obesity.
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The exact impact of bariatric surgery in metabolically "healthy" (MH) or "unhealthy" (MU) phenotypes for the study of the metabolic improvement is still unknown. We applied an untargeted LC-ESI-TripleTOF-MS-driven metabolomics approach in serum samples from 39 patients with morbid obesity (MH and
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