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hyperplasia/triacylglycerol

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Страна 1 од 24 резултати

MicroRNA-27b Depletion Enhances Endotrophic and Intravascular Lipid Accumulation and Induces Adipocyte Hyperplasia in Zebrafish.

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miR-27b has emerged as a regulatory hub in cholesterol and lipid metabolism, and as a potential therapeutic target for treating atherosclerosis and obesity. However, the impact of miR-27b on lipid levels in vivo remains to be determined. Zebrafish lipids are normally stored as triacylglycerols (TGs)

Molecular mechanism driving retroperitoneal adipocyte hypertrophy and hyperplasia in response to a high-sugar diet.

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METHODS We have previously shown an increase in adipocyte size and lipid content in retroperitoneal white adipose tissue (rWAT) induced by an 8-week high-sugar diet (HSD). In this study, we assessed the effect of a HSD on the transcriptional activity of adipogenic genes in a time-course study to

Intestinal adaptation occurs independently of parenteral long-chain triacylglycerol and with no change in intestinal eicosanoids after mid-small bowel resection in rats.

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The role of enteral or parenteral long-chain triacylglycerol (LCT) in the complex process of intestinal adaptation is poorly defined and may involve alterations in eicosanoid synthesis. Our objective was to determine whether provision of parenteral LCT stimulates eicosanoid synthesis and

Effects of trans-10,cis-12 CLA on liver size and fatty acid oxidation under energy restriction conditions in hamsters.

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OBJECTIVE Little evidence exists concerning the effects of trans-10,cis-12 conjugated linoleic acid (CLA) under energy restriction. Thus, the effects of this CLA isomer on adipose tissue size, liver composition, as well as on expression and activity of carnitine-palmitoyl transferase I (CPT-I) and

Coenzyme Q(10) supplementation inhibits aortic lipid oxidation but fails to attenuate intimal thickening in balloon-injured New Zealand white rabbits.

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Oxidized lipoproteins are implicated in atherosclerosis, and some antioxidants attenuate the disease in animals. Coenzyme Q(10) (CoQ(10)) in its reduced form, ubiquinol-10, effectively inhibits lipoprotein oxidation in vitro and in vivo; CoQ(10) supplements also inhibit atherosclerosis in

Effects of dehydroepiandrosterone treatment in rats with diet-induced obesity.

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Previous studies showed that administration of dehydroepiandrosterone (DHEA) to lean and genetically obese Zucker rats reduced body weight. In the present experiments, the effect of DHEA treatment in rats with diet-induced obesity was evaluated. In experiment 1, male Sprague-Dawley rats (300 g) were

Basal adrenergic tone is required for maximal stimulation of rat brown adipose tissue UCP1 expression by chronic PPAR-gamma activation.

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We investigated the involvement of basal sympathetic tone in brown adipose tissue (BAT) recruitment and gene expression profile induced by peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activation. Innervated and surgically denervated BAT pads of rats treated or not with rosiglitazone

Influences of feeding of high-iodine eggs on hypo- and hyperthyroid rats.

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The effects of the feeding of high-iodine eggs to rats with an abnormal thyroid status were investigated. Rats were fed for one week on a commercial diet supplemented with propylthiouracil (PTU) (10 mg/100 g diet) or thyroxine-Na (240 micrograms/100 g diet) respectively, to induce hypo- or

Time course and dynamics of adipose tissue development in obese and lean Zucker rat pups.

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OBJECTIVE To evaluate the ontogeny of adipose tissue dynamics in obese and lean Zucker rat pups, from suckling to puberty. METHODS The trial had a two-group parallel design. Sixty-two male Zucker rat pups shared within 15 litters received deuterated water for 5 days, prior killing at different age.

Changes in activities of some enzymes of glycerolipid synthesis in brown adipose tissue of cold-acclimated rats.

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1. Measurements were made of the activities of the following enzymes of glycerolipid synthesis in homogenates of interscapsular brown adipose tissue obtained from rats subjected to a 4 degrees C environment for time periods of 6 h up to 12 days: fatty acyl-CoA synthetase (FAS), mitochondrial and

HMG-CoA reductase inhibitors perturb fatty acid metabolism and induce peroxisomes in keratinocytes.

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Topical lovastatin stimulates epidermal fatty acid synthesis in vivo; therefore, studies were undertaken to examine the effects of HMG-CoA reductase inhibitors on fatty acid metabolism in cultured keratinocytes. When exposed to fluindostatin or lovastatin for greater than or equal to 24 h,

Loss of the acyl-CoA binding protein (Acbp) results in fatty acid metabolism abnormalities in mouse hair and skin.

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Proper fatty acid metabolism is critical for hair and skin development and maintenance. The acyl-CoA binding protein (Acbp) is a widely expressed protein that binds long-chain fatty acyl-CoA esters and plays a role in fatty acyl-CoA transport and pool formation. However, loss of function of Acbp in

Differentiation of human tumors from nonmalignant tissue by natural-abundance 13C NMR spectroscopy.

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High-quality, high-resolution, proton-decoupled natural-abundance 13C NMR spectra have been obtained in vitro at 100.6 MHz from unprocessed human pathology specimens of tumors and adjacent nonneoplastic control tissues from lung, colon, and prostate. In these preliminary studies, specific molecular

[Obesity and insulin resistance].

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The worldwide epidemic of obesity is a serious threat to public health, because obesity results in insulin resistance, which leads to metabolic syndrome. Obesity is determined by both adipocyte size (adipocyte hypertrophy) and adipocyte number (adipocyte hyperplasia). Recent studies have begun to

Role of adipocyte precursors in the onset of obesity induced by overfeeding in suckling rats.

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Rats were overfed during the suckling period by litter size manipulation in order to investigate the possible contribution of preadipocytes from the stroma-vascular compartment of adipose tissue to the development of obesity. Rats raised in litters of four pups were overfed; for normal feeding we
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