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6 phosphogluconate dehydrogenase/lihavuus
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 17 tuloksia
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,
Dietary soy protein induces hepatic lipogenic enzyme gene expression while suppressing hepatosteatosis in obese female Zucker rats bearing DMBA-initiated mammary tumors.
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Fatty liver is associated with obesity and breast cancer. We used an obese rat model of mammary cancer to examine whether hepatosteatosis is modifiable by diet and associated with altered expression of hepatic lipogenic enzyme genes, thyroid hormone system genes and cholesterol metabolism-related
Metabolic measurements among homozygous (fa/fa) obese, heterozygous (Fa/fa) lean and homozygous (Fa/Fa) lean Zucker rat pups at 17 days of age.
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Factors associated with the development of obesity were compared among obese (fa/fa), heterozygous (Fa/fa) lean and homozygous (Fa/Fa) lean Zucker rats at 17 d of age. Inguinal pad weight, pad-to-body weight ratio and fat cell size were highest in obese pups (fa/fa > Fa/fa > Fa/Fa). Hepatic
An analysis of the relationships among obesity, plasma insulin and hepatic lipogenic enzymes in "viable yellow obese" mice (Avy/a).
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The development of obesity, hyperinsulinemia and six hepatic lipogenic enzymes in Avy/a mice were compared to that in a/a mice. Correlation between body weight, liver weight, plasma insulin concentration and activities of hepatic enzymes was analyzed. In the Avy/a mice, body weight, liver weight and
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
Adaptation in enzyme (metabolic) pathways to obesity, carbohydrate diet and to the occurrence of NIDDM in male and female SHR/N-cp rats.
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Twenty-four male (12 obese and 12 lean) and 21 female (11 obese and 10 lean) SHR/N-cp rats were fed a diet containing either 54% sucrose or starch for periods of 3-4 months. Rats were killed after a 14-16 h fast and liver enzyme activities were determined in both sex groups. Liver
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
Enzymatic activities related to intermediary metabolism of glucose in circulating mononuclear cells from obese humans: relationship to enzyme activity in adipose tissue.
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In order to assess whether enzyme activities of glucose metabolism measured in mononuclear blood cells reflect those in a typical insulin target tissue, we studied hexokinase, 6-phosphofructokinase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase activities in lymphomonocytes
Hepatic drug metabolism and the activities of NADPH generating enzymes and glucose-6-phosphatase in phenobarbital treated genetically obese (ob/ob) mice.
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We aim to evaluate the effects of phenobarbital (PB) on the liver drug metabolism, NADPH production capacity and terminal gluconeogenic enzyme, glucose-6-phosphatase (G6Pase) activity in the diabetic state associated with genetic obesity in mice. The results showed that PB treatment increased the
Selected lipogenic enzyme activities of swine adipose tissue as influenced by genetic phenotype, age, feeding frequency and dietary energy source.
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The effects of genetic phenotype (lean or obese), age, feeding frequency (ad-libitum or meal-fed) and dietary energy source (starch or lard) on selected enzymatic indices of lipogenesis in swine adipose tissue were investigated. The obese line maintained greater specific activities for citrate
Development of lipogenesis and insulin sensitivity in tissues of the ob/ob mouse.
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Lipogenesis and insulin sensitivity are evaluated in adipose tissue, liver, and diaphragm of ob/ob and non-ob/ob mice. In ob/ob mice, hepatic fatty acid synthesis from [U-14C]glucose is elevated by 4 wk of age, and adipose tissue fatty acid synthesis increases at approximately 7 wk. Hepatic
Effect of dietary carbohydrate on liver and kidney enzyme activities and plasma amino acids in the LA/N-cp rat.
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Twenty obese and 20 lean LA/N-cp male rats and 20 male Sprague-Dawley rats were fed a diet containing either 54 percent sucrose or starch for six weeks. After a 14-16 hour fast, rats were killed. Liver and kidney enzyme activities were determined in the LA/N-cp rats while plasma urea and selected
Comparative study of the lipogenic potential of human and rat adipose tissue.
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The reported low activity of lipogenic enzymes (especially adenosine triphosphate [ATP]-citrate lyase) in human adipose tissue led to the general conclusion that in humans lipogenesis occurs primarily in the liver. However, recent studies indicate that the liver plays a minor role in de novo
Effects of rosiglitazone treatment on the pentose phosphate pathway and glutathione-dependent enzymes in liver and kidney of rats fed a high-fat diet.
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BACKGROUND
Animals fed high-fat diets have been shown to develop hyperglycemia, insulin resistance, hyperlipidemia, and moderate obesity, which resemble the human metabolic syndrome. Obesity, the metabolic syndrome, and some thiazolidinediones, which act as insulin sensitizers, may increase
Pharmacological targeting of glucose-6-phosphate dehydrogenase in human erythrocytes by Bay 11-7082, parthenolide and dimethyl fumarate.
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In mature erythrocytes, glucose-6-phosphate dehydrogenase (G6PDH) and 6-phosphogluconate dehydrogenase (6PGDH) yield NADPH, a crucial cofactor of the enzyme glutathione reductase (GR) converting glutathione disulfide (GSSG) into its reduced state (GSH). GSH is essential for detoxification processes
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