pyruvate kinase/비만증

In obese hyperglycemic (ob/ob) mice, as compared to controls, hepatic pyruvate kinase (PK) activity was enhanced by 35.63% (214.75 +/- 13.60 nmol/min/mg protein v 158.33 +/- 10.47, P less than 0.01) when measured at saturating (6.6 mmol/L) concentration of the substrate phosphoenolpyruvate (total

Obesity-dependent insulin resistance and type 2 diabetes mellitus are closely associated with decreased glucose utilization and down-regulation of hepatic glycolytic enzymes expression. Previously, we showed that DNA hypermethylation is involved in age-dependent susceptibility to hepatic insulin

Alterations in hepatic glucose metabolism play a key role in the development of the hyperglycemia observed in type 2 diabetes. Because the transcription factor c-Myc induces hepatic glucose uptake and utilization and blocks gluconeogenesis, we examined whether hepatic overexpression of c-myc

Genetically obese (fa/fa) Zucker rats show oral glucose intolerance, an alteration that has been attributed at least in part to an impaired suppression of hepatic glucose output after the ingestion of glucose. In this work, we studied the influence of different concentrations of glucose (2.5-30 mM)

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

In vivo studies have demonstrated that hepatic glucose production is poorly responsive to insulin in genetically obese Zucker rats. In this work, we have investigated the modulation by insulin of basal gluconeogenesis, fructose 2,6-bisphosphate levels, and pyruvate kinase and 6-phosphofructo

OBJECTIVE To study the mechanism that controls fructose-2,6-bisphosphate (Fru-2,6-P2) accumulation, as well as the mRNAs levels of the glycolytic/gluconeogenic regulatory enzymes in the livers of fed and starved lean (fa/-) and obese (fa/fa) Zucker rats. METHODS Rats were fed a standard chow or

Manganese-Enhanced Magnetic Resonance Imaging (MEMRI), (1)H and (13)C High-Resolution-Magic Angle Spinning (HR-MAS) Spectroscopy, and genomic approaches were used to compare cerebral activation and neuronal and glial oxidative metabolism in ad libitum fed C57BL6/J leptin-deficient, genetically obese

The Wistar fatty rat is a model of obese non-insulin-dependent diabetes mellitus. Males, but not females, develop hyperglycemia, glucouria and polyuria within 8 weeks of age. The regulation of gene expression by insulin has been shown to be differentially impaired in the liver of the fatty rats. The

The possibility that the glucocorticoid-dependence of obesity of the obese fa/fa rat reflects on overactivity of glucocorticoids on the brain has been investigated by studies of enzyme activities and glucocorticoid type II (GR) receptors. The activity of 2 glucocorticoid-sensitive enzymes,

OBJECTIVE Androgen excess in women is frequently associated with muscle insulin resistance, especially in obese women with polycystic ovary syndrome. However, whether this is a primary event or the result of indirect mechanisms is currently debated. METHODS This is an observational study. METHODS We

Altered erythrocyte sodium potassium (Na,K)-stimulated adenosine triphosphatase (ATPase) activity has been cited as having pathophysiologic significance in morbidly obese man. Previous studies have failed to consider obese patients after weight loss and, therefore, did not clarify the role of ATPase

Serotonergic neuronal networks are important for food intake and body weight regulation. Dexfenfluramine (dF), a serotonin releaser and reuptake inhibitor, was used to investigate changes in food intake, body weight development, energy expenditure, respiratory quotient, and substrate oxidation rates

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