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Obesity Rats (obesity + rat)

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Life Sciences100%

Selected Abstracts

Analysis of urinary metabolites for metabolomic study by pressurized CEC

ELECTROPHORESIS, Issue 23 2007
Guoxiang Xie
Abstract A new approach for the metabolomic study of urinary samples using pressurized CEC (pCEC) with gradient elution is proposed as an alternative chromatographic separation tool with higher degree of resolution, selectivity, sensitivity, and efficiency. The pCEC separation of urinary samples was performed on a RP column packed with C18, 5,,m particles with an ACN/water mobile phase containing TFA. The effects of the acid modifiers, applied voltage, mobile phase, and detection wavelength were systematically evaluated using eight spiked standards, as well as urine samples. A typical analytical trial of urine samples from Sprague Dawley (S.D.) rats exposed to high-energy diet was carried out following sample pretreatment. Significant differences in urinary metabolic profiles were observed between the high energy diet-induced obesity rats and the healthy control rats at the 6th,wk postdose. Multivariate statistical analysis revealed the differential metabolites in response to the diet, which were partially validated with the putative standards. This work suggests that such a pCEC-based separation and analysis method may provide a new and cost-effective platform for metabolomic study uniquely positioned between the conventional chromatographic tools such as HPLC, and hyphenated analytical techniques such as LC-MS. [source]

Acute exercise modulates the Foxo1/PGC-1, pathway in the liver of diet-induced obesity rats

THE JOURNAL OF PHYSIOLOGY, Issue 9 2009
Eduardo R. Ropelle
PGC-1, expression is a tissue-specific regulatory feature that is extremely relevant to diabetes. Several studies have shown that PGC-1, activity is atypically activated in the liver of diabetic rodents and contributes to hepatic glucose production. PGC-1, and Foxo1 can physically interact with one another and represent an important signal transduction pathway that governs the synthesis of glucose in the liver. However, the effect of physical activity on PGC-1,/Foxo1 association is unknown. Here we investigate the expression of PGC-1, and the association of PGC-1,/Foxo1 in the liver of diet-induced obese rats after acute exercise. Wistar rats swam for two 3 h-long bouts, separated by a 45 min rest period. Eight hours after the acute exercise protocol, the rats were submitted to an insulin tolerance test (ITT) and biochemical and molecular analysis. Results demonstrate that acute exercise improved insulin signalling, increasing insulin-stimulated Akt and Foxo1 phosphorylation and decreasing PGC-1, expression and PGC-1,/Foxo1 interaction in the liver of diet-induced obesity rats under fasting conditions. These phenomena are accompanied by a reduction in the expression of gluconeogenesis genes, such as phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphate (G6Pase). Thus, these results provide new insights into the mechanism by which exercise could improve fasting hyperglycaemia. [source]

Acute physical exercise reverses S -nitrosation of the insulin receptor, insulin receptor substrate 1 and protein kinase B/Akt in diet-induced obese Wistar rats

THE JOURNAL OF PHYSIOLOGY, Issue 2 2008
José R. Pauli
Early evidence demonstrates that exogenous nitric oxide (NO) and the NO produced by inducible nitric oxide synthase (iNOS) can induce insulin resistance. Here, we investigated whether this insulin resistance, mediated by S -nitrosation of proteins involved in early steps of the insulin signal transduction pathway, could be reversed by acute physical exercise. Rats on a high-fat diet were subjected to swimming for two 3 h-long bouts, separated by a 45 min rest period. Two or 16 h after the exercise protocol the rats were killed and proteins from the insulin signalling pathway were analysed by immunoprecipitation and immunoblotting. We demonstrated that a high-fat diet led to an increase in the iNOS protein level and S -nitrosation of insulin receptor , (IR,), insulin receptor substrate 1 (IRS1) and Akt. Interestingly, an acute bout of exercise reduced iNOS expression and S -nitrosation of proteins involved in the early steps of insulin action, and improved insulin sensitivity in diet-induced obesity rats. Furthermore, administration of GSNO (NO donor) prevents this improvement in insulin action and the use of an inhibitor of iNOS (l- N6 -(1-iminoethyl)lysine; l -NIL) simulates the effects of exercise on insulin action, insulin signalling and S -nitrosation of IR,, IRS1 and Akt. In summary, a single bout of exercise reverses insulin sensitivity in diet-induced obese rats by improving the insulin signalling pathway, in parallel with a decrease in iNOS expression and in the S -nitrosation of IR/IRS1/Akt. The decrease in iNOS protein expression in the muscle of diet-induced obese rats after an acute bout of exercise was accompanied by an increase in AMP-activated protein kinase (AMPK) activity. These results provide new insights into the mechanism by which exercise restores insulin sensitivity. [source]