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Submitted on August 7, 2003
Accepted on December 5, 2003
deficiency does not alter insulin sensitivity in mice maintained on regular or high fat diet: the hyperinsulinemic-euglycemic clamp studies
1 Dept. of Medicine, Faculty of Medicine, Charles University, Prague, Czech Republic; Mouse Metabolism Laboratory, NIDDK, National Institutes of Health, Bethesda, USA; Diabetes Branch, NIDDK, National Institutes of Health, Bethesda, USA
* To whom correspondence should be addressed. E-mail: MHALU{at}LF.CUNI.CZ.
Chronic PPAR-
activation improves glucose metabolism in rodent models of insulin resistance and diabetes; however, PPAR- deficiency was also reported to protect against high fat diet (HFD)-induced insulin resistance. The aim of this study was to clarify the role of PPAR- in the development of insulin resistance using PPAR- knockout mice (PPAR- KO) and wild-type controls (WT). Both WT and PPAR- KO mice on HFD gained significantly more weight relative to chow-fed groups and displayed an increase in insulin levels and decrease in adiponectin levels. Hyperinsulinemic-euglycemic clamp performed in non-fasting state demonstrated that HFD caused a marked reduction in whole body, muscle, white and brown adipose tissue glucose uptake in both WT and PPAR- KO mice relative to chow-fed groups. Suppression of endogenous glucose production during the clamp was markedly blunted in both WT and PPAR- KO HFD-fed mice, indicating liver insulin resistance. The magnitude of HFD-induced changes in the clamp parameters of insulin sensitivity was comparable in PPAR- KO and WT mice. In conclusion, these data show that PPAR- deficiency does not alter insulin sensitivity in mice fed normal chow diet and does not protect against HFD-induced insulin resistance as measured by hyperinsulinemic-euglycemic clamp in non-fasted state.
knockout •
glucose clamp •
fasting
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