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Journal of Lipid Research, Vol. 46, 582-588, March 2005
Copyright © 2005 by American Society for Biochemistry and Molecular Biology

Sixteen hours of fasting differentially affects hepatic and muscle insulin sensitivity in mice

Annemieke C. Heijboer^1,*,, Esther Donga, Peter J. Voshol^*,, Zhi-Chao Dang^*, Louis M. Havekes^,, Johannes A. Romijn^* and Eleonora P. M. Corssmit^*

^* Department of Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands
Netherlands Organization for Applied Scientific Research (TNO) Prevention and Health, Gaubius Laboratory, Leiden, The Netherlands
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands

¹ To whom correspondence should be addressed. e-mail: a.c.heijboer{at}lumc.nl

Fasting readily induces hepatic steatosis. Hepatic steatosis is associated with hepatic insulin resistance. The purpose of the present study was to document the effects of 16 h of fasting in wild-type mice on insulin sensitivity in liver and skeletal muscle in relation to 1) tissue accumulation of triglycerides (TGs) and 2) changes in mRNA expression of metabolically relevant genes. Sixteen hours of fasting did not show an effect on hepatic insulin sensitivity in terms of glucose production in the presence of increased hepatic TG content. In muscle, however, fasting resulted in increased insulin sensitivity, with increased muscle glucose uptake without changes in muscle TG content. In liver, fasting resulted in increased mRNA expression of genes promoting gluconeogenesis and TG synthesis but in decreased mRNA expression of genes involved in glycogenolysis and fatty acid synthesis. In muscle, increased mRNA expression of genes promoting glucose uptake, as well as lipogenesis and ß-oxidation, was found.

In conclusion, 16 h of fasting does not induce hepatic insulin resistance, although it causes liver steatosis, whereas muscle insulin sensitivity increases without changes in muscle TG content. Therefore, fasting induces differential changes in tissue-specific insulin sensitivity, and liver and muscle TG contents are unlikely to be involved in these changes.

Abbreviations: ACC, acetyl-C7oA carboxylase; BGU, body glucose uptake; BHQ1, BlackHoleQuencher-1; Ct, critical threshold; 2-DG, 2-deoxyglucose; DGAT, diacylglycerol acyltransferase; GAPDH, glyceraldehyde phosphate dehydrogenase; GLUT4, glucose transporter 4; GP, glycogen phosphorylase; G6P, glucose-6-phosphatase; HGP, hepatic glucose production; PEPCK, phosphoenolpyruvate carboxykinase; PPAR, peroxisome proliferator-activated receptor; RT-PCR, real-time polymerase chain reaction; SREBP, sterol-regulatory element binding protein; TG, triglyceride

Supplementary key words glucose metabolism • steatosis • insulin action • transcription factors • isotopes

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