Similar changes in muscle lipid metabolism are induced by chronic high‐fructose feeding and high‐fat feeding in C57BL/J6 mice
Authors:
- 8 October 2012
- journal article
- research article
- Published by Wiley in Clinical and Experimental Pharmacology and Physiology
- Vol. 39 (12) , 1011-1018
Abstract
Summary: The aim of the present study was to investigate the effects of high fructose and high fat feeding on muscle lipid metabolism and to illustrate the mechanisms by which the two different dietary factors induce muscle lipid accumulation. C57BL/J6 mice were fed either a standard, high‐fructose (HFru) or high‐fat diet. After 16 weeks feeding, mice were killed and plasma triglyceride (TG) and free fatty acid (FFA) levels were detected. In addition, muscle TG and long chain acyl CoA (LCACoA) content was determined, glucose tolerance was evaluated and the protein content of fatty acid translocase CD36 (FATCD36) in muscle was measured. Mitochondrial oxidative function in the muscle was evaluated by estimating the activity of oxidative enzymes, namely cytochrome oxidase (COx), citrate synthase (CS) and β‐hydroxyacyl CoA dehydrogenase (β‐HAD), and the muscle protein content of carnitine palmitoyltransferase‐1 (CPT‐1), cyclo‐oxygenase (COX)‐1 and proliferator‐activated receptor coactivator (PGC)‐1α was determined. Finally, sterol regulatory element‐binding protein‐1c (SREBP‐1c) gene expression and fatty acid synthase (FAS) protein content were determined in muscle tissues. After 16 weeks, plasma TG and FFA levels were significantly increased in both the HFru and HF groups. In addition, mice in both groups exhibited significant increases in muscle TG and LCACoA content. Compared with mice fed the standard diet (control group), those in the HFru and HF groups developed glucose intolerance and exhibited increased FATCD36 protein levels, enzyme activity related to fatty acid utilization in the mitochondria and protein expressions of CPT‐1, COX‐1 and PGC‐1α in muscle tissue. Finally, mice in both the HFru and HF groups exhibited increase SREBP‐1c expression and FAS protein content. In conclusion, high fructose and high fat feeding lead to similar changes in muscle lipid metabolism in C57BL/J6 mice. Lipid accumulation in the muscle may be associated with increased expression of proteins related to lipid transportation and synthesis.Keywords
This publication has 43 references indexed in Scilit:
- Mechanisms underlying skeletal muscle insulin resistance induced by fatty acids: importance of the mitochondrial functionLipids in Health and Disease, 2012
- Differing Endoplasmic Reticulum Stress Response to Excess Lipogenesis versus Lipid Oversupply in Relation to Hepatic Steatosis and Insulin ResistancePLOS ONE, 2012
- Differential effects of short- and long-term high-fat diet feeding on hepatic fatty acid metabolism in ratsBiochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, 2011
- Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistanceCurrent Opinion in Lipidology, 2008
- Monosaccharide-induced lipogenesis regulates the human hepatic sex hormone–binding globulin geneJournal of Clinical Investigation, 2007
- Effect of L‐Carnitine on Skeletal Muscle Lipids and Oxidative Stress in Rats Fed High‐Fructose DietJournal of Diabetes Research, 2007
- Exercise training and calorie restriction increase SREBP-1 expression and intramuscular triglyceride in skeletal muscleAmerican Journal of Physiology-Endocrinology and Metabolism, 2006
- Impaired plasma fatty acid oxidation in extremely obese womenAmerican Journal of Physiology-Endocrinology and Metabolism, 2004
- In vivo regulation of SREBP-1c in skeletal muscle: effects of nutritional status, glucose, insulin, and leptinAmerican Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2004
- Triacylglycerol accumulation in human obesity and type 2 diabetes is associated with increased rates of skeletal muscle fatty acid transport and increased sarcolemmal FAT/CD36The FASEB Journal, 2004