Muscle-specific overexpression of FAT/CD36 enhances fatty acid oxidation by contracting muscle, reduces plasma triglycerides and fatty acids, and increases plasma glucose and insulin.

摘要: Increasing evidence has implicated the membrane protein CD36 (FAT) in binding and transport of long chain fatty acids (FA). To determine physiological role CD36, we examined effects its overexpression muscle, a tissue that depends on FA for energy needs is responsible clearing major fraction circulating FA. Mice with muscle were generated using promoter creatine kinase gene (MCK). Transgenic (MCK-CD36) mice had slightly lower body weight than control litter mates. This reflected leaner mass less overall adipose tissue, as evidenced by magnetic resonance spectroscopy. Soleus muscles from transgenic animals exhibited greatly enhanced ability to oxidize response stimulation/contraction. increased oxidative was not associated significant alterations histological appearance fibers. blood levels triglycerides reduced triglyceride content very low density lipoproteins. Blood cholesterol lower, but no decrease lipoprotein fractions measured. glucose significantly increased, while insulin similar fed state higher fasted state. However, tolerance curves, determined at 20 weeks age, mice. In summary, study documented, vivo, facilitate cellular uptake. It also illustrated importance uptake process metabolism utilization.