Abstract
BackgroundIn the present study, we tested the hypothesis that carnitine supplementation counteracts obesity-induced muscle fiber transition from type I to type II.Methods24 obese Zucker rats were randomly divided into two groups of 12 rats each (obese control, obese carnitine) and 12 lean Zucker rats were selected for lean control group. A control diet was given to both control groups and a carnitine supplemented diet (3 g/kg diet) was given to obese carnitine group for 4 wk. Components of the muscle fiber transformation in skeletal muscle were examined.ResultsThe plasma level of carnitine were lower in the obese control group compared to the lean control group and higher in the obese carnitine group than in the other groups (P < 0.05). Plasma concentrations of triglycerides and non-esterified fatty acids were increased in obese animals compared to lean animals and the obese carnitine group had lower level compared to the obese control group (P < 0.05). The obese carnitine group had an increased number of type I muscle fibers and higher mRNA levels of type I fiber-specific myosin heavy chain, regulators of muscle fiber transition and of genes involved in carnitine uptake, fatty acid transport, β-oxidation, angiogenesis, tricarboxylic acid cycle and thermo genesis in M. rectus femoris compared to the other groups (P < 0.05).ConclusionThe results demonstrate that carnitine supplementation to obese Zucker a rat counteracts the obesity-induced muscle fiber transition and restores the muscle oxidative metabolic phenotype. Carnitine supplementation is supposed to be beneficial for the treatment of elevated levels of plasma lipids during obesity or diabetes.
Highlights
In the present study, we tested the hypothesis that carnitine supplementation counteracts obesityinduced muscle fiber transition from type I to type II
Due to carnitine supplementation concentrations of free carnitine, acetyl-carnitine and total carnitine in plasma and rectus femoris muscle were greater in the obese carnitine group than in the lean control group (P < 0.05; Table 4)
Expression of genes involved in carnitine uptake, fatty acid transport, fatty acid utilization, and glycolysis in M. rectus femoris The mRNA levels of genes involved in carnitine uptake [SLC22A5 encoding organic cation/carnitine transporter (OCTN2)], fatty acid transport and uptake (FABP3 encoding fatty acid binding protein 3, CD36 encoding fatty acid translocase/CD36, LPL encoding lipoprotein lipase), Table 3 Feed intake and body weight gains of lean rats, obese Zucker rats fed a control diet or obese Zucker rats fed a diet supplemented with 3 g/kg diet carnitine for 4 wk1
Summary
We tested the hypothesis that carnitine supplementation counteracts obesityinduced muscle fiber transition from type I to type II. Genetic and/or high fat diet-induced obesity and diabetes cause an impairment of carnitine status [9,10,11], whereas normalization of carnitine status due to carnitine supplementation reverses mitochondrial dysfunction under these conditions [4,9,10,12,13]. At large, these findings indicate that carnitine supplementation through normalizing carnitine status is able to prevent type I to type II fiber transition and thereby the metabolic shift from oxidative to glycolytic of skeletal muscle under unloading conditions or metabolic stress
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