Abstract

BackgroundRecently, supplementation of L-carnitine to obese rats was found to improve the carnitine status and to counteract an obesity-induced muscle fiber transition from type I to type II. However, it has not been resolved if the change of muscle fiber distribution induced in obese rats and the restoration of the “normal” muscle fiber distribution, which is found in lean rats, in obese rats by supplemental L-carnitine is causally linked with the carnitine status. In the present study we hypothesized that fiber type distribution in skeletal muscle is dependent on carnitine status.MethodsTo test this, an experiment with 48 piglets which were randomly allocated to four groups (n = 12) was performed. All piglets were given orally either 60 mg sodium bicarbonate/kg body weight (group CON), 20 mg L-carnitine and 60 mg sodium bicarbonate/kg body weight (group CARN), 30 mg pivalate (dissolved in sodium bicarbonate)/kg body weight (group PIV) or 20 mg L-carnitine and 30 mg pivalate/kg body weight (group CARN + PIV) each day for a period of 4 weeks.ResultsConcentrations of total carnitine in plasma, liver and longissimus dorsi and biceps femoris muscles were 2.0–2.7 fold higher in group CARN than in group CON, whereas these concentrations were 1.9–2.5-fold lower in group PIV than in group CON. The concentrations of total carnitine in these tissues did not statistically differ between group CARN + PIV and group CON. Fiber type distribution of longissimus dorsi and biceps femoris muscles, mRNA and protein levels of molecular regulators of fiber distribution in longissimus dorsi and biceps femoris muscles and mRNA levels of genes reflecting the metabolic phenotype of longissimus dorsi and biceps femoris muscles did not differ between groups.ConclusionChanges in the systemic carnitine status and the muscle carnitine concentration induced by either supplementing L-carnitine or administering pivalate have no impact on the contractile and metabolic phenotype of skeletal muscles in pigs.

Highlights

  • Supplementation of L-carnitine to obese rats was found to improve the carnitine status and to counteract an obesity-induced muscle fiber transition from type I to type II

  • We have found recently that supplementation of L-carnitine to obese rats counteracts the obesity-induced muscle fiber transition from type I to type II through inducing genes encoding critical molecular regulators of muscle fiber transition, like peroxisome proliferator-activated receptor δ (PPARδ encoded by PPARD), PPARγ coactivator-1α (PGC-1α encoded by PPARGC1A) and PGC-1β (PPARGC1B) [9,10,11,12], and thereby favours an oxidative metabolic phenotype of skeletal muscle [13]

  • We have found in our recent study that obese rats receiving no supplemental L-carnitine had significantly lower tissue carnitine concentrations than healthy lean rats, while supplementation of L-carnitine to the obese rats increased tissue carnitine concentrations to levels found in lean rats [13]

Read more

Summary

Introduction

Supplementation of L-carnitine to obese rats was found to improve the carnitine status and to counteract an obesity-induced muscle fiber transition from type I to type II. In the present study we hypothesized that fiber type distribution in skeletal muscle is dependent on carnitine status. We have found recently that supplementation of L-carnitine to obese rats counteracts the obesity-induced muscle fiber transition from type I to type II through inducing genes encoding critical molecular regulators of muscle fiber transition, like peroxisome proliferator-activated receptor δ (PPARδ encoded by PPARD), PPARγ coactivator-1α (PGC-1α encoded by PPARGC1A) and PGC-1β (PPARGC1B) [9,10,11,12], and thereby favours an oxidative metabolic phenotype of skeletal muscle [13]. Lcarnitine is generally important for proper functioning of intermediary metabolism considering that deficiency of Lcarnitine is associated with impaired fatty acid utilization and with perturbations of glucose utilization and insulin sensitivity [16]

Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call