Cahova 2014 Appl Physiol Nutr Metab
|Cahova M, Chrastina P, Hansikova H, Drahota Z, Trnovska J, Skop V, Spacilova J, Malinska HOliyarnyk O, Papackova Z, Palenickova E,Kazdova L (2014) Carnitine supplementation alleviates lipid metabolism derangements and protects against oxidative stress in non-obese hereditary hypertriglyceridemic rats. Appl Physiol Nutr Metab 40:280-91.|
Abstract: The aim of study was to estimate the effect of carnitine supplementation on lipid disorders and peripheral tissue insulin sensitivity in a non-obese animal model of insulin resistance, hereditary hypertriglyceridemic rats (HHTg). Male HHTg rats were fed a standard diet, and half of them were administered carnitine 500mg/kg b.wt. daily for 8 weeks. Rats of the original Wistar strain were used for comparison. HHTg rats exhibited an increased urinary excretion of free carnitine together with reduced carnitine content in the liver and blood. Carnitine supplementation compensated for this shortage and promoted urinary excretion of acetylcarnitine without any signs of (acyl)carnitine accumulation in skeletal muscle. Carnitine-treated HHTg rats exhibited lower weight gain, reduction of liver steatosis, lower fasting triglyceridemia and greater reduction of free fatty acid serum content after glucose load, compared with their untreated littermates. Carnitine treatment was associated with increased mitochondrial biogenesis and oxidative capacity for fatty acids, amelioration of oxidative stress, and restored substrate switching in the liver. In skeletal muscle (diaphragm) carnitine supplementation was associated with significantly higher palmitate oxidation and more favorable complete to incomplete oxidation products ratio. It further enhanced insulin sensitivity ex vivo. No effects on whole body glucose tolerance were observed. Our data suggest that some metabolic syndrome related disorders, particularly fatty acid oxidation, steatosis, and oxidative stress in the liver, could be attenuated by carnitine supplementation. The effect of carnitine could be explained, at least partly, by enhanced substrate oxidation and increased fatty acid transport from tissues in the form of short-chain acylcarnitines.
• Keywords: Metabolic syndrome, Insulin resistance, Antioxidant, Liver steatosis, Mass spectrometry
Labels: MiParea: Respiration Pathology: Diabetes Stress:Oxidative stress;RONS Organism: Rat Tissue;cell: Liver Preparation: Isolated mitochondria
Coupling state: OXPHOS Pathway: F, N, S HRR: Oxygraph-2k