Carnitine supplementation alleviates lipid metabolism derangements and protects against oxidative stress in non-obese hereditary hypertriglyceridemic rats
Language English Country Canada Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
- Keywords
- antioxidant, antioxydant, insulin resistance, insulinorésistance, liver steatosis, mass spectrometry, metabolic syndrome, spectrométrie de masse, stéatose hépatique, syndrome métabolique,
- MeSH
- Genetic Predisposition to Disease MeSH
- Homeostasis MeSH
- Hypertriglyceridemia genetics metabolism MeSH
- Insulin Resistance MeSH
- Liver metabolism MeSH
- Carnitine administration & dosage analogs & derivatives blood metabolism pharmacology urine MeSH
- Muscle, Skeletal metabolism MeSH
- Rats MeSH
- Kidney drug effects metabolism MeSH
- Lipid Metabolism drug effects MeSH
- DNA, Mitochondrial genetics MeSH
- Oxidative Stress drug effects MeSH
- Dietary Supplements MeSH
- Gene Expression Regulation drug effects physiology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- acylcarnitine MeSH Browser
- Carnitine MeSH
- DNA, Mitochondrial MeSH
The aim of this 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, the hereditary hypertriglyceridemic (HHTg) rat. Male HHTg rats were fed a standard diet, and half of them received daily doses of carnitine (500 mg·kg(-1) body weight) for 8 weeks. Rats of the original Wistar strain were used for comparison. HHTg rats exhibited increased urinary excretion of free carnitine and 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. Compared with their untreated littermates, carnitine-treated HHTg rats exhibited lower weight gain, reduced liver steatosis, lower fasting triglyceridemia, and greater reduction of serum free fatty acid content after glucose load. 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 a more favorable complete to incomplete oxidation products ratio. Carnitine supplementation 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.
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