Lack of phosphatidylethanolamine N -methyltransferase in mice does not promote fatty acid oxidation in skeletal muscle
| Autor: | Jean E. Vance, Guergana Tasseva, Jelske N. van der Veen, Dennis E. Vance, Susanne Lingrell, René L. Jacobs |
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| Rok vydání: | 2016 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Phosphatidylethanolamine N-Methyltransferase Primary Cell Culture Gene Expression Biology Diet High-Fat Mice 03 medical and health sciences chemistry.chemical_compound Oxygen Consumption 0302 clinical medicine Internal medicine medicine Animals Myocyte Respiratory function Obesity Muscle Skeletal Molecular Biology Beta oxidation Mice Knockout chemistry.chemical_classification Muscle Cells Phosphatidylethanolamines Fatty Acids Skeletal muscle Fatty acid Cell Biology Dietary Fats Mitochondria Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure Malonyl-CoA Endocrinology Liver chemistry Phosphatidylethanolamine N-methyltransferase Phosphatidylcholines Insulin Resistance Energy Metabolism Energy source Oxidation-Reduction 030217 neurology & neurosurgery |
| Zdroj: | Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids. 1861:119-129 |
| ISSN: | 1388-1981 |
| DOI: | 10.1016/j.bbalip.2015.11.008 |
| Popis: | Phosphatidylethanolamine N-methyltransferase (PEMT) converts phosphatidylethanolamine (PE) to phosphatidylcholine (PC) in the liver. Mice lacking PEMT are protected from high-fat diet-induced obesity and insulin resistance, and exhibit increased whole-body energy expenditure and oxygen consumption. Since skeletal muscle is a major site of fatty acid oxidation and energy utilization, we determined if rates of fatty acid oxidation/oxygen consumption in muscle are higher in Pemt(-/-) mice than in Pemt(+/+) mice. Although PEMT is abundant in the liver, PEMT protein and activity were undetectable in four types of skeletal muscle. Moreover, amounts of PC and PE in the skeletal muscle were not altered by PEMT deficiency. Thus, we concluded that any influence of PEMT deficiency on skeletal muscle would be an indirect consequence of lack of PEMT in liver. Neither the in vivo rate of fatty acid uptake by muscle nor the rate of fatty acid oxidation in muscle explants and cultured myocytes depended upon Pemt genotype. Nor did PEMT deficiency increase oxygen consumption or respiratory function in skeletal muscle mitochondria. Thus, the increased whole body oxygen consumption in Pemt(-/-) mice, and resistance of these mice to diet-induced weight gain, are not primarily due to increased capacity of skeletal muscle for utilization of fatty acids as an energy source. |
| Databáze: | OpenAIRE |
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