Insulin acutely improves mitochondrial function of rat and human skeletal muscle by increasing coupling efficiency of oxidative phosphorylation☆
Autor: | Charles Affourtit, Raid B. Nisr |
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Jazyk: | angličtina |
Rok vydání: | 2014 |
Předmět: |
DMEM
Dulbecco's modified Eagle medium medicine.medical_treatment Palmitic Acid Mitochondrion Biochemistry Hepes 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid Oxidative Phosphorylation 0302 clinical medicine Uncoupling protein Insulin Glycolysis Anaerobiosis FCCP trifluorocarbonylcyanide phenylhydrazone 0303 health sciences Insulin sensitivity 3. Good health Mitochondria medicine.anatomical_structure Glycogenesis UCP uncoupling protein Protons Mitochondrial proton leak Cell respiratory control medicine.medical_specialty Cell Respiration Biophysics Skeletal muscle cells Oxidative phosphorylation Biology Article Cell Line 03 medical and health sciences Oxygen Consumption Internal medicine medicine 2DG 2-deoxyglucose Animals Humans Muscle Skeletal 030304 developmental biology ECAR extracellular acidification rate Mitochondrial coupling efficiency Skeletal muscle Cell Biology Rats Endocrinology Glucose Anaerobic glycolysis BSA bovine serum albumin FCS fetal calf serum 030217 neurology & neurosurgery |
Zdroj: | Biochimica et Biophysica Acta |
ISSN: | 0006-3002 |
Popis: | Insulin is essential for the regulation of fuel metabolism and triggers the uptake of glucose by skeletal muscle. The imported glucose is either stored or broken down, as insulin stimulates glycogenesis and ATP synthesis. The mechanism by which ATP production is increased is incompletely understood at present and, generally, relatively little functional information is available on the effect of insulin on mitochondrial function. In this paper we have exploited extracellular flux technology to investigate insulin effects on the bioenergetics of rat (L6) and human skeletal muscle myoblasts and myotubes. We demonstrate that a 20-min insulin exposure significantly increases (i) the cell respiratory control ratio, (ii) the coupling efficiency of oxidative phosphorylation, and (iii) the glucose sensitivity of anaerobic glycolysis. The improvement of mitochondrial function is explained by an insulin-induced immediate decrease of mitochondrial proton leak. Palmitate exposure annuls the beneficial mitochondrial effects of insulin. Our data improve the mechanistic understanding of insulin-stimulated ATP synthesis, and reveal a hitherto undisclosed insulin sensitivity of cellular bioenergetics that suggests a novel way of detecting insulin responsiveness of cells. Highlights • Insulin acutely improves mitochondrial function of skeletal muscle cells. • Mitochondrial proton leak of skeletal muscle cells is attenuated by insulin. • Insulin sensitises anaerobic glycolysis of skeletal muscle cells to glucose. • Bioenergetic insulin effects offer novel assays for cellular insulin sensitivity. |
Databáze: | OpenAIRE |
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