Insulin acutely improves mitochondrial function of rat and human skeletal muscle by increasing coupling efficiency of oxidative phosphorylation☆

Autor: Charles Affourtit, Raid B. Nisr
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