Phielix 2012 Diabetes: Difference between revisions
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Revision as of 17:34, 6 August 2013
Phielix E, Meex R, Ouwens DM, Sparks L, Hoeks J, Schaart G, Moonen-Kornips E, Hesselink MK, Schrauwen P (2012) High oxidative capacity due to chronic exercise training attenuates lipid-induced insulin resistance. Diabetes 61: 2472-2478 |
Phielix E, Meex R, Ouwens DM, Sparks L, Hoeks J, Schaart G, Moonen-Kornips E, Hesselink MK, Schrauwen P (2012) Diabetes
Abstract: Fat accumulation in skeletal muscle combined with low mitochondrial oxidative capacity is associated with insulin resistance (IR). Endurance-trained athletes, characterized by a high oxidative capacity, have elevated intramyocellular lipids, yet are highly insulin sensitive. We tested the hypothesis that a high oxidative capacity could attenuate lipid-induced IR. Nine endurance-trained (age = 23.4 ยฑ 0.9 years; BMI = 21.2 ยฑ 0.6 kg/m(2)) and 10 untrained subjects (age = 21.9 ยฑ 0.9 years; BMI = 22.8 ยฑ 0.6 kg/m(2)) were included and underwent a clamp with either infusion of glycerol or intralipid. Muscle biopsies were taken to perform high-resolution respirometry and protein phosphorylation/expression. Trained subjects had โผ32% higher mitochondrial capacity and โผ22% higher insulin sensitivity (P < 0.05 for both). Lipid infusion reduced insulin-stimulated glucose uptake by 63% in untrained subjects (P < 0.05), whereas this effect was blunted in trained subjects (29%, P < 0.05). In untrained subjects, lipid infusion reduced oxidative and nonoxidative glucose disposal (NOGD), whereas trained subjects were completely protected against lipid-induced reduction in NOGD, supported by dephosphorylation of glycogen synthase. We conclude that chronic exercise training attenuates lipid-induced IR and specifically attenuates the lipid-induced reduction in NOGD. Signaling data support the notion that high glucose uptake in trained subjects is maintained by shuttling glucose toward storage as glycogen. โข Keywords: Lipid-induced insulin resistance (IR), nonoxidative glucose disposal (NOGD), exercise training, glucose
โข O2k-Network Lab: NL Maastricht Schrauwen P, DE Duesseldorf Roden M
Labels:
Pathology: Diabetes
Stress:Mitochondrial Disease; Degenerative Disease and Defect"Mitochondrial Disease; Degenerative Disease and Defect" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property.
Organism: Human
Tissue;cell: Skeletal muscle
Preparation: Permeabilized tissue
Regulation: Anaerobic metabolism"Anaerobic metabolism" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property., Respiration"Respiration" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property., Substrate; Glucose; TCA Cycle"Substrate; Glucose; TCA Cycle" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property. Coupling state: OXPHOS
HRR: Oxygraph-2k