Difference between revisions of "Phielix 2012 Diabetes"
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{{Publication | {{Publication | ||
|title=Phielix E, Meex R, Ouwens DM, Sparks LM, 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- | |title=Phielix E, Meex R, Ouwens DM, Sparks LM, 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 61:2472-8. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/22787138 PMID: 22787138] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/22787138 PMID: 22787138] | ||
|authors=Phielix E, Meex R, Ouwens DM, Sparks | |authors=Phielix E, Meex R, Ouwens DM, Sparks LM, Hoeks J, Schaart G, Moonen-Kornips E, Hesselink MK, Schrauwen P | ||
|year=2012 | |year=2012 | ||
|journal=Diabetes | |journal=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 ± 0.9 years; BMI = 21.2 ± 0.6 kg/m(2)) and 10 untrained subjects (age = 21.9 ± 0.9 years; BMI = 22.8 ± 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 ∼32% higher mitochondrial capacity and ∼22% 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. | |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 ± 0.9 years; BMI = 21.2 ± 0.6 kg/m(2)) and 10 untrained subjects (age = 21.9 ± 0.9 years; BMI = 22.8 ± 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 ∼32% higher mitochondrial capacity and ∼22% 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. | ||
|keywords=Lipid-induced insulin resistance (IR), nonoxidative glucose disposal (NOGD), exercise training, glucose | |keywords=Lipid-induced insulin resistance (IR), nonoxidative glucose disposal (NOGD), exercise training, glucose | ||
|mipnetlab=NL Maastricht Schrauwen P, DE Duesseldorf Roden M, | |mipnetlab=NL Maastricht Schrauwen P, DE Duesseldorf Roden M, US FL Orlando Sparks LM | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
| Line 14: | Line 14: | ||
|tissues=Skeletal muscle | |tissues=Skeletal muscle | ||
|preparations=Permeabilized tissue | |preparations=Permeabilized tissue | ||
|injuries=Mitochondrial | |injuries=Mitochondrial disease | ||
|diseases=Diabetes | |diseases=Diabetes | ||
|topics=Aerobic glycolysis, Substrate | |topics=Aerobic glycolysis, Substrate | ||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=BMI, VO2max | |||
}} | }} | ||
Latest revision as of 15:46, 6 May 2016
| Phielix E, Meex R, Ouwens DM, Sparks LM, 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 61:2472-8. |
Phielix E, Meex R, Ouwens DM, Sparks LM, 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 ± 0.9 years; BMI = 21.2 ± 0.6 kg/m(2)) and 10 untrained subjects (age = 21.9 ± 0.9 years; BMI = 22.8 ± 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 ∼32% higher mitochondrial capacity and ∼22% 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. • Keywords: Lipid-induced insulin resistance (IR), nonoxidative glucose disposal (NOGD), exercise training, glucose
• O2k-Network Lab: NL Maastricht Schrauwen P, DE Duesseldorf Roden M, US FL Orlando Sparks LM
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style, mt-Medicine
Pathology: Diabetes
Stress:Mitochondrial disease
Organism: Human
Tissue;cell: Skeletal muscle
Preparation: Permeabilized tissue
Regulation: Aerobic glycolysis, Substrate Coupling state: OXPHOS
HRR: Oxygraph-2k
BMI, VO2max
