Difference between revisions of "Phielix 2008 Diabetes"
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{{Publication | {{Publication | ||
|title=Phielix E, Schrauwen-Hinderling VB, Mensink M, Lenaers E, Meex R, Hoeks J, Kooi ME, Moonen-Kornips E, Sels JP, Hesselink MK, Schrauwen P (2008) Lower intrinsic ADP-stimulated mitochondrial respiration underlies in vivo mitochondrial dysfunction in muscle of male type 2 diabetic patients. Diabetes 57: 2943- | |title=Phielix E, Schrauwen-Hinderling VB, Mensink M, Lenaers E, Meex R, Hoeks J, Kooi ME, Moonen-Kornips E, Sels JP, Hesselink MK, Schrauwen P (2008) Lower intrinsic ADP-stimulated mitochondrial respiration underlies ''in vivo'' mitochondrial dysfunction in muscle of male type 2 diabetic patients. Diabetes 57:2943-9. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/18678616 PMID: 18678616] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/18678616 PMID: 18678616 Open Access] | ||
|authors=Phielix E, Schrauwen-Hinderling VB, Mensink M, Lenaers E, Meex R, Hoeks J, Kooi ME, Moonen-Kornips E, Sels JP, Hesselink MK, Schrauwen P | |authors=Phielix E, Schrauwen-Hinderling VB, Mensink M, Lenaers E, Meex R, Hoeks J, Kooi ME, Moonen-Kornips E, Sels JP, Hesselink MK, Schrauwen P | ||
|year=2008 | |year=2008 | ||
|journal=Diabetes | |journal=Diabetes | ||
|abstract=Objective A lower in vivo mitochondrial function has been reported in (first-degree relatives (FDR) of) diabetic patients (T2DM). The nature of this reduction is unknown. Here we tested the hypothesis that a lower intrinsic mitochondrial respiratory capacity may underlie lower in vivo mitochondrial function observed in T2DM. | |abstract=Objective A lower ''in vivo'' mitochondrial function has been reported in (first-degree relatives (FDR) of) diabetic patients (T2DM). The nature of this reduction is unknown. Here we tested the hypothesis that a lower intrinsic mitochondrial respiratory capacity may underlie lower ''in vivo'' mitochondrial function observed in T2DM. | ||
Research Design and Methods Ten overweight T2DM, twelve FDR, and sixteen control subjects - all males - matched for age and BMI participated in this study. Insulin sensitivity was measured with a hyperinsulineamic euglyceamic clamp. Ex vivo intrinsic mitochondrial respiratory capacity was determined in permeabilized skinned muscle fibers using high-resolution respirometry and normalized for mitochondrial content. In vivo mitochondrial function was | Research Design and Methods Ten overweight T2DM, twelve FDR, and sixteen control subjects - all males - matched for age and BMI participated in this study. Insulin sensitivity was measured with a hyperinsulineamic euglyceamic clamp. Ex vivo intrinsic mitochondrial respiratory capacity was determined in permeabilized skinned muscle fibers using high-resolution respirometry and normalized for mitochondrial content. ''In vivo'' mitochondrial function was | ||
determined by measuring post-exercise PCr recovery half-time (PCrt1/2) using 31Phosphorus | determined by measuring post-exercise PCr recovery half-time (PCrt1/2) using 31Phosphorus | ||
Magnetic Resonance Spectroscopy. | Magnetic Resonance Spectroscopy. | ||
Results Insulin-stimulated glucose disposal (μmol/kgFFM/min) was lower in T2DM compared to control subjects (11.2 ± 2.8 vs 28.9 ± 3.7, respectively; p=0.003), with intermediate values for FDR (22.1 ± 3.4). In vivo mitochondrial function was 25% lower in T2DM (p=0.034) and 23% lower in FDR, but the latter did not reach statistical significance (p=0.08). Interestingly, ADPstimulated | Results Insulin-stimulated glucose disposal (μmol/kgFFM/min) was lower in T2DM compared to control subjects (11.2 ± 2.8 vs 28.9 ± 3.7, respectively; p=0.003), with intermediate values for FDR (22.1 ± 3.4). ''In vivo'' mitochondrial function was 25% lower in T2DM (p=0.034) and 23% lower in FDR, but the latter did not reach statistical significance (p=0.08). Interestingly, ADPstimulated | ||
basal respiration was 35% lower in T2DM (p=0.031) and FCCP-driven maximal | basal respiration was 35% lower in T2DM (p=0.031) and FCCP-driven maximal | ||
mitochondrial respiratory capacity was 31% lower in T2DM (p=0.05) compared to control subjects with intermediate values for FDR. | mitochondrial respiratory capacity was 31% lower in T2DM (p=0.05) compared to control subjects with intermediate values for FDR. | ||
Conclusions A reduced basal ADP-stimulated and maximal mitochondrial respiratory capacity underlies the reduction in in vivo mitochondrial function, independent of mitochondrial content. | Conclusions A reduced basal ADP-stimulated and maximal mitochondrial respiratory capacity underlies the reduction in ''in vivo'' mitochondrial function, independent of mitochondrial content. | ||
A reduced capacity at both the level of the electron transport chain and phosphorylation system underlies this impaired mitochondrial capacity. | A reduced capacity at both the level of the electron transport chain and phosphorylation system underlies this impaired mitochondrial capacity. | ||
|mipnetlab= | |mipnetlab=NL Maastricht Schrauwen P | ||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|tissues=Skeletal muscle | |||
|diseases=Diabetes | |||
|couplingstates=OXPHOS | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
}} | }} | ||
Latest revision as of 16:00, 20 March 2015
| Phielix E, Schrauwen-Hinderling VB, Mensink M, Lenaers E, Meex R, Hoeks J, Kooi ME, Moonen-Kornips E, Sels JP, Hesselink MK, Schrauwen P (2008) Lower intrinsic ADP-stimulated mitochondrial respiration underlies in vivo mitochondrial dysfunction in muscle of male type 2 diabetic patients. Diabetes 57:2943-9. |
Phielix E, Schrauwen-Hinderling VB, Mensink M, Lenaers E, Meex R, Hoeks J, Kooi ME, Moonen-Kornips E, Sels JP, Hesselink MK, Schrauwen P (2008) Diabetes
Abstract: Objective A lower in vivo mitochondrial function has been reported in (first-degree relatives (FDR) of) diabetic patients (T2DM). The nature of this reduction is unknown. Here we tested the hypothesis that a lower intrinsic mitochondrial respiratory capacity may underlie lower in vivo mitochondrial function observed in T2DM. Research Design and Methods Ten overweight T2DM, twelve FDR, and sixteen control subjects - all males - matched for age and BMI participated in this study. Insulin sensitivity was measured with a hyperinsulineamic euglyceamic clamp. Ex vivo intrinsic mitochondrial respiratory capacity was determined in permeabilized skinned muscle fibers using high-resolution respirometry and normalized for mitochondrial content. In vivo mitochondrial function was determined by measuring post-exercise PCr recovery half-time (PCrt1/2) using 31Phosphorus Magnetic Resonance Spectroscopy. Results Insulin-stimulated glucose disposal (μmol/kgFFM/min) was lower in T2DM compared to control subjects (11.2 ± 2.8 vs 28.9 ± 3.7, respectively; p=0.003), with intermediate values for FDR (22.1 ± 3.4). In vivo mitochondrial function was 25% lower in T2DM (p=0.034) and 23% lower in FDR, but the latter did not reach statistical significance (p=0.08). Interestingly, ADPstimulated basal respiration was 35% lower in T2DM (p=0.031) and FCCP-driven maximal mitochondrial respiratory capacity was 31% lower in T2DM (p=0.05) compared to control subjects with intermediate values for FDR. Conclusions A reduced basal ADP-stimulated and maximal mitochondrial respiratory capacity underlies the reduction in in vivo mitochondrial function, independent of mitochondrial content. A reduced capacity at both the level of the electron transport chain and phosphorylation system underlies this impaired mitochondrial capacity.
• O2k-Network Lab: NL Maastricht Schrauwen P
Labels:
Pathology: Diabetes
Tissue;cell: Skeletal muscle
Coupling state: OXPHOS
HRR: Oxygraph-2k
