| Impact of exercise training on insulin sensitivity, physical fitness, and muscle oxidative capacity in first-degree relatives of type 2 diabetic patients. | |
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MedLine Citation:
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PMID: 16352678 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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First-degree relatives of type 2 diabetic patients (offspring) are often characterized by insulin resistance and reduced physical fitness (VO2 max). We determined the response of healthy first-degree relatives to a standardized 10-wk exercise program compared with an age-, sex-, and body mass index-matched control group. Improvements in VO2 max (14.1 +/- 11.3 and 16.1 +/- 14.2%; both P < 0.001) and insulin sensitivity (0.6 +/- 1.4 and 1.0 +/- 2.1 mg x kg(-1) x min(-1); both P < 0.05) were comparable in offspring and control subjects. However, VO2 max and insulin sensitivity in offspring were not related at baseline as in the controls (r = 0.009, P = 0.96 vs. r = 0.67, P = 0.002). Likewise, in offspring, exercise-induced changes in VO2 max did not correlate with changes in insulin sensitivity as opposed to controls (r = 0.06, P = 0.76 vs. r = 0.57, P = 0.01). Skeletal muscle oxidative capacity tended to be lower in offspring at baseline but improved equally in both offspring and controls in response to exercise training (delta citrate synthase enzyme activity 26 vs. 20%, and delta cyclooxygenase enzyme activity 25 vs. 23%. Skeletal muscle fiber morphology and capillary density were comparable between groups at baseline and did not change significantly with exercise training. In conclusion, this study shows that first-degree relatives of type 2 diabetic patients respond normally to endurance exercise in terms of changes in VO2 max and insulin sensitivity. However, the lack of a correlation between the VO2 max and insulin sensitivity in the first-degree relatives of type 2 diabetic patients indicates that skeletal muscle adaptations are dissociated from the improvement in VO2 max. This could indicate that, in first-degree relatives, improvement of insulin sensitivity is dissociated from muscle mitochondrial functions. |
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Authors:
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Torben Østergård; Jesper L Andersen; Birgit Nyholm; Sten Lund; K Sreekumaran Nair; Bengt Saltin; Ole Schmitz |
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Publication Detail:
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Type: Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2005-12-13 |
Journal Detail:
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Title: American journal of physiology. Endocrinology and metabolism Volume: 290 ISSN: 0193-1849 ISO Abbreviation: Am. J. Physiol. Endocrinol. Metab. Publication Date: 2006 May |
Date Detail:
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Created Date: 2006-04-10 Completed Date: 2006-06-19 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 100901226 Medline TA: Am J Physiol Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: E998-1005 Citation Subset: IM |
Affiliation:
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Dept. of Endocrinology & Diabetes M, Aarhus Univ. Hospital, Aarhus Sygehus, Nørrebrogade 42-44, DK-8000 Aarhus C, Denmark. oest@dadlnet.dk |
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Blood Glucose / metabolism Body Mass Index C-Peptide / blood Citrate (si)-Synthase / metabolism Diabetes Mellitus, Type 2 / blood, genetics, physiopathology* Electron Transport Complex IV / metabolism Exercise / physiology* Exercise Test Family Health Female Humans Insulin / blood Insulin Resistance / physiology* Lipid Metabolism / physiology Male Muscle, Skeletal / cytology, metabolism* Oxidation-Reduction Oxygen / metabolism Physical Fitness / physiology* Regression Analysis |
| Grant Support | |
ID/Acronym/Agency:
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R01 DK-41973/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Blood Glucose; 0/C-Peptide; 11061-68-0/Insulin; 7782-44-7/Oxygen; EC 1.9.3.1/Electron Transport Complex IV; EC 2.3.3.1/Citrate (si)-Synthase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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