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Cited by 75Metabolism, Diabetes, and CancerCardiovascular and exercise physiologyGenetics and Physical Performance

Short-term exercise training does not stimulate skeletal muscle ATP synthesis in relatives of humans with type 2 diabetes.

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Kacerovsky-Bielesz, Gertrud, Chmelik, Marek, Ling, Charlotte, Pokan, Rochus, Szendroedi, Julia, Farukuoye, Michaela, Kacerovsky, Michaela, Schmid, Albrecht I. +7 more·2009·Diabetes
DOI 10.2337/db08-1240PMC PMC2682667
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Abstract

OBJECTIVE: We tested the hypothesis that short-term exercise training improves hereditary insulin resistance by stimulating ATP synthesis and investigated associations with gene polymorphisms. RESEARCH DESIGN AND METHODS: We studied 24 nonobese first-degree relatives of type 2 diabetic patients and 12 control subjects at rest and 48 h after three bouts of exercise. In addition to measurements of oxygen uptake and insulin sensitivity (oral glucose tolerance test), ectopic lipids and mitochondrial ATP synthesis were assessed using(1)H and(31)P magnetic resonance spectroscopy, respectively. They were genotyped for polymorphisms in genes regulating mitochondrial function, PPARGC1A (rs8192678) and NDUFB6 (rs540467). RESULTS: Relatives had slightly lower (P = 0.012) insulin sensitivity than control subjects. In control subjects, ATP synthase flux rose by 18% (P = 0.0001), being 23% higher (P = 0.002) than that in relatives after exercise training. Relatives responding to exercise training with increased ATP synthesis (+19%, P = 0.009) showed improved insulin sensitivity (P = 0.009) compared with those whose insulin sensitivity did not improve. A polymorphism in the NDUFB6 gene from respiratory chain complex I related to ATP synthesis (P = 0.02) and insulin sensitivity response to exercise training (P = 0.05). ATP synthase flux correlated with O(2)uptake and insulin sensitivity. CONCLUSIONS: The ability of short-term exercise to stimulate ATP production distinguished individuals with improved insulin sensitivity from those whose insulin sensitivity did not improve. In addition, the NDUFB6 gene polymorphism appeared to modulate this adaptation. This finding suggests that genes involved in mitochondrial function contribute to the response of ATP synthesis to exercise training.

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  • Additional mechanisms potentially linking impaired mitochondrial oxidative function to insulin resistance include reduced ATP synthesis for energy-requiring functions, abnormalities in calcium homeostasis, and reduced ATP production during exercise.

    “Additional mechanisms potentially linking impaired mitochondrial oxidative function to insulin resistance include: 1) reduced ATP synthesis for energyrequiring functions such as insulin-stimulated glucose uptake; 2) abnormalities in calcium homeostasis (necessary for exercise-induced glucose uptake) (103-105); and 3) reduced ATP production during exercise (106), potentially contributing to reduced”

    From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [106]

  • Mild deficiencies in mitochondrial activity, and/or an inability to increase activity and capacity in response to cellular energy demand, could explain the reduced exercise ability seen in individuals with a family history of DM.

    “With regard to the first question, mild deficiencies in mitochondrial activity, and/or an inability to increase activity and capacity in response to cellular energy demand, could explain the reduced exercise ability seen in individuals with a family history of DM (106).”

    From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [106]

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Authors
Kacerovsky-Bielesz, G., Chmelik, M., Ling, C., Pokan, R., Szendroedi, J., Farukuoye, M., Kacerovsky, M., Schmid, A. I., Gruber, S., Wolzt, M., Moser, E., Pacini, G., Smekal, G., Groop, L., & Roden, M.
Affiliations
  • Hanusch Hospital (AT)
  • Karl-Landsteiner Institute for Endocrinology and Metabolism, Vienna, Austria;
  • Lund University (SE)
  • University of Vienna (AT)
  • Medical University of Vienna (AT)
  • National Research Council (IT)
Corresponding author
Roden, Michael
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
2009-03-05
Volume
58
Issue
6
Pages
1333-1341
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/db08-1240
PMC
PMC2682667
OpenAlex
W2156223798
Cited by
75
References
54
Citations by year
2026: 1 · 2024: 2 · 2023: 1 · 2022: 4 · 2021: 13 · 2020: 5 · 2019: 1 · 2018: 3 · 2017: 3 · 2016: 6 · 2015: 3 · 2014: 4 · 2013: 2 · 2012: 10
FWCI
3.62
Type
journal article
Language
en
Open access
Licence
Locations
  • Diabetes (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Phaidra (Universität Wien) (submittedVersion, cc-by-nc-nd)
  • Lund University Publications (Lund University) (submittedVersion)
Funders
  • Eli Lilly and Company
  • GlaxoSmithKline
  • Sanofi
  • European Foundation for the Study of Diabetes
  • Universität Wien
  • Oesterreichische Nationalbank (OENB 11459)
  • Novo Nordisk
  • Vetenskapsrådet
  • Regione del Veneto
  • Österreichische Diabetes Gesellschaft
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Physical Performance
Keywords
type 2 diabetes, first-degree relatives, short-term exercise training, insulin sensitivity, insulin resistance, mitochondrial function, PGC-1α, genetic polymorphism, respiratory chain complex I, oxygen consumption
MeSH terms
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Adenosine Triphosphatases, Adenosine Triphosphate, Diabetes Mellitus, Type 2, Family, Feeding Behavior, Heat-Shock Proteins, Humans, NADH, NADPH Oxidoreductases, Polymorphism, Genetic, Surveys and Questionnaires, Transcription Factors, Exercise, DNA Primers, Muscle, Skeletal, Electron Transport Complex I

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