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

Autor: Charlotte Ling, Marek Chmelik, Gertrud Kacerovsky-Bielesz, Michaela Kacerovsky, Michael Wolzt, Giovanni Pacini, Michael Roden, Gerhard Smekal, Leif Groop, Julia Szendroedi, Rochus Pokan, Michaela Farukuoye, Albrecht Ingo Schmid, Stephan Gruber, Ewald Moser
Jazyk: angličtina
Rok vydání: 2009
Předmět:
medicine.medical_specialty
Endocrinology
Diabetes and Metabolism

030209 endocrinology & metabolism
Physical exercise
Type 2 diabetes
Biology
Pathophysiology
03 medical and health sciences
0302 clinical medicine
Insulin resistance
Adenosine Triphosphate
Internal medicine
Surveys and Questionnaires
Internal Medicine
medicine
Humans
Family
NADH
NADPH Oxidoreductases

Muscle
Skeletal

Exercise
Heat-Shock Proteins
030304 developmental biology
DNA Primers
Adenosine Triphosphatases
0303 health sciences
Electron Transport Complex I
Polymorphism
Genetic

ATP synthase
Skeletal muscle
Feeding Behavior
medicine.disease
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
medicine.anatomical_structure
NDUFB6
Endocrinology
Diabetes Mellitus
Type 2

biology.protein
Original Article
PPARGC1A
Gene polymorphism
Transcription Factors
Zdroj: Diabetes (N.Y.N.Y.) (2009). doi:10.2337/db08-1240
info:cnr-pdr/source/autori: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./titolo:Short-term exercise training does not stimulate skeletal muscle ATP synthesis in relatives of humans with type 2 diabetes/doi:10.2337%2Fdb08-1240/rivista:Diabetes (N.Y.N.Y.)/anno:2009/pagina_da:/pagina_a:/intervallo_pagine:/volume
Diabetes
DOI: 10.2337/db08-1240
Popis: 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 using1H and31P 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 O2uptake 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.
Databáze: OpenAIRE