m.3243A>G mutation in mitochondrial DNA leads to decreased insulin sensitivity in skeletal muscle and to progressive beta-cell dysfunction (Articolo in rivista)

Type
Label
  • m.3243A>G mutation in mitochondrial DNA leads to decreased insulin sensitivity in skeletal muscle and to progressive beta-cell dysfunction (Articolo in rivista) (literal)
Anno
  • 2009-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.2337/db08-0981 (literal)
Alternative label
  • Lindroos MM, Majamaa K, Tura A, Mari A, Kalliokoski KK, Taittonen MT, Iozzo P, Nuutila P. Lindroos, M. M., Majamaa, K., Tura, A., Mari, A., Kalliokoski, K. K., Taittonen, M. T., Iozzo, P. and Nuutila, P., (2009)
    m.3243A>G mutation in mitochondrial DNA leads to decreased insulin sensitivity in skeletal muscle and to progressive beta-cell dysfunction
    in Diabetes (N.Y.N.Y.); American Diabetes Association, Alexandria (Stati Uniti d'America)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Lindroos MM, Majamaa K, Tura A, Mari A, Kalliokoski KK, Taittonen MT, Iozzo P, Nuutila P. Lindroos, M. M., Majamaa, K., Tura, A., Mari, A., Kalliokoski, K. K., Taittonen, M. T., Iozzo, P. and Nuutila, P., (literal)
Pagina inizio
  • 543 (literal)
Pagina fine
  • 549 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url
  • http://diabetes.diabetesjournals.org/content/58/3/543.long (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 58 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • University of Turku, Turku, Finland National Research Council (CNR), Institute of Clinical Physiology, Pisa and Institute of Biomedical Engineering, Padova, Italy (literal)
Titolo
  • m.3243A>G mutation in mitochondrial DNA leads to decreased insulin sensitivity in skeletal muscle and to progressive beta-cell dysfunction (literal)
Abstract
  • OBJECTIVE-To study insulin sensitivity and perfusion in skeletal muscle together with the beta-cell function in subjects with the m.3243A>G mutation in mitochondrial DNA, the most common cause of mitochondrial diabetes. RESEARCH DESIGN AND METHODS-We measured skeletal muscle glucose uptake and perfusion using positron emission tomography and 2-[(18)F]fluoro-2-deoxyglucose and [(15)O]H(2)O during euglycemic hyperinsulinemia in 15 patients with m.3243A>G. These patients included five subjects with no diabetes as defined by the oral glucose tolerance test (OGTT) (group 1), three with GHb <6.1% and newly found diabetes by OGTT (group 2), and seven with a previously diagnosed diabetes (group 3). Control subjects consisted of 13 healthy individuals who were similar to the carriers of m.3243A>G with respect to age and physical activity. beta-Cell function was assessed using the OGTT and Subsequent mathematical modeling. RESULTS-Skeletal muscle glucose uptake was significantly lower in groups 1, 2, and 3 than in the control subjects. The glucose sensitivity of beta-cells in group 1 patients was similar to that of the control subjects, whereas in group 2 and 3 patients, the glucose sensitivity was significantly lower. The insulin secretion parameters correlated strongly with the proportion of m.3243A>G mutation in muscle. CONCLUSIONS-Our findings show that subjects with m.3243A>G are insulin resistant in skeletal muscle even when beta-cell function is not markedly impaired or glucose control compromised. We suggest that both the skeletal muscle insulin sensitivity and the beta-cell function are affected before the onset of the mitochondrial diabetes caused by the m.3243A>G mutation. Diabetes 58:543-549, 2009 (literal)
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