作者: Tomas F Gianotti , Silvia Sookoian , Guillermo Dieuzeide , Silvia I García , Carolina Gemma
DOI: 10.1038/OBY.2008.253
关键词: Mitochondrial DNA 、 TFAM 、 Genotyping 、 Biology 、 Population 、 Genotype 、 Mitochondrial biogenesis 、 Restriction fragment length polymorphism 、 Genetics 、 Molecular biology 、 Insulin resistance 、 Nutrition and Dietetics 、 Medicine (miscellaneous) 、 Endocrinology, Diabetes and Metabolism 、 Endocrinology
摘要: The aim of this study was to investigate whether mitochondrial DNA (mtDNA) content is associated with insulin resistance (IR) in a sample adolescents features metabolic syndrome. We further studied the link between polymorphisms three genes involved biogenesis and presence deleted mtDNA content. Data blood samples were collected from 175 out cross-sectional, population-based 934 high school students. On basis median value homeostasis model assessment IR (HOMA-IR) whole (2.2), population divided into two groups: noninsulin (NIR) IR. quantification using nuclear (nDNA) as reference carried real-time quantitative PCR method. Genotyping for peroxisome proliferator-activated receptor-γ (PPAR-γ) (pro12Ala), PPAR- γ coactivator-1α (PGC-1α) (Gly482Ser), Tfam (rs1937 rs12247015) performed by PCR-based restriction fragment length polymorphism. Long-extension amplify genome. mtDNA/nDNA ratio significantly lower group (median: 9.08, range: 68.94) comparison NIR (12.24, 71.92) (P < 0.03). Besides, inversely correlated HOMA (R: −0.18, P 0.02), glucose −0.21, 0.008), uric acid Genotypes γ, PGC-1α, variants not ratio. did show significant levels deletions. In conclusion, our findings indicate that reduced peripheral leukocytes This result seems be related previously mentioned regulation biogenesis.