Genetic studies of association earlier suggested a strong link between genes MSRA (methionine sulfoxide reductase A), LYPLAL1 (Lysophospholipase-like protein 1) and TFAP2B (transcription factor activating enhancer binding protein 2 beta), and adiposity of abdomen (fatty condition of the latter). Sulfoxide reductase A methionine is an enzyme that reduces oxidative stress (aggression components of the cell due to reactive oxygen species), or the increased oxidative stress is responsible for the destruction of pancreatic beta cells that leads to the development of diabetes Type II. Similarly, Lysophospholipase-like protein 1 regulates the metabolism (mobilization and storage) fatty acids, while the increase in the flow of these fatty acids increase the risk of developing type II diabetes. TFAP2B protein was associated with insulin resistance in adolescents and type II diabetes in adults. Thus, an American team has looked for nucleotide variations in these genes in patients with type II diabetes in order to high light their involvement in this disease.
They showed that a variant in the gene associated MSRA was a significant risk of developing type II diabetes but only in men. Moreover, this genetic alteration is associated, in women, at a lower rate of adiponectin, a protein produced by adipose tissue that has an anti-diabetes by increasing insulin sensitivity. Furthermore, this decrease is often observed in obesity. The variant found in the gene is only weakly LYPLAL1 associated with type II diabetes. However, genetic variation in the gene identified TFAP2B is not associated with type II diabetes but is associated with leptin levels much lower and thus more appetite important.Cette a landmark study suggests that the gene and LYPLAL1 MSRA, two genes of abdominal adiposity, predispose to type II diabetes in humans. Subsequent studies identified will have their mechanisms of action in the development of type II diabetes.
