đề xuất như là một nguyên nhân gây ra T2DM42 có thể thông qua một tình trạng quá tải ngoài tử cung của axit béo và lipotoxicity của mỡ không vai trò cho resistin do đó có thể được hình dung trong hội chứng kháng insulin prediabetic nhờ khả | 418 GENETICS OF THE METABOLIC SYNDROME proposed as a cause of T2DM42 possibly through an ectopic overload of fatty acids and lipotoxicity of non-adipose A role for resistin could therefore be envisioned in the prediabetic syndrome of insulin resistance by virtue of its ability to block adipocyte differentiation. At the genic level SNPS in non-coding regions of the human resistin gene were either not significantly associated with insulin resistance G1326C in 3 UTR -167C 4 T 157C 4 T 299G 4 A in introns 168 169 or associated with an insulin sensitivity index in the case of a promoter SNP 394C 4 G 170 Table . A genetic variant in intron 2 IVS2 181G 4 A was significantly involved in a possible interaction between obesity and the association between T2DM and the A study that combined population data from the Quebec Family Study and the Saguenay-Lac-St-Jean region of Quebec found two promoter SNPs 537A 4 C and 420C 4 G to be associated with increased risk for BMI but this result was not replicated in a population from A trinucleotide ATG repeat at the 3 UTR of the gene was on the other hand associated with a decreased risk of insulin It is too early at this point to draw any definitive conclusions regarding the role of resistin in the aetiology of the metabolic syndrome but its proposed physiological role and early genetic studies suggest a link between resistin and the metabolic syndrome. However its effects may be mediated by intermediate factors such as oxidative stress or population-specific environmental factors. PC-1 Plasma cell membrane glycoprotein-1 PC-1 inhibits insulin receptor IR tyrosine kinase activity and subsequent cellular signalling possibly by inhibiting the IR by directly interacting with a specific region in the IR IR kinase activity is impaired in muscle fibroblasts and other tissues of many patients with T2DM but abnormalities in the insulin receptor gene are not the cause of .
