瘦素受体基因(Arg223Glu)不同基因型缺血性心脏病和肥胖症患者的代谢状况

O. Kadykova, K. Borovyk, N. Ryndina
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引用次数: 0

摘要

本研究的目的是评估瘦素受体基因(Arg223Glu)不同基因型的冠心病和肥胖患者的代谢状态,即碳水化合物和脂质代谢。材料和方法。该研究包括220名患有冠心病和肥胖症的患者。对照组为体重正常的冠心病患者113例。对照组包括35名健康个体。此外,根据瘦素受体基因(Arg223Glu)的基因型,将冠心病和肥胖患者分为亚组:第一亚组包括A/A基因型携带者(n=57),第二- G/A基因型携带者(n=90),第三- G/G基因型携带者(n=73)。结果和讨论。根据瘦素受体基因(Arg223Gln)基因型对冠心病和肥胖症患者碳水化合物代谢的分析表明,G/G基因型携带者的碳水化合物代谢紊乱更为明显,表现为高胰岛素血症,组织对胰岛素的敏感性降低,而G/A和A/A基因型携带者对葡萄糖代谢紊乱的抵抗力更强。G/G基因型携带者的体重指数最高,分别比G/A和A/A基因型携带者高19.19%和19.53%。因此,冠心病和肥胖患者的G/G基因型与体重指数相关。冠心病合并肥胖患者脂质代谢受损定义为高甘油三酯血症,与瘦素受体基因多态性(Arg223Gln)的G/G基因型相关。我们的研究结果表明瘦素受体基因多态性位点(Arg223Gln)参与了碳水化合物和脂质代谢紊乱的形成,这与文献相符。有研究表明,瘦素受体基因的结构变化不仅与肥胖的发生有关,而且与2型糖尿病的发生有关。结论。确定冠心病与肥胖合并病程的特点:高胰岛素血症和胰岛素抵抗与Arg223Gln瘦素受体基因多态性位点G等位基因和G/G基因型相关(r=0.76, p<0.05);高甘油三酯血症的脂质谱重排受瘦素受体基因Arg223Gln基因多态性位点G等位基因的同质性影响(r=0.73, p<0.05)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Metabolic Status in Patients with Ischemic Heart Disease and Obesity with Different Genotypes of Leptin Receptor Gene (Arg223Glu)
The purpose of the study was to assess the metabolic status, namely carbohydrate and lipid metabolism, in patients with coronary heart disease and obesity with different genotypes of the leptin receptor gene (Arg223Glu). Materials and methods. The study included 220 patients with coronary heart disease and obesity. The comparison group consisted of 113 patients with coronary heart disease with normal body weight. The control group included 35 healthy individuals. Additionally, patients with coronary heart disease and obesity were divided into subgroups depending on the genotype of the leptin receptor gene (Arg223Glu): the first subgroup included carriers of the A/A genotype (n=57), the second – G/A genotype (n=90), the third – G/G genotype (n=73). Results and discussion. The analysis of carbohydrate metabolism depending on the genotypes of the leptin receptor gene (Arg223Gln) in patients with coronary heart disease and obesity showed that carriers of the G/G genotype have more pronounced disorders of carbohydrate metabolism in the form of hyperinsulinemia and decreased tissue sensitivity to insulin while carriers of the genotypes G/A and A/A have greater resistance to glucose-metabolic disorders. Body mass index in carriers of G/G genotype had the highest value, which is 19.19% and 19.53% more than in carriers of genotypes G/A and A/A. Thus, the G/G genotype in patients with coronary heart disease and obesity was associated with body mass index. The impaired lipid metabolism in patients with coronary heart disease in combination with obesity was defined as hypertriglyceridemia, which is associated with the G/G genotype of the leptin receptor gene polymorphism (Arg223Gln). The results obtained in our work indicate the involvement of the polymorphic locus of the leptin receptor gene (Arg223Gln) in the formation of disorders of carbohydrate and lipid metabolism, which corresponds to the literature. It has been suggested that structural changes in the leptin receptor gene are associated not only with the development of obesity but also with the development of type 2 diabetes mellitus. Conclusion. The features of the combined course of coronary heart disease and obesity were identified: hyperinsulinemia and insulin resistance are associated with the G allele and G/G genotype of the polymorphic locus Arg223Gln leptin receptor gene (r=0.76, p<0.05); the rearrangement of the lipid spectrum due to hypertriglyceridemia is influenced by the homogeny of the G allele of the polymorphic locus of the Arg223Gln gene of the leptin receptor gene (r=0.73, p<0.05)
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