Krempler F, Hell E, Winkler C, Breban D, Patsch W
Departments of Internal Medicine and Surgery, Krankenhaus Hallein, and the Department of Laboratory Medicine Landeskrankenanstalten, Salzburg, Austria.
Arterioscler Thromb Vasc Biol. 1998 Nov;18(11):1686-90. doi: 10.1161/01.atv.18.11.1686.
Obesity is associated with insulin resistance and other major cardiovascular risk factors. A common amino acid polymorphism at codon 972 of the insulin receptor substrate-1 (IRS-1) has been shown to interact with obesity in the expression of insulin resistance. The plasma concentration of the adipocyte-specific hormone leptin is increased in obesity and is correlated with adipose tissue mass. Because in vitro studies demonstrated inhibitory effects of leptin on insulin signaling, leptin may be involved in obesity-associated insulin resistance. To gain insight into the relationship between insulin and leptin in obesity, we studied plasma leptin levels and several cardiovascular risk factors, as well as their modification by the IRS-1 codon 972 genotype, in 156 obese individuals and 131 lean control subjects. In both groups, 10% of the subjects were heterozygous for the IRS-1 codon 972 variant. Obese individuals harboring the IRS-1 variant displayed significantly lower plasma concentrations of leptin than obese subjects without the polymorphism (means, 26.7 versus 37.8 ng/mL, P<0.0293). In a subgroup of obese patients, leptin mRNA abundance was measured in the adipose tissue and was significantly lower in carriers of the IRS-1 variant than in subjects with the wild-type variant (P<0.0291). Our data suggest that insulin signaling influences plasma leptin concentrations at the mRNA expression level and argue against leptin as a major causative factor of insulin resistance.
肥胖与胰岛素抵抗及其他主要心血管危险因素相关。胰岛素受体底物-1(IRS-1)第972位密码子处常见的氨基酸多态性已被证明在胰岛素抵抗的表达中与肥胖相互作用。脂肪细胞特异性激素瘦素的血浆浓度在肥胖时升高,且与脂肪组织量相关。由于体外研究表明瘦素对胰岛素信号传导有抑制作用,瘦素可能参与了肥胖相关的胰岛素抵抗。为深入了解肥胖中胰岛素与瘦素之间的关系,我们研究了156名肥胖个体和131名瘦对照受试者的血浆瘦素水平及几种心血管危险因素,以及IRS-1第972位密码子基因型对它们的影响。在两组中,10%的受试者为IRS-1第972位密码子变异的杂合子。携带IRS-1变异的肥胖个体的血浆瘦素浓度显著低于无该多态性的肥胖受试者(均值分别为26.7与37.8 ng/mL,P<0.0293)。在一组肥胖患者亚组中,测量了脂肪组织中瘦素mRNA丰度,携带IRS-1变异的个体显著低于野生型变异个体(P<0.0291)。我们的数据表明胰岛素信号传导在mRNA表达水平影响血浆瘦素浓度,且不支持瘦素是胰岛素抵抗的主要致病因素。