Lazarin Mary A C T, Bennini João R, Pereira Carlos L C, Astiarraga Brenno D, Ferrannini Ele, Muscelli Elza
Department of Internal Medicine, School of Medical Sciences, State University of Campinas, UNICAMP, São Paulo, Brazil.
Obes Res. 2004 Apr;12(4):621-6. doi: 10.1038/oby.2004.71.
Offspring of diabetic or hypertensive patients are insulin resistant at a prediabetic/prehypertensive stage. We tested the hypothesis that insulin action may be impaired in the offspring of obese nondiabetic parents.
Twenty-one lean offspring of nonobese subjects [(OL) 22 +/- 3 years of age] were matched to 23 lean offspring of obese subjects (OOb) by gender distribution, age, BMI, and waist circumference. Anthropometry, oral glucose tolerance, in vivo insulin sensitivity [by a euglycemic insulin clamp (6 pmol/min per kilogram(FFM); where FFM represents fat-free mass)], and thermogenesis (by indirect calorimetry) were measured in each subject. The study subjects were from a population of 267 nuclear families (one offspring and both his/her parents) in which there was statistically significant (chi2 = 30.2, p = 0.001) concordance of BMI between parents and offspring.
In comparing OOb with OL, no statistically significant difference or trend toward a difference was detected in fasting plasma glucose and insulin concentrations, glucose and insulin responses to oral glucose, insulin sensitivity [metabolism value = 45 +/- 12 (OOb) vs. 47 +/- 17 micro mol/min per kilogram(FFM) (OL)], insulin-induced inhibition of protein and lipid oxidation, stimulation of glucose oxidation and nonoxidative glucose disposal, respiratory quotient, resting energy expenditure, and glucose-induced thermogenesis.
The metabolic similarity between lean offspring of obese parents and those of nonobese parents suggests that insulin resistance and its correlates are not co-inherited with the predisposition to develop obesity.
糖尿病或高血压患者的后代在糖尿病前期/高血压前期阶段存在胰岛素抵抗。我们检验了这样一个假设,即肥胖非糖尿病父母的后代可能存在胰岛素作用受损的情况。
21名非肥胖受试者的瘦后代([OL],年龄22±3岁),根据性别分布、年龄、体重指数(BMI)和腰围,与23名肥胖受试者的瘦后代(OOb)进行匹配。对每位受试者进行人体测量、口服葡萄糖耐量测试、体内胰岛素敏感性测定[采用正常血糖胰岛素钳夹技术(每千克去脂体重6 pmol/min;其中去脂体重代表无脂肪体重)]以及产热测定(采用间接测热法)。研究对象来自267个核心家庭(一名后代及其父母双方)组成的群体,父母与后代之间的BMI存在统计学显著一致性(χ2 = 30.2,p = 0.001)。
在比较OOb与OL时,未检测到空腹血糖和胰岛素浓度、口服葡萄糖后的血糖和胰岛素反应、胰岛素敏感性[代谢值 = 45±12(OOb)对47±17微摩尔/分钟每千克去脂体重(OL)]、胰岛素诱导的蛋白质和脂质氧化抑制、葡萄糖氧化和非氧化葡萄糖处置刺激、呼吸商、静息能量消耗以及葡萄糖诱导的产热方面存在统计学显著差异或差异趋势。
肥胖父母的瘦后代与非肥胖父母的瘦后代之间的代谢相似性表明,胰岛素抵抗及其相关因素并非与肥胖易感性共同遗传。