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首页> 外文期刊>The American Journal of Clinical Nutrition: Official Journal of the American Society for Clinical Nutrition >Familial influences and obesity-associated metabolic risk factors contribute to the variation in resting energy expenditure: the Kiel Obesity Prevention Study.
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Familial influences and obesity-associated metabolic risk factors contribute to the variation in resting energy expenditure: the Kiel Obesity Prevention Study.

机译:家族影响和肥胖相关的代谢危险因素导致静息能量消耗的变化:基尔肥胖预防研究。

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摘要

BACKGROUND: A low metabolic rate may be inherited and predispose to obesity, whereas a higher metabolic rate in obesity may be acquired by obesity-associated cardiometabolic risk. OBJECTIVE: We aimed to explain the interindividual variation in resting energy expenditure (REE) by assessing 1) the association between REE and body composition, thyroid hormones, and obesity-related cardiometabolic risk factors, and 2) the familial (genetic and environmental) contribution to REE. DESIGN: REE and metabolic risk factors (ie, blood pressure and plasma insulin, glucose, and C-reactive protein concentrations) were assessed in 149 two- or three-generation families, including at least one overweight or obese member. Heritability of REE, respiratory quotient (RQ), thyroid hormones [thyrotropin (TSH), free triiodothyronine (FT3) and free thyroxine (FT4)], and body composition (fat-free mass and fat mass) were estimated by using variance components-based quantitative genetic models. RESULTS: REE adjusted for body composition, sex, and age (REEadj) significantly correlated with systolic and diastolic blood pressure, plasma insulin and glucose concentrations, and the homeostasis model assessment (HOMA) (r = 0.14-0.31, P < 0.05). Thyroid hormones had a modest influence on REE variance only. Heritability was 0.30 +/- 0.07 for REEadj and 0.29 +/- 0.08 for REE after additional adjustment for thyroid hormones and metabolic risk. Furthermore, heritability was estimated to be 0.22 +/- 0.08 for RQ, 0.37 +/- 0.08 for TSH, 0.68 +/- 0.06 for FT4, and 0.69 +/- 0.05 for FT3 (all significantly larger than zero). CONCLUSIONS: Obesity-related cardiometabolic risk factors contribute to interindividual variation in REE, with hypertension and insulin resistance being associated with a higher REE. REE was moderately heritable, independent of body composition, sex, age, thyroid function, and cardiometabolic risk.
机译:背景:低代谢率可能是遗传性的,并易患肥胖症,而肥胖症相关的心脏代谢风险可能导致肥胖者代谢率较高。目的:我们旨在通过评估1)REE与身体成分,甲状腺激素和肥胖相关的心脏代谢危险因素之间的关联,以及2)家族(遗传和环境)影响来解释静息能量消耗(REE)的个体差异。到稀土。设计:在149个两代或三代家庭中评估了REE和代谢危险因素(即血压和血浆胰岛素,葡萄糖和C反应蛋白浓度),包括至少一个超重或肥胖成员。 REE的遗传力,呼吸商(RQ),甲状腺激素[促甲状腺激素(TSH),游离三碘甲状腺素(FT3)和游离甲状腺素(FT4)]和身体成分(无脂肪量和脂肪量)通过以下方差估算-基于定量遗传模型。结果:针对身体组成,性别和年龄(REEadj)进行调整的REE与收缩压和舒张压,血浆胰岛素和葡萄糖浓度以及体内稳态模型评估(HOMA)显着相关(r = 0.14-0.31,P <0.05)。甲状腺激素仅对REE变异有中等影响。进一步调整甲状腺激素和代谢风险后,REEadj的遗传力为0.30 +/- 0.07,REE的遗传力为0.29 +/- 0.08。此外,RQ的遗传力估计为0.22 +/- 0.08,TSH的遗传力估计为0.37 +/- 0.08,FT4的遗传力为0.68 +/- 0.06,FT3的遗传力为0.69 +/- 0.05(均显着大于零)。结论:肥胖相关的心脏代谢危险因素导致个体间REE的变化,其中高血压和胰岛素抵抗与更高的REE相关。 REE具有中等遗传性,与身体组成,性别,年龄,甲状腺功能和心脏代谢风险无关。

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