Familial influences and obesity-associated metabolic risk factors contribute to the variation in resting energy expenditure:: the Kiel Obesity Prevention Study

被引:37
作者
Bosy-Westphal, Anja [1 ]
Wolf, Andreas [2 ]
Buehrens, Frederike [1 ]
Hitze, Britta [1 ]
Czech, Norbert [3 ]
Moenig, Heiner [4 ]
Selberg, Oliver [5 ]
Settler, Uta [1 ]
Pfeuffer, Maria [6 ]
Schrezenmeir, Juergen [6 ]
Krawczak, Michael [2 ]
Mueller, Manfred J. [1 ]
机构
[1] Univ Kiel, Inst Humanernahrung & Lebensmittelkunde, Agrar & Ernahrungswissensch Fak, D-24105 Kiel, Germany
[2] Univ Kiel, Inst Med Informat & Stat, D-24105 Kiel, Germany
[3] Univ Kiel, Abt Nukl Med, Radiol Diagnost Klin, D-24105 Kiel, Germany
[4] Univ Kiel, Klin Allgemeine Innere Med, D-24105 Kiel, Germany
[5] Stadt Klinikum Braunschweig, Klin Chem Abt, Braunschweig, Germany
[6] Bundesforschungsanstalt Ernahrung & Lebensmittel, Kiel, Germany
关键词
D O I
10.1093/ajcn/87.6.1695
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
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.
引用
收藏
页码:1695 / 1701
页数:7
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