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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^1,2,3

¹ From the Institut für Humanernährung und Lebensmittelkunde, Christian-Albrechts-Universität, Kiel, Germany (AB-W, FB, BH, US, and MJM); the Institut für Medizinische Informatik und Statistik, Universitäts klinikum Schleswig-Holstein, Kiel, Germany (AW and MK); the Klinik für Diagnostische Radiologie, Abt Nuklearmedizin, Universitäts klinikum Schleswig-Holstein, Kiel, Germany (NC); the Klinik für Allgemeine Innere Medizin, Universitäts-klinikum Schleswig-Holstein, Kiel, Germany (HM); the Städtisches Klinikum Braunschweig, Abt Klinische Chemie, Braunschweig, Germany (OS); and the Bundesforschungsanstalt für Ernährung und Lebensmittel, Kiel, Germany (MP and JS)

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.

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				A. Bosy-Westphal, E. Kossel, K. Goele, W. Later, B. Hitze, U. Settler, M. Heller, C.-C. Gluer, S. B Heymsfield, and M. J Muller Contribution of individual organ mass loss to weight loss-associated decline in resting energy expenditure Am. J. Clinical Nutrition, October 1, 2009; 90(4): 993 - 1001. [Abstract] [Full Text] [PDF]