Maryam Pourhassan1, Anja Bosy-Westphal, Britta Schautz, Wiebke Braun, Claus-C Glüer, Manfred J Müller. 1. Institute of Human Nutrition and Food Science, Christian-Albrechts University, Kiel, Germany (MP, AB-W, BS, WB, and MJM); the Klinik für Diagnostische Radiologie, Sektion Biomedizinische Bildgebung, Molecular Imaging North Competence Center CC, Universitätsklinikum (University Medical Center) Schleswig Holstein, Kiel, Germany (C-CG); and the Institute of Nutritional Medicine, University of Hohenheim, Stuttgart, Germany (AB-W).
Abstract
BACKGROUND: Weight change affects resting energy expenditure (REE) and metabolic risk factors. The impact of changes in individual body components on metabolism is unclear. OBJECTIVE: We investigated changes in detailed body composition to assess their impacts on REE and insulin resistance. DESIGN: Eighty-three healthy subjects [body mass index (BMI; in kg/m²) range: 20.2-46.8; 50% obese] were investigated at 2 occasions with weight changes between -11.2 and +6.5 kg (follow-up periods between 23.5 and 43.5 mo). Detailed body composition was measured by using the 4-component model and whole-body magnetic resonance imaging. REE, plasma thyroid hormone concentrations, and insulin resistance were measured by using standard methods. RESULTS: Weight loss was associated with decreases in fat mass (FM) and fat-free mass (FFM) by 72.0% and 28.0%, respectively. A total of 87.9% of weight gain was attributed to FM. With weight loss, sizes of skeletal muscle, kidneys, heart, and all fat depots decreased. With weight gain, skeletal muscle, liver, kidney masses, and several adipose tissue depots increased except for visceral adipose tissue (VAT). After adjustments for FM and FFM, REE decreased with weight loss (by 0.22 MJ/d) and increased with weight gain (by 0.11 MJ/d). In a multiple stepwise regression analysis, changes in skeletal muscle, plasma triiodothyronine, and kidney masses explained 34.9%, 5.3%, and 4.5%, respectively, of the variance in changes in REE. A reduction in subcutaneous adipose tissue rather than VAT was associated with the improvement of insulin sensitivity with weight loss. Weight gain had no effect on insulin resistance. CONCLUSION: Beyond a 2-compartment model, detailed changes in organ and tissue masses further add to explain changes in REE and insulin resistance.
BACKGROUND: Weight change affects resting energy expenditure (REE) and metabolic risk factors. The impact of changes in individual body components on metabolism is unclear. OBJECTIVE: We investigated changes in detailed body composition to assess their impacts on REE and insulin resistance. DESIGN: Eighty-three healthy subjects [body mass index (BMI; in kg/m²) range: 20.2-46.8; 50% obese] were investigated at 2 occasions with weight changes between -11.2 and +6.5 kg (follow-up periods between 23.5 and 43.5 mo). Detailed body composition was measured by using the 4-component model and whole-body magnetic resonance imaging. REE, plasma thyroid hormone concentrations, and insulin resistance were measured by using standard methods. RESULTS:Weight loss was associated with decreases in fat mass (FM) and fat-free mass (FFM) by 72.0% and 28.0%, respectively. A total of 87.9% of weight gain was attributed to FM. With weight loss, sizes of skeletal muscle, kidneys, heart, and all fat depots decreased. With weight gain, skeletal muscle, liver, kidney masses, and several adipose tissue depots increased except for visceral adipose tissue (VAT). After adjustments for FM and FFM, REE decreased with weight loss (by 0.22 MJ/d) and increased with weight gain (by 0.11 MJ/d). In a multiple stepwise regression analysis, changes in skeletal muscle, plasma triiodothyronine, and kidney masses explained 34.9%, 5.3%, and 4.5%, respectively, of the variance in changes in REE. A reduction in subcutaneous adipose tissue rather than VAT was associated with the improvement of insulin sensitivity with weight loss. Weight gain had no effect on insulin resistance. CONCLUSION: Beyond a 2-compartment model, detailed changes in organ and tissue masses further add to explain changes in REE and insulin resistance.
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