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Author(s): Manfred J. Müller [sup.1], Anja Bosy-Westphal [sup.1] Author Affiliations: (1) Institute of Human Nutrition and Food Science, Faculty of Agriculture and Food Sciences, Christian-Albrecht-University Kiel, Kiel, Germany The philosopher [...]

Aim The objective of this study is to generate metabolic phenotypes based on structure-function relationships. Methods In 459 healthy adults (54% females, 18 and 40 years old), we analyzed body composition by air-displacement densitometry (to assess fat mass, (FM) and fat-free mass (FFM)) and whole-body magnetic resonance imaging (to assess skeletal muscle mass (SMM) and masses of brain, heart, liver, kidneys, and subcutaneous (SAT) and visceral adipose tissue (VAT)), resting energy expenditure (REE) by indirect calorimetry, and plasma concentrations of insulin (Ins) and leptin (Lep). Results Three 'functional body composition-derived phenotypes' (FBCPs) were derived: (1) REE on FFM-FBCP, (2) Lep on FM-FBCP, and (3) Ins on VAT-FBCP. Assuming that being within the [plus or minus] 5% range of the respective regression lines reflects a 'normal' structure-function relationship, three 'normal' FBCPs were generated with prevalences of 9.0%, 5.1%, and 6.8%, respectively, of the study population. The three 'FBCPs' did not overlap and were independent from each other. When compared with the two other FBCPs, the 'Lep on FM-FBCP' was leanest, whereas the 'REE on FFM-FBCP' had the highest BMI and SAT. Taking into account FFM composition, a hierarchical multi-level model is proposed with brain at level 1, the liver at level 2, and SMM and FM at level 3 with insulin coordinating the interplay between level 1 and 2, whereas variance in plasma insulin levels impacts energy and substrate metabolism in SMM and AT. Conclusion Structure-function relationships can be used to generate FBCPs. Different FBCPs reflect different dimensions of normality (or health). This is evidence for the idea that there is no across the board 'normal' state., Author(s): Manfred J. Müller [sup.1] , Corinna Geisler [sup.1] , Mark Hübers [sup.1] , Maryam Pourhassan [sup.2] , Anja Bosy-Westphal [sup.1] Author Affiliations: (1) Institute of Human Nutrition and Food [...]

Common obesity-associated hepatic steatosis (nonalcoholic fatty liver disease (NAFLD)) and insulin resistance are mainly caused by dysfunctional adipose tissue. This adipose tissue dysfunction leads to increased delivery of NEFA and glycerol to the liver that (i) drives hepatic gluconeogenesis and (ii) facilitates the accumulation of lipids and insulin signaling inhibiting lipid intermediates. Dysfunctional adipose tissue can be caused by impaired lipid storage (overflow hypothesis, characterized by large visceral adipocytes) or increased lipolysis (due to impaired postprandial suppression of lipolysis in inflamed, insulin-resistant adipocytes). In line with the adipose tissue expandability hypothesis the amount and distribution of adipose tissue correlate with its dysfunction and thus with liver fat. This relationship is however modified by endocrine effects on lipid storage and lipolysis as well as dietary effects on hepatic lipogenesis and lipid oxidation. The association between body composition characteristics like visceral obesity or fat cell size and ectopic liver fat is modified by these influences. Phenotyping obesity according to metabolic risk should integrate body composition characteristics, endocrine parameters and information on diet., Author(s): Anja Bosy-Westphal [sup.1] , Wiebke Braun [sup.1] , Viktoria Albrecht [sup.1] , Manfred J. Müller [sup.1] Author Affiliations: (1) Institute for Human Nutrition and Food Science, Christian-Albrechts-University Kiel, Kiel, [...]

Body mass in humans and animals is strongly associated with the rate of heat production as defined by resting energy expenditure (REE). Beginning with the ancient Greeks up to the present time, philosophers and scientists have endeavored to understand the nature and sources of bodily heat. Today we recognize that body mass consists of organs and tissues, each of which produces a specified amount of heat at rest. An individual organ's REE can now be estimated in vivo as the product of its assumed mass-specific metabolic rate and its imaging-derived mass; whole-body REE reflects the sum of organ and tissue metabolic rates. The sizes of organs and total body mass in adults are governed by two main factors, a person's stature or height, and their level of adiposity. With greater body size, as represented by adult height independent of adiposity, organs remain stable or increase in mass according to distinct 'scaling' patterns. Similarly, with greater relative adiposity organs adaptively accommodate to the increase in imposed mechanical and metabolic loading conditions. Through a detailed analysis of these stature and adiposity effects, we show how classical statistical REE prediction models can be mechanistically understood at the anatomic body composition level., Author(s): Steven B. Heymsfield [sup.1] , Diana M. Thomas [sup.2] , Anja Bosy-Westphal [sup.3] , Manfred J. Müller [sup.3] Author Affiliations: (1) Pennington Biomedical Research Center, Baton Rouge, USA (2) [...]