Body composition phenotypes in pathways to obesity and the metabolic syndrome

Abstract

Dynamic changes in body weight have long been recognized as important indicators of risk for debilitating diseases. While weight loss or impaired growth can lead to muscle wastage, as well as to susceptibility to infections and organ dysfunctions, the development of excess fat predisposes to type 2 diabetes and cardiovascular diseases, with insulin resistance as a central feature of the disease entities of the metabolic syndrome. Although widely used as the phenotypic expression of adiposity in population and gene-search studies, body mass index (BMI), that is, weight/height 2 (H 2 ), which was developed as an operational definition for classifying both obesity and malnutrition, has considerable limitations in delineating fat mass (FM) from fat-free mass (FFM), in particular at the individual level. After an examination of these limitations within the constraints of the BMI-FM% relationship, this paper reviews recent advances in concepts about health risks related to body composition phenotypes, which center upon (i) the partitioning of BMI into an FM index (FM/H 2 ) and an FFM index (FFM/H 2 ), (ii) the partitioning of FFM into organ mass and skeletal muscle mass, (iii) the anatomical partitioning of FM into hazardous fat and protective fat and (iv) the interplay between adipose tissue expandability and ectopic fat deposition within or around organs/tissues that constitute the lean body mass. These concepts about body composition phenotypes and health risks are reviewed in the light of race/ethnic variability in metabolic susceptibility to obesity and the metabolic syndrome.

Effect of protein intake and weight gain velocity on body fat mass at 6 months of age: The EU Childhood Obesity Programme

“…All measured isotope ratios, 2 H/ 1 H and 18 O/ 16 O were normalized to the SMOW/SLAP scale using the internal standards. In the case of the 18 O determinations, the isotope ratios were first expressed relative to PDB for Craig correction 24 before normalization to the SMOW/SLAP scale.…”

“…2 H analysis was performed using equilibration with hydrogen gas over a platinum catalyst using an Isoprep system (Micromass Ltd, Manchester, UK) coupled to a Sira 10 dual inlet mass spectrometer (VG Isogas Ltd, Middlewich, Cheshire, UK). 18 O enrichment was determined by equilibration with CO 2 gas followed by analysis by continuous flow isotope ratio mass spectrometry (AP 2003, Analytical Precision Ltd, Northwich, Cheshire, UK). Each batch of postdosing urine samples were analysed together with their corresponding basal sample, a gravimetrically diluted sample of the dosing solution and a number of internal standards traceable to the primary reference materials PDB, VSMOW2 and SLAP2 (IAEA, Vienna, Austria).…”

“…15 While adiposity in childhood is related to insulin resistance in adulthood, 16 lean mass has an important role on insulin-mediated glucose uptake 17 and basal metabolic rate. 18 Therefore, both adipose and lean tissues may be key factors for later cardiovascular risk. 15,19 Precise assessment of body composition in infants is still a challenge, since most of the accessible methods have poor accuracy (for example, anthropometry and bioimpedance).…”

Metabolic Damage: do Negative Metabolic Adaptations During Underfeeding Persist After Refeeding in Non-Obese Populations?

“…Furthermore, the same researchers suggested that weight loss diets make "the lean fatter," because CR-induced feedback signals suppress RMR normalization until the initial fat mass (FM) is fully recovered ("fat-stores memory") [8,7]. The post-diet shift towards an unfavorable body composition may result in repeated dieting attempts and increase the risk of becoming overweight [8].…”

“…Metabolic slowing, originating from adaptive thermogenesis (AT) in a calorie- recovery and proposed that it is the reason for favorable fat gain after CR [6][7][8].…”