Deep body composition phenotyping during weight cycling: relevance to metabolic efficiency and metabolic risk.

Weight cycling may lead to adverse effects on metabolic efficiency (i.e. adaptive thermogenesis or 'metabolic slowing') and metabolic risks (e.g. increased risk for insulin resistance and the metabolic syndrome). In order to investigate these topics, the partitioning of fat and lean mass (i.e. the change in the proportion of both compartments) needs to be extended to the organ and tissue level because metabolic risk differs between adipose tissue depots and lean mass is metabolically heterogeneous being composed of organs and tissues differing in metabolic rate. Contrary to data obtained with severe weight loss and regain in lean people, weight cycling most likely has no adverse effects on fat distribution and metabolic risk in obese patients. There is even evidence for an increased ability of fat storage in subcutaneous fat depots (at the trunk in men and at the limbs in women) with weight cycling that may provide a certain protection from ectopic lipid deposition and thus explain the preservation of a favourable metabolic profile despite weight regain. On the other hand, the mass-specific metabolic rate of lean mass may increase with weight gain and decrease with weight loss mainly because of an increase and respective decrease in the proportion (and/or activity) of metabolically active organ mass. Obese people could therefore have a higher slope of the regression line between resting energy expenditure (REE) and fat-free mass that leads to an overestimation of metabolic efficiency when applied to normalize REE data after weight loss. Furthermore, in addressing the impact of macronutrient composition of the diet on partitioning of lean and fat mass, and the old controversy about whether a calorie is a calorie, we discuss recent evidence in support of a low glycaemic weight maintenance diet in countering weight regain and challenge this concept for weight loss by proposing the opposite.

Carbohydrate intake and glycemic index affect substrate oxidation during a controlled weight cycle in healthy men.

BACKGROUND/OBJECTIVES: Because both, glycemic index (GI) and carbohydrate content of the diet increase insulin levels and could thus impair fat oxidation, we hypothesized that refeeding a low GI, moderate-carbohydrate diet facilitates weight maintenance. SUBJECTS/METHODS: Healthy men (n=32, age 26.0±3.9 years; BMI 23.4±2.0 kg/m(2)) followed 1 week of controlled overfeeding, 3 weeks of caloric restriction and 2 weeks of hypercaloric refeeding (+50, -50 and +50% energy requirement) with low vs high GI (41 vs 74) and moderate vs high CHO intake (50% vs 65% energy). We measured adaptation of fasting macronutrient oxidation and the capacity to supress fat oxidation during an oral glucose tolerance test. Changes in fat mass were measured by quantitative magnetic resonance. RESULTS: During overfeeding, participants gained 1.9±1.2 kg body weight, followed by a weight loss of -6.3±0.6 kg and weight regain of 2.8±1.0 kg. Subjects with 65% CHO gained more body weight compared with 50% CHO diet (P<0.05) particularly with HGI meals (P<0.01). Refeeding a high-GI diet led to an impaired basal fat oxidation when compared with a low-GI diet (P<0.02), especially at 65% CHO intake. Postprandial metabolic flexibility was unaffected by refeeding at 50% CHO but clearly impaired by 65% CHO diet (P<0.05). Impairment in fasting fat oxidation was associated with regain in fat mass (r=0.43, P<0.05) and body weight (r=0.35; P=0.051). CONCLUSIONS: Both higher GI and higher carbohydrate content affect substrate oxidation and thus the regain in body weight in healthy men. These results argue in favor of a lower glycemic load diet for weight maintenance after weight loss.

Effect of weight loss and regain on adipose tissue distribution, composition of lean mass and resting energy expenditure in young overweight and obese adults.

BACKGROUND: Although weight cycling is frequent in obese patients, the adverse consequences on body composition and an increased propensity to weight gain remain controversial. OBJECTIVE: We investigated the effect of intentional weight loss and spontaneous regain on fat distribution, the composition of lean mass and resting energy expenditure (REE). DESIGN: Weight regainers (≥ 30% of loss, n=27) and weight-stable subjects (within <± 20% of weight change, n=20) were selected from 103 overweight and obese subjects (body mass index 28-43 kg m(-2), 24-45 years) who passed a 13-week low-calorie diet intervention. REE and body composition (by densitometry and whole-body magnetic resonance imaging) were examined at baseline, after weight loss and at 6 months of follow-up. RESULTS: Mean weight loss was -12.3 ± 3.3 kg in weight-stable subjects and -9.0 ± 4.3 kg in weight regainers (P<0.01). Weight regain was incomplete, accounting for 83 and 42% of weight loss in women and men. Regain in total fat and different adipose tissue depots was in proportion to weight regain except for a higher regain in adipose tissue of the extremities in women and a lower regain in extremity and visceral adipose tissue in men. In both genders, regain in skeletal muscle of the trunk lagged behind skeletal muscle regain at the extremities. In contrast to weight-stable subjects, weight regainers showed a reduced REE adjusted for changes in organ and tissue masses after weight loss (P<0.001). CONCLUSION: Weight regain did not adversely affect body fat distribution. Weight loss-associated adaptations in REE may impair weight loss and contribute to weight regain.

Beyond the body mass index: tracking body composition in the pathogenesis of obesity and the metabolic syndrome.

Body composition is related to various physiological and pathological states. Characterization of individual body components adds to understand metabolic, endocrine and genetic data on obesity and obesity-related metabolic risks, e.g. insulin resistance. The obese phenotype is multifaceted and can be characterized by measures of body fat, leg fat, liver fat and skeletal muscle mass rather than by body mass index. The contribution of either whole body fat or fat distribution or individual fat depots to insulin resistance is moderate, but liver fat has a closer association with (hepatic) insulin resistance. Although liver fat is associated with visceral fat, its effect on insulin resistance is independent of visceral adipose tissue. In contrast to abdominal fat, appendicular or leg fat is inversely related to insulin resistance. The association between 'high fat mass + low muscle mass' (i.e. 'sarcopenic adiposity') and insulin resistance deserves further investigation and also attention in daily clinical practice. In addition to cross-sectional data, longitudinal assessment of body composition during controlled under- and overfeeding of normal-weight healthy young men shows that small decreases and increases in fat mass are associated with corresponding decreases and increases in insulin secretion as well as increases and decreases in insulin sensitivity. However, even under controlled conditions, there is a high intra- and inter-individual variance in the changes of (i) body composition; (ii) the 'body composition-glucose metabolism relationship' and (iii) glucose metabolism itself. Combining individual body components with their related functional aspects (e.g. the endocrine, metabolic and inflammatory profiles) will provide a suitable basis for future definitions of a 'metabolically healthy body composition'.

Effects of brief perturbations in energy balance on indices of glucose homeostasis in healthy lean men.

BACKGROUND: Little is known about the effects of short-term caloric restriction (CR) and overfeeding (OF) on glucose homeostasis in healthy lean individuals. In addition, it remains unclear whether the effects of CR and OF are reversed by a complementary feeding period. METHODS: Ten healthy men participated in two cycles of controlled 7-day periods of CR and refeeding (RF; protocol A), and OF and CR (protocol B) at ±60% energy requirement. At baseline, insulin sensitivity (IS) was assessed by euglycemic clamp (M). Before and during each feeding cycle, fasting and oral glucose tolerance test-derived indices were used to estimate glucose tolerance, IS and glucose-stimulated insulin secretion. RESULTS: Clamp tests revealed normal IS at baseline (M-values 9.4±2.1 mg kg⁻¹ min⁻¹, coefficient of variation (CV)(inter) 22%). M-values were significantly correlated with indices of IS. In protocol A, CR-induced weight loss (-3.0±0.4 kg) was associated with an increase in fasting IS. Postprandial IS and glucose-stimulated insulin secretion remained unchanged, but glucose tolerance decreased. RF decreased fasting and postprandial IS at increased glucose-stimulated insulin secretion. In protocol B, OF significantly increased the body weight (+1.6±0.9 kg). Concomitantly, fasting and postprandial IS decreased at increased glucose-stimulated insulin secretion. Subsequent CR reversed these effects. Inter-individual variability in indices of glucose metabolism was high with coefficients of variation ranging from 9 to 59%. CONCLUSION: Significant changes in glucose metabolism are evident within 7-day periods of controlled OF and underfeeding. Although IS was impaired at the end of the CR-RF cycle, IS was normalized after the OF-CR cycle. At different feeding regimens, homeostatic responses of glucose metabolism were highly variable.