Abdul G. Dulloo’s research while affiliated with University of Fribourg and other places

Background/Aims Coronary heart disease morbidity and mortality are higher in people of South Asian origin than in those of African origin. We investigated whether as young adults without diabetes, people in Mauritius of South Asian descent (Indians) would show a more adverse cardiovascular risk profile that those of predominantly African descent (Creoles), and whether this could be explained by ethnic differences in visceral adiposity or other fat distribution patterns. Methods The study was conducted in 189 young non-physically active adults, with the following measurements conducted after an overnight fast: anthropometry (weight, height, waist circumference), whole-body and regional body composition by dual-energy x-ray absorptiometry, blood pressure, and blood assays for glycemic (glucose and HbA1c) and lipid profile (triglycerides and cholesterols). Results The results indicate higher serum triglycerides and lower HDL cholesterol in men than in women, and in Indians than in Creoles (p < 0.001). No significant differences due to sex or ethnicity are observed in body mass index and waist circumference, but indices of visceral adiposity (visceral/android, visceral/subcutaneous) and visceral-to-peripheral adiposity ratio (visceral/gynoid, visceral/limb) were significantly higher in men than in women, and in Indians than in Creoles. The significant effects of sex and ethnicity on blood lipid profile were either completely abolished or reduced to a greater extent after adjusting for the ratio of visceral-to-peripheral adiposity than for visceral adiposity per se. Conclusions In young adults in Mauritius, Indians show a more adverse pattern of body fat distribution and blood lipid risk profile than Creoles. Differences in their fat distribution patterns, however, only partially explain their differential atherogenic lipid risk profile, amid a greater impact of visceral-to-peripheral adiposity ratio than that of visceral adiposity per se on sex and ethnic differences in cardiovascular risks; the former possibly reflecting the ratio of hazardous (visceral) adiposity and protective (peripheral) superficial subcutaneous adiposity.

This chapter covers the key concepts of energy balance and body weight regulation. The long-term constancy of body weight is achieved through a highly complex network of regulatory systems through which changes in food intake, body composition, and energy expenditure are interlinked. Failure of regulations results in either obesity and its co-morbidities or protein-energy malnutrition and cachexia in disease states. Thus, achieving energy balance and weight homeostasis is central to the quality of life. The chapter then details how energy expenditure changes in response to undernutrition and overnutrition before examining the components of models of energy intake and energy expenditure.

Depending on the nature of their sports, athletes may be engaged in successive weight loss (WL) and regain, conducing to “weight cycling.” The aims of this paper were to systematically (and meta‐analytically when possible) analyze the post‐WL recovery of (i) body weight and (ii) fat mass; fat‐free mass; and performance and metabolic responses in weight cycling athletes (18–55 years old, body mass index < 30 kg.m ⁻² ). MEDLINE, Embase, and SPORTDiscus databases were explored. The quality and risk of bias of the 74 included studies were assessed using the quality assessment tool for quantitative studies. Thirty‐two studies were eligible for meta‐analyses. Whatever the type of sports or methods used to lose weight, post‐WL body weight does not seem affected compared with pre‐WL. While similar results are observed for fat‐free mass, strength sports athletes (also having longer WL and regain periods) do not seem to fully recover their initial fat mass (ES: −0.39, 95% CI: [−0.77; −0.00], p = 0.048, I ² = 0.0%). Although the methods used by athletes to achieve WL might prevent them from a potential post‐WL fat overshooting, further studies are needed to better understand WL episodes consequences on athletes' performance as well as short‐ and long‐term physical, metabolic, and mental health.

The concept of dual-adaptive thermogenesis underlying metabolic adaptation to prolonged energy deficit posits that there are two control systems that govern energy sparing: a rapid-reacting system to energy deficit and a slow-reacting system to fat store depletion. The latter control system, referred to as the "adipose-specific" control of thermogenesis, contributes to accelerating fat store replenishment (catch-up fat) during weight regain. The case is put forward here that, whereas adaptive thermogenesis during weight loss results primarily from central suppression of the sympathetic nervous system and hypothalamic-pituitary-thyroid axis, during weight regain it operates primarily through peripheral tissue resistance to the actions of this neurohormonal network. Emerging evidence that altered deiodination of thyroid hormones within the skeletal muscle and liver is a key determinant of such peripheral resistance therefore offers entry points toward elucidating the molecular mechanisms that underlie the adipose-specific control of thermogenesis and unraveling tissue-specific targets to counter obesity recidivism.

While there is an increasing prevalence of dieting in the overall population, weight loss practices could be a risk factor for weight gain in normal-weight individuals. The aim of the present work was to systematically review all the studies implicating diet restriction and body weight evolution in normal-weight people. The literature search was registered in PROSPERO (CRD42021281442) and was performed in three databases from April 2021 to June 2022 for articles involving healthy normal-weight adults. From a total of 1487 records initially identified, 18 were selected in the systematic review. Of the 8 dieting interventional studies, only one found a higher body weight after weight recovery, but 75% of them highlighted metabolic adaptations in response to weight loss favoring weight regain and persisting during/after body weight recovery. Eight of the 10 observational studies showed a relationship between dieting and major later weight gain while the meta-analysis of observational studies results indicated that ‘dieters’ have a higher body weight than ‘non-dieters’. However, considering the high methodological heterogeneity and the publication bias of the studies, this result should be taken with caution. Moreover, the term ‘diet’ was poorly described and we observed a large heterogeneity of the methods used to assess dieting status. Present results suggest that dieting could be a major risk factor for weight gain in the long term in normal-weight individuals. There is however a real need for prospective randomized controlled studies specifically assessing the relationship between weight loss induced by diet and subsequent weight in this population.

Obesity is often considered to result from the failure of homeostatic mechanisms that regulate body weight to cope with an environment that encourages overeating and sedentarity. Understanding how short‐term deviations in body weight are corrected by changes in energy intake, energy expenditure (EE), or both, still remains a challenging issue for human research today. In such a dynamic state within which weight homeostasis occurs, it is likely that long‐term constancy of body weight is achieved through a highly complex network of autoregulatory control systems and subsystems through which changes in food intake, body composition and EE are interlinked. Since many factors can lead to underestimation or overestimation of energy intake, thereby causing a bias in energy balance, it is not surprising that energy requirements are preferentially based on estimates of EE rather than on energy intake estimates.

For most of their evolutionary history, humans have been faced with frequent periods of food scarcity and famine, specific nutrient deficiencies and sometimes food abundance. In such a lifestyle of famine-and-feast, it is conceivable that adaptive mechanisms—operating through adjustments in energy expenditure and in management of the body's main energy-containing compartments (fat and protein)—have evolved as key control systems in the regulation of body weight. What are these control systems, and how they function to enable the human body to adapt to nutritional stresses and to achieve weight homeostasis is the focus of this article.

Societal erosion of daily life low-level physical activity has had a great influence on the obesity epidemic. Given that low fat oxidation is also a risk factor for obesity, we investigated, in a repeated measures design, the dynamics of fat oxidation from a resting state to a light-intensity leg cycling exercise (0–50 watts) in inactive, healthy young adults. Using indirect calorimetry, energy expenditure and the respiratory quotient (RQ) were assessed in a sitting posture at rest and during a cycling exercise in 35 subjects (20 women). The rate of perceived exhaustion (RPE) was assessed using the Borg Scale. During graded leg cycling, the mean RPE did not exceed values corresponding to the exercise being perceived as ‘light’. However, analysis of individual data at 50 watts revealed two distinct subgroups among the subjects: those having RPE values corresponding to the exercise being perceived as ‘very light to light’ and showing no increase in RQ relative to resting levels, as opposed to an increase in RQ in those who perceived the exercise as being ‘somewhat hard to hard’ (p < 0.001). Our study in inactive individuals showing that high fat oxidation was maintained during ‘light-perceived’ physical activity reinforced the potential importance of light physical activity in the prevention of obesity.