Coping with climate change. Using genebanks to protect farmers' livelihoods

Poster presented at World Bank Development Marketplace. Washington D.C. (USA), 10 - 13 Nov 200

Collateral fattening: when a deficit in lean body mass drives overeating

In his last review entitled “Some Adventures in Body Composition,” Gilbert Forbes reminded us that “lean body mass and body fat are in a sense companions.” To what extent the lean body mass (or fat-free mass) component in this companionship impacts on energy intake is rarely a topic for discussion, amid a dominant adipocentric view of appetite control. Yet an analysis of the few human studies that have investigated the relationships between objectively measured food intake and body composition reveals a potentially important role for both an increase and a decrease in fat-free mass in the drive to eat. These studies are highlighted here, together with the implications of their findings for research directed as much toward the elucidation of peripheral signals and energy-sensing mechanisms that drive hunger and appetite, as toward understanding the mechanisms by which dieting and sedentariness predispose to fatness

Nutrition, movement and sleep behaviours: their interactions in pathways to obesity and cardiometabolic diseases

Among the multitude of dietary and lifestyle behaviours that have been proposed to contribute to the obesity epidemic, those that have generated considerable research scrutiny in the past decade are centred upon sleep behaviours, sedentary behaviours (sitting or lying while awake) and diminished low-level physical activities of everyday life, with each category of behaviours apparently presenting an independent risk for obesity and/or cardiometabolic diseases. These behaviours are highly complex, operate in synergy with each other, disrupt the link between regulation of the circadian clock and metabolic physiology and impact on various components of daily energy expenditure and feeding behaviours to promote obesity and hinder the outcome of obesity therapy. As such, this behavioural triad (nutrition, movement and sleep) presents plenty of scope for intervention and optimization in the context of body weight regulation and lifestyle-related disease prevention. It is against this background that recent advances relevant to the theme of ‘Nutrition, Movement & Sleep Behaviors: their interactions in pathways to obesity and cardiometabolic diseases’ are addressed in this overview and the nine review articles in this supplement reporting the proceedings of the 8th Fribourg Obesity Research Conference

Collateral fattening in body composition autoregulation: its determinants and significance for obesity predisposition

Collateral fattening refers to the process whereby excess fat is deposited as a result of the body’s attempt to counter a deficit in lean mass through overeating. Its demonstration and significance to weight regulation and obesity can be traced to work on energy budget strategies in growing mammals and birds, and to men recovering from experimental starvation. The cardinal features of collateral fattening rests upon (i) the existence of a feedback system between lean tissue and appetite control, with lean tissue deficit driving hyperphagia, and (ii) upon the occurrence of a temporal desynchronization in the recovery of body composition, with complete recovery of fat mass preceeding that of lean mass. Under these conditions, persistent hyperphagia driven by the need to complete the recovery of lean tissue will result in the excess fat deposition (hence collateral fattening) and fat overshooting. After reviewing the main lines of evidence for the phenomenon of collateral fattening in body composition autoregulation, this article discusses the causes and determinants of the desynchronization in fat and lean tissue recovery leading to collateral fattening and fat overshooting, and points to their significance in the mechanisms by which dieting, developmental programming and sedentariness predispose to obesity

Uncoupling proteins: their roles in adaptive thermogenesis and substrate metabolism reconsidered

During the past few years, there have been two major developments, if not revolutions, in the field of energy balance and weight regulation. The first at the molecular level, which was catalysed by developments in DNA screening technology together with the mapping of the human genome, has been the tremendous advances made in the identification of molecules that play a role in the control of food intake and metabolic rate. The second, at the systemic level, which centered upon the use of modern technologies or more robust analytical techniques for assessing human energy expenditure in response to starvation and overfeeding, has been the publication of several papers providing strong evidence that adaptive thermogenesis plays a much more important role in the regulation of body weight and body composition than previously thought. Within these same few years, several new members of the mitochondrial carrier protein family have been identified in a variety of tissues and organs. All apparently possess uncoupling properties in genetically-modified systems, with two of them (uncoupling protein (UCP) 2 and UCP3) being expressed in adipose tissues and skeletal muscles, which are generally recognised as important sites for variations in thermogenesis and/or in substrate oxidation. Considered as breakthrough discoveries, the cloning of these genes has generated considerable optimism for rapid advances in our molecular understanding of adaptive thermogenesis, and for the identification of new targets for pharmacological management of obesity and cachexia. The present paper traces first, from a historical perspective, the landmark events in the field of thermogenesis that led to the identification of these genes encoding candidate UCP, and then addresses the controversies and on-going debate about their physiological importance in adaptive thermogenesis, in lipid oxidation or in oxidative stress. The general conclusion is that UCP2 and UCP3 may have distinct primary functions, with UCP3 implicated in regulating the flux of lipid substrates across the mitochondria and UCP2 in the control of mitochondrial generation of reactive oxygen species. The distinct functions of these two UCP1 homologues have been incorporated in a conceptual model to illustrate how UCP2 and UCP3 may act in concert in the overall regulation of lipid oxidation concomitant to the prevention of lipid-induced oxidative damag

The control of partitioning between protein and fat during human starvation: its internal determinants and biological significance

Human subjects vary in the extent to which their body's protein and fat compartments are mobilized for fuel during starvation. Although an inverse association between the initial adiposity and the contribution of protein as fuel during starvation has been known for nearly a century, interest in the quantitative importance and functional significance of the initial percentage fat as a determinant of biological variation in energy-partitioning between protein and fat (and hence in determining the partitioning characteristic of the individual) is relatively recent. The present paper addresses these issues by revisiting the classic Minnesota experiment of semi-starvation and refeeding from a standpoint of system physiology. In a quantitative analysis of the relationship between the initial body composition (ratio FAT0:fat-free mass (FFM)0) and the composition of weight loss (ratio ΔFAT:ΔFFM) in the thirty-two men in the Minnesota study, the arguments are put forward that the fraction of FFM lost when the fat stores reach total depletion is independent of the initial percentage fat, and that this fraction represents the ‘dispensible' component of the protein compartment that is compatible with life (i.e. the protein energy-reserve, rp). The concepts are developed that (1) the initial percentage body fat (which reflects the initial ratio FAT0:FFM0) provides a ‘memory of partitioning' which dictates the control of partitioning between protein and fat in such a way that both the protein energy-reserve (rp) and the fat energy-reserve (rf) reach complete depletion simultaneously, a strategy that would ensure maximum length of survival during long-term food scarcity, and that (2) variability in the relative sizes of these two energy reserves (i.e. in rf:rp) could, in addition to the initial percentage fat, also contribute to human variability in energy-partitioning. The basic assumptions underlying this re-analysis of the Minnesota data, and the concepts that are derived from it, have been integrated in the simple mathematical model for predicting the partitioning characteristic of the individual. This model is used to explain how variability in the fraction of the protein compartment that could function as an energy reserve (rp) can be as important as the initial percentage fat in determining inter-individual variability in protein-sparing during the early phase of starvation, in fuel partitioning during prolonged starvation, or in the maximum percentage weight loss during starvation. The elucidation of factors underlying variability in the size of the protein energy-reserve may have important implications for our understanding of the pathophysiology of starvation and age-associated susceptibility to muscle wasting, and in the clinical management of cachexia and obesit