Body composition during nutritional repletion of severely undernourished men

Barac‐Nieto, Mario; Spurr, G. B.; Lotero, H; Maksud, Michael G.; Dahners, H. W.

doi:10.1093/ajcn/32.5.981

Cited by 61 publications

(24 citation statements)

References 13 publications

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“…For 80 more days, they were fed 9.4 MJ/day, 19.7% protein. Nitrogen balance became more positive (5-8 g) and the ratio of intracellular water to total body water increased to 36-38% (Barac-Nieto et al, 1979). This is only a correlation between nitrogen balance and cellular hydration, which does not prove a causality effect.…”

Section: Changes In Water Compartments In Diseased Humansmentioning

confidence: 82%

Effects of changes in water compartments on physiology and metabolism

et al. 2003

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There is paramount evidence to suggest the importance of cell volume changes for the regulation of cell function, including protein metabolism. Among many other effects, cell swelling inhibits proteolysis and stimulates protein synthesis. However, most of the data pertinent to this theory relate to in vitro experiments. This paper reviews the evidence about the relevance of cell swelling and changes in water compartments to regulation of metabolism at the whole body level in animals and humans. Protein metabolism is most likely regulated by cellular hydration in health and disease. Cellular hydration appears to bear no effect on energy metabolism. The relationship between cellular hydration and lipolysis deserves to be verified. There appears to be a possible weak effect on glucose metabolism. Further studies are therefore necessary to challenge the cell swelling theory. If confirmed, strategies to modify cellular hydration could be used to improve metabolic orientations especially in the critically ill.

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Section: Changes In Water Compartments In Diseased Humansmentioning

confidence: 82%

Effects of changes in water compartments on physiology and metabolism

et al. 2003

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“…Although their body weight returned to pre-entry values 6 months after exit, the weight regained was found to be almost exclusively accounted for by an increase in body fat. Over the past few decades, this phenomenon of fat recovery predominating over muscle reconstitution has also been reported in hospitalized adult patients recovering from severe weight losses due to poverty-related undernutrition, 35 anorexia nervosa, 36 and various pathophysiological 'hypermetabolic' conditions including cancer, 37 septic shock 38 and AIDS. 39 Explanations for this phenomenon of catch-up fat and poor recovery of lean tissues have in the past centered upon inadequate intake of dietary protein or other nutrients for optimal protein deposition, or that the absolute amount of food consumed may greatly exceed the energy requirements for maintenance, tissue synthesis and physical work, such that the extra energy ingested is deposited as fat.…”

Section: The Catch-up Fat Phenomenonmentioning

confidence: 93%

Pathways from weight fluctuations to metabolic diseases: focus on maladaptive thermogenesis during catch-up fat

2002

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It has long been known that obesity is a high risk factor for cardiovascular diseases. In more recent years, the analysis of several large epidemiological databases has also revealed that, independently of excess weight, large fluctuations in body weight at some point earlier in life represent an independent risk factor for type 2 diabetes and hypertension -two major contributors to cardiovascular diseases. High cardiovascular morbidity and mortality have indeed been reported in men and women who in young adulthood experienced weight fluctuations (involving the recovery of body weight after weight loss due to disease, famine or voluntary slimming), or when weight fluctuations occurred much earlier in life and involved catch-up growth after fetal or neonatal growth retardation. This paper addresses the pathways from weight fluctuations to chronic metabolic diseases by focusing on the phenomenon of accelerated fat recovery (ie catch-up fat) after weight loss or growth retardation. Arguments are put forward that, during catch-up growth or weight recovery on our modern refined foods, the mechanisms of adaptive thermogenesis that regulate catch-up fat are pushed beyond the limits for which they were meant to operate and turn maladaptive. The consequences are enhanced susceptibilities towards skeletal muscle insulin resistance and overactive sympathetic activity, both of which are major contributors to the pathogenesis of chronic metabolic diseases. Since weight fluctuation earlier in life (independently of excess weight later in life) is an independent risk factor for metabolic diseases, the mechanisms by which body fat is acquired would seem to be at least as important as the consequences of excess fat per se in the pathogenesis of diabetes, hypertension and cardiovascular diseases. International Journal of Obesity (2002) 26, Suppl 2, S46 -S57. doi:10.1038=sj.ijo.0802127Keywords: obesity; diabetes; hypertension; catch-up growth; weight cycling; fetal programming Weight fluctuations through the agesCardiovascular diseases are well recognized to be among the most common debilitating complications of excess body fat. According to some reports, as many as 50% of obese people have high blood pressure and type 2 diabetes, which are both major contributors to their high predispositions to cardiovascular diseases.1,2 While restriction of energy intake and weight loss improve insulin sensitivity and lower blood pressure, the long-term prognosis of treatment is poor. In the vast majority of patients, the phase of weight loss is followed by a return towards the obese state, together with the associated metabolic complications and high cardiovascular risks. In fact, several lines of evidence suggest that the process of recovering body weight is itself an independent risk factor for the development of cardiovascular diseases.First, the analysis of several large epidemiological databases 3 -7 has revealed a higher cardiovascular morbidity and mortality in men and women who previously experienced marked fluctuations in body weigh...

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Section: Catch-up Fat In Infants Born Pretermmentioning

confidence: 97%

The thrifty ‘catch-up fat’ phenotype: its impact on insulin sensitivity during growth trajectories to obesity and metabolic syndrome

et al. 2006

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The analyses of large epidemiological databases have suggested that infants and children who show catch-up growth, or adiposity rebound at a younger age, are predisposed to the development of obesity, type 2 diabetes and cardiovascular diseases later in life. The pathophysiological mechanisms by which these growth trajectories confer increased risks for these diseases are obscure, but there is compelling evidence that the dynamic process of catch-up growth per se, which often overlaps with adiposity rebound at a younger age, is characterized by hyperinsulinemia and by a disproportionately higher rate in the recovery of body fat than lean tissue (i.e. preferential 'catch-up fat'). This paper first focuses upon the almost ubiquitous nature of this preferential 'catch-up fat' phenotype across the life cycle as a risk factor for obesity and insulin-related complications -not only in infants and children who experienced catch-up growth after earlier fetal or neonatal growth retardation, or after preterm birth, but also in adults who show weight recovery after substantial weight loss owing to famine, disease-cachexia or periodic dieting. It subsequently reviews the evidence indicating that such preferential catch-up fat is primarily driven by energy conservation (thrifty) mechanisms operating via suppressed thermogenesis, with glucose thus spared from oxidation in skeletal muscle being directed towards de novo lipogenesis and storage in white adipose tissue. A molecular-physiological framework is presented which integrates emerging insights into the mechanisms by which this thrifty 'catch-up fat' phenotype crosslinks with early development of insulin and leptin resistance. In the complex interactions between genetic constitution of the individual, programming earlier in life, and a subsequent lifestyle of energy dense foods and low physical activity, this thrifty 'catch-up fat' phenotype -which probably evolved to increase survival capacity in a hunter-gatherer lifestyle of periodic food shortages -is a central event in growth trajectories to obesity and to diseases that cluster into the insulin resistance (metabolic) syndrome.

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Body composition during nutritional repletion of severely undernourished men

Cited by 61 publications

References 13 publications

Effects of changes in water compartments on physiology and metabolism

Effects of changes in water compartments on physiology and metabolism

Pathways from weight fluctuations to metabolic diseases: focus on maladaptive thermogenesis during catch-up fat

The thrifty ‘catch-up fat’ phenotype: its impact on insulin sensitivity during growth trajectories to obesity and metabolic syndrome

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