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Determinants of energy expenditure and energy balance.
ARTICLE IN PRESS Abstracts / Appetite 49 (2007) 272–341
Determinants of energy expenditure and energy balance
K.R. WESTERTERP. Department of Human Biology, Maastricht University, 6200 MD Maastricht, The Netherlands Energy metabolism of an individual is a function of body size, body composition, behaviour including food intake and physical activity, and health status. The analysis of determinants of energy expenditure is illustrated in relation to gender differences. Women have on average a lower energy intake and a lower average daily metabolic rate due to a lower body mass, fat-free mass, and a higher % body fat. Activity-induced energy expenditure, the energy expenditure associated with muscular contractions to perform body postures and—movements excluding exercise, is the most variable component of total energy expenditure. Determinants of activity-induced energy expenditure are presented to get a view whether it is an obligatory or a facultative phenomenon. Twin studies showed that most of the between subject variation in activity-induced energy expenditure is explained by genetic factors. Activity-induced energy expenditure of subjects in the confined environment of a respiration chamber was on average halve the value as observed in the same subjects in free-living conditions with doubly labeled water. In young adults, exercise training does not affect non-training activity. However, in elderly subjects, exercise training induced an equivalent compensatory decline in non-training activity. Similarly, activity-induced energy expenditure is reduced during energy restriction and in patients with chronic disease increasing resting energy expenditure. Studies with exercise training showed the reduction is difficult to overcome. There is little evidence for a compensatory increase in activity-induced energy expenditure during overfeeding.
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of leptin resistance. Twenty-eight days of high-fat (HF) feeding increased body weight and fat pad weights (Po0.05) compared to low-fat (LF), and also increased PTP1B protein levels in the mediobasal hypothalamus (P=0.003). To define a mechanism underlying this HF-induced increase in PTP1B, the independent effects of hyperleptinemia and exposure to a high-fat diet were tested. Leptin-deficient ob/ob mice were fed LF or HF diets and treated with leptin or saline for 14 days. Leptin treatment increased hypothalamic PTP1B in the LF mice (P=0.003), but had no effect in HF mice. However, HF mice exhibited a marked increase in hypothalamic PTP1B mRNA irrespective of leptin treatment (Po0.001). These data are consistent with the hypothesis that increases in hypothalamic PTP1B contribute to leptin resistance in response to a high-fat diet. While chronic increases in circulating leptin are sufficient to increase PTP1B, HF diets also directly stimulate hypothalamic PTP1B via a leptinindependent mechanism. 10.1016/j.appet.2007.03.214
10.1016/j.appet.2007.03.213
In utero programming of metabolic dysregulation: Focus on CNS mechanisms K.W. WHITAKER, T.M. REYES. University
of Pennsylvania, School of Medicine, Philadelphia, PA 19104, USA
PTP1B: A molecular mediator of leptin resistance C.L. WHITE,
M.J. BARNES, A. WHITTINGTON, Z. WANG, W.T. CEFALU, G.A. BRAY, C.D. MORRISON. Pennington Biomedical Research Center, Baton Rouge, LA 70808, USA Leptin acts in the brain to suppress food intake and body adiposity, but in most cases obesity is associated with a resistance to leptin action. Protein tyrosine phosphatase 1B (PTP1B) dephosphorylates key components of the leptin receptor signaling cascade, and represents a molecular mediator of leptin resistance. Our recent work demonstrates that hypothalamic PTP1B levels are elevated in a model of aging-induced leptin resistance, and that acute inhibition of PTP1B improves hypothalamic leptin sensitivity in this setting. We therefore tested whether hypothalamic PTP1B is increased in diet-induced obesity, another model
We have used a model of restricted maternal nutrition (8% protein) in mice to examine the consequences for feeding and metabolism in the offspring. Dams are maintained on control or low-protein diets throughout breeding and lactation. At weaning, pups are divided into groups that are fed either control or high fat (60%) diets. Food and water intake, metabolic rate and activity were monitored for 6 months. Animals from low protein pregnancies weighed significantly less at weaning, and had a significantly greater rate of weight gain. Additionally, animals from low protein pregnancies were hyperphagic and hypermetabolic. These effects were influenced by the weaning diet. Differences in hypothalamic levels of protein and mRNA levels of NPY and melanocortin peptides will be presented. Additionally, pilot data show that low birth weight animals have an altered stress response. Animals from the maternal low protein pregnancies had significantly fewer Fos-ir+ cells in the PVH in response to a 30 min restraint stress as compared to animals from control pregnancies. These phenotypic findings will be discussed in the context of the potential long term consequence for health and disease. 10.1016/j.appet.2007.03.215
Determinants of energy expenditure and energy balance
K.R. WESTERTERP. Department of Human Biology, Maastricht University, 6200 MD Maastricht, The Netherlands Energy metabolism of an individual is a function of body size, body composition, behaviour including food intake and physical activity, and health status. The analysis of determinants of energy expenditure is illustrated in relation to gender differences. Women have on average a lower energy intake and a lower average daily metabolic rate due to a lower body mass, fat-free mass, and a higher % body fat. Activity-induced energy expenditure, the energy expenditure associated with muscular contractions to perform body postures and—movements excluding exercise, is the most variable component of total energy expenditure. Determinants of activity-induced energy expenditure are presented to get a view whether it is an obligatory or a facultative phenomenon. Twin studies showed that most of the between subject variation in activity-induced energy expenditure is explained by genetic factors. Activity-induced energy expenditure of subjects in the confined environment of a respiration chamber was on average halve the value as observed in the same subjects in free-living conditions with doubly labeled water. In young adults, exercise training does not affect non-training activity. However, in elderly subjects, exercise training induced an equivalent compensatory decline in non-training activity. Similarly, activity-induced energy expenditure is reduced during energy restriction and in patients with chronic disease increasing resting energy expenditure. Studies with exercise training showed the reduction is difficult to overcome. There is little evidence for a compensatory increase in activity-induced energy expenditure during overfeeding.
339
of leptin resistance. Twenty-eight days of high-fat (HF) feeding increased body weight and fat pad weights (Po0.05) compared to low-fat (LF), and also increased PTP1B protein levels in the mediobasal hypothalamus (P=0.003). To define a mechanism underlying this HF-induced increase in PTP1B, the independent effects of hyperleptinemia and exposure to a high-fat diet were tested. Leptin-deficient ob/ob mice were fed LF or HF diets and treated with leptin or saline for 14 days. Leptin treatment increased hypothalamic PTP1B in the LF mice (P=0.003), but had no effect in HF mice. However, HF mice exhibited a marked increase in hypothalamic PTP1B mRNA irrespective of leptin treatment (Po0.001). These data are consistent with the hypothesis that increases in hypothalamic PTP1B contribute to leptin resistance in response to a high-fat diet. While chronic increases in circulating leptin are sufficient to increase PTP1B, HF diets also directly stimulate hypothalamic PTP1B via a leptinindependent mechanism. 10.1016/j.appet.2007.03.214
10.1016/j.appet.2007.03.213
In utero programming of metabolic dysregulation: Focus on CNS mechanisms K.W. WHITAKER, T.M. REYES. University
of Pennsylvania, School of Medicine, Philadelphia, PA 19104, USA
PTP1B: A molecular mediator of leptin resistance C.L. WHITE,
M.J. BARNES, A. WHITTINGTON, Z. WANG, W.T. CEFALU, G.A. BRAY, C.D. MORRISON. Pennington Biomedical Research Center, Baton Rouge, LA 70808, USA Leptin acts in the brain to suppress food intake and body adiposity, but in most cases obesity is associated with a resistance to leptin action. Protein tyrosine phosphatase 1B (PTP1B) dephosphorylates key components of the leptin receptor signaling cascade, and represents a molecular mediator of leptin resistance. Our recent work demonstrates that hypothalamic PTP1B levels are elevated in a model of aging-induced leptin resistance, and that acute inhibition of PTP1B improves hypothalamic leptin sensitivity in this setting. We therefore tested whether hypothalamic PTP1B is increased in diet-induced obesity, another model
We have used a model of restricted maternal nutrition (8% protein) in mice to examine the consequences for feeding and metabolism in the offspring. Dams are maintained on control or low-protein diets throughout breeding and lactation. At weaning, pups are divided into groups that are fed either control or high fat (60%) diets. Food and water intake, metabolic rate and activity were monitored for 6 months. Animals from low protein pregnancies weighed significantly less at weaning, and had a significantly greater rate of weight gain. Additionally, animals from low protein pregnancies were hyperphagic and hypermetabolic. These effects were influenced by the weaning diet. Differences in hypothalamic levels of protein and mRNA levels of NPY and melanocortin peptides will be presented. Additionally, pilot data show that low birth weight animals have an altered stress response. Animals from the maternal low protein pregnancies had significantly fewer Fos-ir+ cells in the PVH in response to a 30 min restraint stress as compared to animals from control pregnancies. These phenotypic findings will be discussed in the context of the potential long term consequence for health and disease. 10.1016/j.appet.2007.03.215