Food demand and energy balance: A neuroeconomic analysis of melanocortin system and exercise
Başlık çevirisi mevcut değil.
- Tez No: 402182
- Danışmanlar: DR. NEIL E. ROWLAND
- Tez Türü: Doktora
- Konular: Beslenme ve Diyetetik, Ekonomi, Nutrition and Dietetics, Economics
- Anahtar Kelimeler: Belirtilmemiş.
- Yıl: 2010
- Dil: İngilizce
- Üniversite: University of Florida
- Enstitü: Yurtdışı Enstitü
- Ana Bilim Dalı: Belirtilmemiş.
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: 114
Özet
Özet yok.
Özet (Çeviri)
One of the main factors contributing to the obesity epidemic is the obesity favorable food environment of today's modern societies that promotes excessive energy intake while minimizing the energy expenditure. The purpose of the present work is to combine the analyses of the effects of both positive and negative energy balance on food demand and meal size by exploring the some of the physiological and neuronal mechanisms of the melanocortin system and the effects of physical activity. Homozygous deletion of the melanocortin-4 receptors (MC4R-/-) is known to result in positive energy balance as MC4R-/- mice and humans develop obesity, while those with deletion of the melanocortin-3 receptors (MC3R-/-) do not become markedly obese. In the first part of this dissertation, the effects of positive energy demand on food demand were examined. MC3R-/-, MC4R-/- mice with wild type (WT) and mice lacking both of these receptors (double knockout, DKO) were compared on select feeding and neuroanatomical dimensions. In a food demand protocol, DKO and MC4R-/- were hyperphagic at low unit costs for food, due primarily to increased meal size. However, at higher costs, their intake dropped below that of WT and MC3R-/- indicating increased elasticity of food demand. To determine whether this higher elasticity was due either to the genotype or to the positive energy balance per se, the same food demand protocol was conducted in dietary obese mice. The difference between the demand functions of WT and dietary obese mice was smaller compared to that of WT and genetically obese mice. To assess a mechanism for the larger meal size in MC4R-/- and DKO, we examined the acute anorectic effect of peripherally-administered cholecystokinin (CCK) and subsequently the induction of Fos-immunoreactivity in select brain regions. The anorectic effect of CCK was comparable in MC4R-/-, DKO, and WT, but was unexpectedly absent in MC3R-/-. CCK-8 induced c-Fos was lower in PVN in MC3R-/- than the other genotypes. The second part of this dissertation examines the effects of negative energy balance on food demand. Physical activity has long been suggested as a method to better maintain weight loss and that obesity induced by a high fat diet can be treated without energy restriction by exercise. The effects of running wheel activity on food intake and meal patterns were measured under several economic conditions in CD 1 mice. Voluntary wheel running activity increased daily food intake and running animals consumed bigger but fewer meals compared to the sedentary. Although they ate more, running mice had significantly lower body fat, especially in subcutaneous depots. In the foraging protocol, when food intake was contingent on the running wheel activity, mice were able to emit more responses compared to when food is contingent upon a nose poke response. In both voluntary and foraging running protocols mice had inelastic demand functions compared to the non-running groups indicating that negative energy balance affects how much mice are willing to work for food.
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