ABSTRACT
Simulation models (SMs) combine information from a variety of sources to provide a useful tool for examining how the effects of obesity unfold over time and impact population health. SMs can aid in the understanding of the complex interaction of the drivers of diet and activity and their relation to health outcomes. As emphasized in a recently released report of the Institute or Medicine, SMs can be especially useful for considering the potential impact of an array of policies that will be required to tackle the obesity problem. The purpose of this paper is to present an overview of existing SMs for obesity. First, a background section introduces the different types of models, explains how models are constructed, shows the utility of SMs and discusses their strengths and weaknesses. Using these typologies, we then briefly review extant obesity SMs. We categorize these models according to their focus: health and economic outcomes, trends in obesity as a function of past trends, physiologically based behavioural models, environmental contributors to obesity and policy interventions. Finally, we suggest directions for future research.
Subject(s)
Health Policy , Models, Biological , Obesity/epidemiology , Body Mass Index , Computer Simulation , HumansABSTRACT
Electrolytic lesions of the basomedial hypothalamus eliminated food-deprivation-induced stabilimeter activity in rats that were prevented from becoming obese. Knife cuts lateral to the basomedial area (separating the medial and lateral hypothalamus) potentiated this activity, as did transections posterior to the basomedial region. Anterior transections (between anterior and medial hypothalamus), however, eliminated the effect. Lesions of the stria terminalis and amygdala likewise abolished deprivation-induced locomotor activity, but elevated ab-lib activity to a level comparable with that after deprivation in intact animals. Animals with combined basomedial-stria terminalis lesions behaved like animals with basomedial lesions. These results suggest that food-deprivation-induced locomotor activity in stabilimeter cages is due to a disinhibition of the basomedial hypothalamus by the amygdala via the stria terminalis.
Subject(s)
Amygdala/physiology , Arousal/physiology , Food Deprivation , Hypothalamus/physiology , Motor Activity/physiology , Animals , Body Weight/drug effects , Dextroamphetamine/pharmacology , Diabetes Mellitus, Experimental/physiopathology , Drinking Behavior , Feeding Behavior , Housing, Animal , Hypothalamus, Anterior/physiology , Hypothalamus, Middle/physiology , Inhibition, Psychological/physiology , Male , Motor Activity/drug effects , Rats , Time FactorsABSTRACT
Locomotor activity was studied in rats with lesions of the basomedial hypothalamus following food deprivation (0, 1, 2, and 4 days) and amphetamine (0, .5, 1.0, and 2.0 mg/kg). Control animals showed the normal potentiation of amphetamine-induced locomotor activity by starvation. Animals with lesions, however, did not differ, when deprived, from satiated control animals in their response to amphetamine. These results suggest that behavioral arousal produced by food deprivation is mediated by the basomedial hypothalamus.
