The pattern of food consumption can influence body weight and composition. This dissertation utilizes a recently developed meal pattern program created for the studies presented here to examine how high-fat diet and social stress alter the pattern of food consumption and how these changes, along with individual-vulnerability to stress, may contribute to known diet and stress-related effects on body weight and composition.
The established meal pattern program was validated by exposing rats to a high-fat diet, which resulted in the gain of body weight and adipose tissue and a decreased meal frequency and increased meal size. Furthermore, meal size was shown to have a positive correlation with the gain of adipose mass. All of these results have been previously reported allowing us to verify the system for use in our laboratory model of chronic social stress: the visible burrow system (VBS) and for the first time measure meal patterns during social stress exposure. Dominant (DOM) animals lose a minimal amount of weight and adipose tissue during VBS exposure, but quickly recover their weight and body composition to controls (CON) levels once removed from the VBS. Subordinate (SUB) animals lose a significant amount of body weight, adipose and lean tissue during VBS housing, and upon recovery from stress regain body weight preferentially as adipose tissue.
DOM and SUB are hypophagic during initial exposure to the VBS. DOM initially had a reduced meal frequency, but once the hierarchy was established showed no signs of disrupted ingestive behavior. SUB took smaller, fewer meals during the formation of the hierarchy, but once stable, only took fewer meals although had other signs of disrupted ingestive behavior such as increased meal duration, Intrameal interval and Intermeal interval along with an interrupted circadian pattern of feeding suggested by their increased meal frequency in the light cycle. These changes are likely a result of adaptation to the VBS environment. Expression of neuropeptide Y (NPY), a potent orexigenic agent expressed in the hypothalamus, was increased immediately following VBS exposure in both the DOM and SUB population suggesting that another mechanism is blocking or impairing the NPY signal to stimulate food intake during VBS housing.
During recovery, DOM and SUB were hyperphagic. SUB accomplished this through taking larger meals. This in combination with the slight decrease in meal number likely contributes to the gain in adipose tissue present in this population following VBS exposure. Furthermore, the circadian pattern of feeding remained altered during the initial recovery period and meal duration and intermeal interval were longer than DOM and CON throughout the 3-week recovery period. After 1- and 3-weeks of recovery hypothalamic NPY expression was not different among the groups suggesting that, in this case, NPY does not mediate the hyperphagia following VBS exposure.
Together, these studies suggest that pattern of ingestive behavior is an important factor in the body weight and composition changes associated with the VBS models of chronic social stress; however, individual vulnerability may also contribute to these changes. The OMEGA phenotype, as established through behavior within the VBS, loses a considerable amount of body weight, adipose and lean tissue and is hyporesponsive to a novel acute restraint stress test. An increase in NPY expression in the central and basolateral nucleus suggest an impaired anxiety mechanism in this maladaptive phenotype.
|Advisor:||Woods, Stephen C.|
|School:||University of Cincinnati|
|School Location:||United States -- Ohio|
|Source:||DAI-B 70/08, Dissertation Abstracts International|
|Subjects:||Nutrition, Physiological psychology|
|Keywords:||Body composition, Food intake, High-fat diets, Neuropeptide Y, Social stress, Social subordination|
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