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Abstract

It has been suggested that high-fat diets (HF) exaggerate stress-induced activation of the hypothalamic-pituitary-adrenal axis and glucocorticoid release. Experiments in this thesis investigated whether the exaggerated response in HF-fed Sprague Dawley rats was caused by dietary fat or increased adiposity. We found that exposure to HF-diet and not adiposity exaggerates the glucocorticoid and weight loss response to mild stress but not to a greater stress of repeated restraint. The mechanisms by which HF-diet exaggerates the stress response are unknown, therefore, we measured aspects of the stress pathway. Corticortrophin releasing factor (CRF) mRNA expression in the paraventricular nucleus of the hypothalamus and of urocortin I in the Edinger Westphal nucleus were not increased in HF-fed rats and corticosterone release following third ventricle CRF injection was not changed. This suggests that acute exposure to HF-diet increases stress-responsiveness by modify an aspect of the stress pathway down-stream of the hypothalamic CRF receptors.

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