Variations in 11B-Hydroxysteroid Dehydrogenase Type1 in Two Rat Models of Obesity

Abstract

Obesity is an epidemic that has been estimated to cost the United States over $117 billion every year. Glucocorticoids have long been implicated in the maintenance of energy homeostasis due to their involvement with the hypothalamic-pituitary-adrenal axis. 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD-1) is an enzyme that interconverts the glucocorticoids cortisol and cortisone, and their rat counterparts corticosterone and 11-dehydrocorticosterone. We predicted an association between hepatic levels of this enzyme and either genetic obesity or dietary-induced obesity from any of two fat levels (high fat, low fat) or three fat sources (saturated, polyunsaturated, or monounsaturated). Our results indicated that hepatic 11β-HSD-1 is downregulated in genetic obesity, as has been previously found. High fat diets also caused reductions in hepatic enzyme message, although these were not statistically significant. There did not appear to be any effect of fat type.