Abstract

Bimatoprost is a synthetic prostamide F2α analog that down-regulates adipogenesis in vitro. This effect has been attributed to participation in a negative feedback loop that regulates anandamide-induced adipogenesis. A follow-on investigation has now been conducted into the broader metabolic effects of bimatoprost using rats under both normal state and obesity-inducing conditions. Chronic bimatoprost administration attenuated weight gain in a dose dependent-manner in rats fed either standard [max effect −7%] or obesity-promoting diets [max effect −23%] over a 9–10 week period. Consistent with these findings, bimatoprost promoted satiety as measured by decreased food intake [max effect, −7%], gastric emptying [max effect, −33–50%] and decreased circulating concentrations of the gut hormones, ghrelin and GLP-1 [max effect, −33–50%]. Additionally, subcutaneous, and visceral fat mass were distinctly affected by treatment [−30% diet independent]. Taken together, these results suggest that bimatoprost regulates energy homeostasis through promoting satiety and a decrease in food intake. These newly reported activities of bimatoprost reveal an additional method of metabolic disease intervention for potential therapeutic exploitation.

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