Clayton Spada , Chau Vu , Iona Raymond , Warren Tong , Chia-Lin Chuang , Christopher Walker , Kerry Loomes , David F. Woodward , Neil J. Poloso
{"title":"Bimatoprost promotes satiety and attenuates body weight gain in rats fed standard or obesity-promoting diets.","authors":"Clayton Spada , Chau Vu , Iona Raymond , Warren Tong , Chia-Lin Chuang , Christopher Walker , Kerry Loomes , David F. Woodward , Neil J. Poloso","doi":"10.1016/j.plefa.2022.102511","DOIUrl":null,"url":null,"abstract":"<div><p>Bimatoprost is a synthetic prostamide F<sub>2α</sub> 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.</p></div>","PeriodicalId":94179,"journal":{"name":"Prostaglandins, leukotrienes, and essential fatty acids","volume":null,"pages":null},"PeriodicalIF":3.0000,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0952327822001211/pdfft?md5=d0abb812458fb17f5a4a0935bf8b6a3e&pid=1-s2.0-S0952327822001211-main.pdf","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Prostaglandins, leukotrienes, and essential fatty acids","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0952327822001211","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
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.