While kisspeptin was initially found to function as a metastasis suppressor, after identification of its receptor KISS1R and their expression profiles in tissues such as the hypothalamus and adrenals, kisspeptin and KISS1R were predominantly assigned endocrine functions, including regulating puberty and fertility through their actions on hypothalamic gonadotropin releasing hormone production. More recently, an alter ego for kisspeptin has emerged, with a significant role in regulating glucose homeostasis, insulin secretion, as well as food intake and body composition, and deficient kisspeptin signaling results in reduced locomotor activity and increased adiposity. This review highlights these recent observations on the role of kisspeptin in metabolism as well as several key questions that need to be addressed in the future. Kisspeptin and its class I G protein-coupled receptor KISS1R regulate not only (i) puberty and fertility but also (ii) glucose homeostasis, locomotor activity, and body-weight control. Glucagon stimulates liver kisspeptin production. Kisspeptin inhibits insulin secretion via activating KISS1R located on pancreatic β cells. In the absence of KISS1R signaling, locomotor activity is profoundly reduced, accompanied by a slight reduction in food intake and energy expenditure, leading to adiposity. An absence of KISS1R signaling results in increased body weight and impaired glucose homeostasis in female but not male mice.
- Sexual dimorphism
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism