Abstract

In mammals, leptin is a peripheral satiety factor that inhibits feeding by regulating a variety of appetite-related hormones in the brain. However, most of the previous studies examining leptin in fish feeding were performed with mammalian leptins, which share very low sequence homologies with fish leptins. To elucidate the function and mechanism of endogenous fish leptins in feeding regulation, recombinant goldfish leptin-AI and leptin-AII were expressed in methylotrophic yeast and purified by immobilized metal ion affinity chromatography (IMAC). By intraperitoneal (IP) injection, both leptin-AI and leptin-AII were shown to inhibit the feeding behavior and to reduce the food consumption of goldfish in 2 h. In addition, co-treatment of leptin-AI or leptin-AII could block the feeding behavior and reduce the food consumption induced by neuropeptide Y (NPY) injection. High levels of leptin receptor (lepR) mRNA were detected in the hypothalamus, telencephalon, optic tectum and cerebellum of the goldfish brain. The appetite inhibitory effects of leptins were mediated by downregulating the mRNA levels of orexigenic NPY, agouti-related peptide (AgRP) and orexin and upregulating the mRNA levels of anorexigenic cocaine-amphetamine-regulated transcript (CART), cholecystokinin (CCK), melanin-concentrating hormone (MCH) and proopiomelanocortin (POMC) in different areas of the goldfish brain. Our study, as a whole, provides new insights into the functions and mechanisms of leptins in appetite control in a fish model.

Highlights

  • Leptin, the protein product of the obese gene, was first identified in mouse adipose tissue by positional cloning [1]

  • Leptin plays a major role as a satiety factor in feeding termination [2] by blocking the synthesis and secretion of orexigenic neuropeptide Y (NPY) [3] and agouti-related peptide (AgRP) [4] and promoting the expression and secretion of anorexigenic proopiomelanocortin (POMC) [5] and cocaine-amphetamine-regulated transcript (CART) [6] in the central nervous system

  • A study in tilapia showed that mouse leptin cannot promote STAT-3 signaling in the tilapia leptin receptor (lepR)-transfected COS7 cells, and STAT-3 signaling is necessary for leptin regulation of appetite [41]

Read more

Summary

Introduction

The protein product of the obese gene, was first identified in mouse adipose tissue by positional cloning [1]. Leptin plays a major role as a satiety factor in feeding termination [2] by blocking the synthesis and secretion of orexigenic neuropeptide Y (NPY) [3] and agouti-related peptide (AgRP) [4] and promoting the expression and secretion of anorexigenic proopiomelanocortin (POMC) [5] and cocaine-amphetamine-regulated transcript (CART) [6] in the central nervous system. At least six transcripts from a single lepR gene have been reported to produce multiple lepR isoforms in mammals, but only the long form (lepRb) is responsible for the actions of leptin [9]. In the hypothalamus in particular, lepR was found to be a crucial link between peripheral leptin and the central appetite regulators [11,12]

Methods
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call