Abstract
Leptin actions at the pituitary level have been extensively investigated in mammalian species, but remain insufficiently characterized in lower vertebrates, especially in teleost fish. Prolactin (PRL) is a pituitary hormone of central importance to osmoregulation in fish. Using goldfish as a model, we examined the global and brain-pituitary distribution of a leptin receptor (lepR) and examined the relationship between expression of lepR and major pituitary hormones in different pituitary regions. The effects of recombinant goldfish leptin-AI and leptin-AII on PRL mRNA expression in the pituitary were further analysed, and the mechanisms underlying signal transduction for leptin-induced PRL expression were determined by pharmacological approaches. Our results showed that goldfish lepR is abundantly expressed in the brain-pituitary regions, with highly overlapping PRL transcripts within the pituitary. Recombinant goldfish leptin-AI and leptin-AII proteins could stimulate PRL mRNA expression in dose- and time-dependent manners in the goldfish pituitary, by both intraperitoneal injection and primary cell incubation approaches. Moreover, the PI3K/Akt/mTOR, MKK3/6/p38MAPK, and MEK1/2/ERK1/2—but not JAK2/STAT 1, 3 and 5 cascades—were involved in leptin-induced PRL mRNA expression in the goldfish pituitary.
Highlights
Leptin is the protein product of the obese gene, and was first identified in mouse adipose tissue by positional cloning in 1994 [1]
The p38MAPK inhibitor SB02190 (100 nM) could only block the leptin-AI, but not the leptin-AII-induced PRL expression. These results indicate that the PI3K/Akt/mTOR, MKK3/6/p38MAPK, and MEK1/2/ERK1/2 cascades were involved in the regulation of PRL mRNA expression by leptin in the goldfish pituitary
The production and/or secretion of PRL could be enhanced by gonadotropin-releasing hormoneho(rTmRoHne),(GpnroRlHa)c,tginh-rreelilne,aPsAinCgApP,eepsttirdadeio(Pl (RE2P),),tepstiotustietraornye a(Td)e, TnRyHla,tGe Hcy, LclHa,sien-saucltiniv-laiktienggropwetphtide (PACAP) and prolactin-releasing peptide (PRP), stimulate PRL secretion in the anterior pituitary, while other factors, such as dopamine (DA) and somatostatin (SS), inhibit the secretion of PRL [53]
Summary
Leptin is the protein product of the obese gene, and was first identified in mouse adipose tissue by positional cloning in 1994 [1]. Mammalian leptin is primarily secreted by white adipose tissue, and was initially identified as an anti-obesity hormone [2,3,4]. Additional studies have shown increasing evidence suggesting that leptin is a multifunctional hormone that plays other roles in the regulation of reproduction [5], metabolism [6], immunity [7], and pituitary hormone synthesis and secretion [8]. Leptin signalling in fish possibly serves as an integrating system that includes energy metabolism, reproduction, and stress [17,18]. The role of leptin as a satiety factor in fish still remains controversial, and is not as dogmatically defined as its counterparts in mammals [18]
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