Comparative transcriptome analysis of hypothalamus-regulated feed intake induced by exogenous visfatin in chicks

Abstract

BackgroundThe intracerebroventricular injection of visfatin increases feed intake. However, little is known about the molecular mechanism in chicks. This study was conducted to assess the effect of visfatin on the feeding behavior of chicks and the associated molecular mechanism.ResultsIn response to the intraventricular injection of 40 ng and 400 ng visfatin, feed intake in chicks was significantly increased, and the concentrations of glucose, insulin, TG, HDL and LDL were significantly altered. Using RNA-seq, we identified DEGs in the chick hypothalamus at 60 min after injection with various doses of visfatin. In total, 325, 85 and 519 DEGs were identified in the treated chick hypothalamus in the LT vs C, HT vs C and LT vs HT comparisons, respectively. The changes in the expression profiles of DEGs, GO functional categories, KEGG pathways, and PPI networks by visfatin-mediated regulation of feed intake were analyzed. The DEGs were grouped into 8 clusters based on their expression patterns via K-mean clustering; there were 14 appetite-related DEGs enriched in the hormone activity GO term. The neuroactive ligand-receptor interaction pathway was the key pathway affected by visfatin. The PPI analysis of DEGs showed that POMC was a hub gene that interacted with the maximum number of nodes and ingestion-related pathways, including POMC, CRH, AgRP, NPY, TRH, VIP, NPYL, CGA and TSHB.ConclusionThese common DEGs were enriched in the hormone activity GO term and the neuroactive ligand-receptor interaction pathway. Therefore, visfatin causes hyperphagia via the POMC/CRH and NPY/AgRP signaling pathways. These results provide valuable information about the molecular mechanisms of the regulation of food intake by visfatin.Electronic supplementary materialThe online version of this article (10.1186/s12864-018-4644-7) contains supplementary material, which is available to authorized users.

Plasma level and expression of visfatin in the porcine hypothalamus during the estrous cycle and early pregnancy

“…Its expression in the structures responsible for GnRH production may suggest that visfatin is also engaged in the control of GnRH generation. The intracerebroventricular injection of visfatin stimulated GnRH-I gene expression in chicks 48 . The adipokine also enhanced Fos gene expression in the mouse hypothalamic explants 49 , a marker of neuroendocrine cell activation 50 .…”

Recent advances in neuropeptide-related omics and gene editing: Spotlight on NPY and somatostatin and their roles in growth and food intake of fish

“…It has been reported that in broiler chickens, dietary stevioside (STE) supplementation promoted feed intake, and the analysis of RNA-Seq in the hypothalamus of the STE-supplemented group compared with the control group showed that several appetite-related genes, such as NPY and NPY5R, were differentially expressed, and it was suggested that dietary STE supplementation promoted feed intake through the regulation of the hypothalamic neuroactive ligand-receptor interaction pathway and the alteration of intestinal microbiota composition ( 85 ). On the contrary, SS is involved in suppressing feeding, especially important in studying the mechanism of feed additives ( 28 ) and environmental influences on feeding ( 30 ). In yellow catfish ( Tachysurus fulvidraco ), it has been reported that sertraline (SER) increased shoaling, decreased food consumption, higher cannibalism rate and RNA-seq results showed that transcript levels of SS reduced in the brain following SER exposure, indicating that SER disturbs neuropeptides which may be unrelated to its antidepressant effects in vertebrates ( 30 ).…”

Visfatin and Its Role in the Regulation of the Reproductive System

“…Недавно было показано, что интрацеребральное введение 40 и 400 нг висфатина курам вызывало изменение соотношения активности гипоталамических нейронов, экспрессирующих про-опиомеланокортин, предшественник анорексигенных меланокортиновых пептидов, и нейронов, экспрессирующих орексигенные нейропептид Y и агути-подобный пептид. Изменение соотношения орексигенных и анорексигенных факторов, как можно полагать, является основным механизмом усиления аппетита под действием висфатина и в значительной степени определяет регуляторное влияние висфатина на активность гипоталамических нейронов, экспрессирующих гонадолиберин [56]. Таким образом, некоторые эффекты висфатина при его центральном введении птицам и млекопитающим являются сходными и направлены как на усиление аппетита, так и на подавление активности ГГГ-оси.…”