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Ghrelin and obestatin are two gastrointestinal peptides obtained by post-translational processing of a common precursor, preproghrelin. The effect of obestatin on food intake is still controversial. The aim of the present study was to investigate the effects of ghrelin and obestatin on food intake in grass carp, Ctenopharyngodon idellus . Fish received intraperitoneal (IP) injection of saline, ghrelin (100 ng g − 1 BW), obestatin-like (25 ng g − 1 BW) and ghrelin in combination with obestatin-like. Ghrelin stimulation of food intake varied considerably among individual fish with 70.8% eliciting a robust response. In these high-responders, food intake was significantly increased by IP ghrelin within 2 h. Co-administration of ghrelin and obestatin-like resulted in a decrease in food intake, indicating that obestatin was able to antagonize the effect of ghrelin. However, IP obestatin-like alone could not regulate food intake in grass carp. RT-PCR analysis demonstrated that IP ghrelin peptide led to a significant increase in mRNA abundance of NPY, Y8a and Y8b genes compared to saline injected fish, while in combination with obestatin-like peptide decreased ghrelin-induced gene expressions of these three genes. IP sole obestatin-like peptide did not modify the expression levels of NPY, Y8a, Y8b, CART and POMC compared to the control group. Therefore, IP administration of obestatin-like peptide, partially blocking the ghrelin-induced appetite, investigated the possible involvement of obestatin as a mediator of the ghrelin stimulatory action on food intake, at least in “high-responders” grass carp. [ABSTRACT FROM AUTHOR]

Abstract: The R/L type pyruvate kinase (PKLR) gene was cloned from liver of grass carp (Ctenopharyngodon idella) by degenerate oligonucleotide primed PCR, including a complete open reading frame (ORF) of 1617bp. Homological protein analysis showed that the PKLR in grass carp shared a high degree of sequence identity with other known PK sequences. In addition, tissue distribution analysis showed that the highest expression of the PKLR was detected in liver. Then triplicate groups of grass carp (9 tanks) were fed twice daily to satiation with 91.8, 192.9, and 402.6gkg−1 carbohydrate diets for 8weeks, respectively. Dietary 402.6gkg−1 carbohydrate decreased growth performance, feed intake and feed utilization. With increasing dietary carbohydrates, the hepatic PK activity and mRNA expression of grass carp were up-regulated significantly. The results indicated that the PKLR play a modulation role in the adaptation of hepatic glycolysis to dietary high carbohydrates in grass carp. [Copyright &y& Elsevier]

As typical herbivorous fish, grass carp possesses greater capability to utilize carbohydrate than carnivorous and omnivorous fish. However, mechanism of carbohydrate utilization in herbivorous fish was unclear. This study is intended to investigate response of grass carp to insufficient or excessive dietary carbohydrate. Grass carp accepted isonitrogenous diets with different carbohydrate levels (15.90, 21.81 and 45.45 g 100 g −1 ) were cultured. After 8 weeks, weight gain and feed intake were highest in fish fed with medium-carbohydrate diet compared with others. Gene expression data indicated that expressions of glucose-6-phosphatase (G6Pase) were down-regulated and gene expressions of glycogen synthase (GS) were up-regulated in fish accepted lower-carbohydrate diet. In high-carbohydrate group, glucose catabolism was increased by enhanced expressions of glucokinase genes (GK). Meanwhile, fatty acid synthase (FAS) and acetyl coenzyme-A carboxylase (ACC1) genes were significantly up-regulated and lipoprotein lipase and carnitine palmitoyltransferase 1 (CPT1) genes expressions were down-regulate, inducing more lipid deposition. Subsequently, serum cholesterol and total lipid contents were significantly increased, and then induced appetite suppression through up-regulation of leptin and anorexigenic genes expressions. Furthermore, depressed food intake caused lower growth rate in grass carp with excessive carbohydrate intake. [ABSTRACT FROM AUTHOR]

A study was conducted to determine the effects of dietary non-protein energy sources on growth, tissue lipid accumulation and lipid metabolism-related genes expression of grass carp. Triplicate groups of fish were fed for 9 weeks on four isonitrogenous (300 g kg−1) experimental diets with four levels of non-protein energy (6.52 kJ g−1 control diet, 5.32 kJ g−1 high- CEL diet, 8.46 kJ g−1 high- CHO diet and 8.53 kJ g−1 high- LIP diet respectively). Increasing dietary non-protein energy source levels did not improve the growth, and the high- CEL diet reduced the growth of grass carp. The high- CHO diet tended to induce high hepatosomatic index, with high fat and glycogen content of liver. However, the high- LIP diet caused the high mesenteric fat index, but did not increase liver fat. The m RNA abundance and activities of hepatic lipogenic enzymes were significantly increased in the high- CHO diet group, whereas the opposite tendencies were observed in the high- LIP diet group. Peroxisome proliferator-actived receptor-α ( PPARα) in liver and PPARγ in mesenteric adipose tissue were up-regulated in the high- CEL diet group. Lipoprotein lipase ( LPL) gene expression was significantly increased both in liver and mesenteric adipose tissue of fish fed the high- LIP diet, while the LPL gene expression was up-regulated in liver but down-regulated in mesenteric adipose tissue of fish fed the high- CEL diet. These findings suggest that an increase in dietary non-protein energy sources alters the genes expression of lipid metabolism and increased lipid deposition. [ABSTRACT FROM AUTHOR]