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ORIGINAL PAPER
Acetate induces anorexia via up-regulating
the hypothalamic pro-opiomelanocortin (POMC)
gene expression in rabbits
1
Shandong Agricultural University,
Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention,
61 Daizong Street, Taian, Shandong 271018, P.R. China
Publication date: 2017-08-11
Corresponding author
F. Li
Shandong Agricultural University, Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, 61 Daizong Street, Taian, Shandong 271018, P.R. China
Shandong Agricultural University, Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, 61 Daizong Street, Taian, Shandong 271018, P.R. China
J. Anim. Feed Sci. 2017;26(3):266-273
KEYWORDS
TOPICS
ABSTRACT
The aim of the study was to describe the effects of acetate on
hypothalamic G-protein-coupled receptor (GPR) 41 or 43, 5’-AMP-activated
protein kinase (AMPK) signalling, mitogen-activated protein kinases (MAPKs)
signalling and (an)orexigenic neuropeptides. Forty rabbits (Hyla, 35-day old)
were randomly assigned to one of two treatment groups: intravenous injection
of acetate (0.5 mg · kg−1 body weight) or vehicle (control). The acetate treatment
decreased the rabbit feed intake within 5 h as compared with the control
(P < 0.05). Although the acetate treatment had no effect on hypothalamic neuropeptide
Y, agouti-related protein, cocaine-amphetamine-regulated transcript,
GPR41, acetyl-CoA carboxylase, fatty acid synthase and carnitine palmitoyltransferase-
1 mRNA levels (P > 0.05), it significantly increased the gene expression
of the pro-opiomelanocortin (POMC) and GPR43 (P < 0.05). Moreover,
intravenous injection of acetate did not affect the protein levels of phosphorylated
extracellular signal-regulated kinases, AMPK or p38 MAPK in comparison
with the control group (P > 0.05); however, there was a significant increase in
GPR43 protein level and decrease in phosphorylated c-Jun N-terminal kinases
(JNK) level (P < 0.05). So, acetate induced anorexia via the up-regulation of hypothalamic
POMC gene expression, which may be associated with membrane
GPR43 and intracellular JNK signalling.
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