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Acetate alters the process of lipid metabolism in rabbits

Published online by Cambridge University Press:  04 December 2017

C. Fu ,
L. Liu  and
F. Li
C. Fu
Affiliation:
Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Department of Animal Science and Technology, Shandong Agricultural University, Taian 271018, China Poultry Institute, Shandong Academy of Agricultural Sciences, Jinan 250023, China
L. Liu*
Affiliation:
Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Department of Animal Science and Technology, Shandong Agricultural University, Taian 271018, China
F. Li*
Affiliation:
Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Department of Animal Science and Technology, Shandong Agricultural University, Taian 271018, China
*
†E-mail: liusanshi1985@126.com or chlf@sdau.edu.cn
†E-mail: liusanshi1985@126.com or chlf@sdau.edu.cn
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Abstract

An experiment was conducted to investigate the effect of acetate treatment on lipid metabolism in rabbits. New Zealand Rabbits (30 days, n=80) randomly received a subcutaneous injection (2 ml/injection) of 0, 0.5, 1.0 or 2.0 g/kg per day body mass acetate (dissolved in saline) for 4 days. Our results showed that acetate induced a dose-dependent decrease in shoulder adipose (P<0.05). Although acetate injection did not alter the plasma leptin and glucose concentration (P>0.05), acetate treatment significantly decreased the plasma adiponectin, insulin and triglyceride concentrations (P<0.05). In adipose, acetate injection significantly up-regulated the gene expression of peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα), differentiation-dependent factor 1 (ADD1), adipocyte protein 2 (aP2), carnitine palmitoyltransferase 1 (CPT1), CPT2, hormone-sensitive lipase (HSL), G protein-coupled receptor (GPR41), GPR43, adenosine monophosphate-activated protein kinase α1 (AMPKα1), adiponectin receptor (AdipoR1), AdipoR2 and leptin receptor. In addition, acetate treatment significantly increased the protein levels of phosphorylated AMPKα, extracellular signaling-regulated kinases 1 and 2 (ERK1/2), p38 mitogen-activated protein kinase (P38 MAPK) and c-jun amino-terminal kinase (JNK). In conclusion, acetate up-regulated the adipocyte-specific transcription factors (PPARγ, C/EBPα, aP2 and ADD1), which were associated with the activated GPR41/43 and MAPKs signaling. Meanwhile, acetate decreased fat content via the upregulation of the steatolysis-related factors (HSL, CPT1 and CPT2), and AMPK signaling may be involved in the process.

Keywords

acetateadipocyte differentiationrabbitssignaling pathwaysteatolysis
Type
Research Article
Information
animal , Volume 12 , Issue 9 , September 2018 , pp. 1895 - 1902
Copyright
© The Animal Consortium 2017 

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