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.
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