Abstract

BackgroundIn avian species, liver is the main site of de novo lipogenesis, and hepatic lipid metabolism relates closely to adipose fat deposition. Using our fat and lean chicken lines of striking differences in abdominal fat content, post-hatch lipid metabolism in both liver and adipose tissues has been studied extensively. However, whether molecular discrepancy for hepatic lipid metabolism exists in chicken embryos remains obscure.ResultsWe performed transcriptome and proteome profiling on chicken livers at five embryonic stages (E7, E12, E14, E17 and E21) between the fat and lean chicken lines. At each stage, 521, 141, 882, 979 and 169 differentially expressed genes were found by the digital gene expression, respectively, which were significantly enriched in the metabolic, PPAR signaling and fatty acid metabolism pathways. Quantitative proteomics analysis found 20 differentially expressed proteins related to lipid metabolism, PPAR signaling, fat digestion and absorption, and oxidative phosphorylation pathways. Combined analysis showed that genes and proteins related to lipid transport (intestinal fatty acid-binding protein, nucleoside diphosphate kinase, and apolipoprotein A-I), lipid clearance (heat shock protein beta-1) and energy metabolism (NADH dehydrogenase [ubiquinone] 1 beta subcomplex subunit 10 and succinate dehydrogenase flavoprotein subunit) were significantly differentially expressed between the two lines.ConclusionsFor hepatic lipid metabolism at embryonic stages, molecular differences related to lipid transport, lipid clearance and energy metabolism exist between the fat and lean chicken lines, which might contribute to the striking differences of abdominal fat deposition at post-hatch stages.

Highlights

  • In avian species, liver is the main site of de novo lipogenesis, and hepatic lipid metabolism relates closely to adipose fat deposition

  • In previous studies, using adipose and liver tissues from the fat and lean chickens at various post-hatch stages (1, 4 and 7 weeks of age), we have found a number of differentially expressed genes (DEGs) and proteins (DEPs) related to lipid metabolism by the microarray and proteomics methods, such as peroxisome proliferatoractivated receptor gamma (PPARγ), liver basic fatty acids binding protein (LBFABP), lipoprotein lipase (LPL), adipocyte fatty acid-binding protein (AFABP), apolipoprotein A-I (ApoA-I), and long-chain acyl-coenzyme A dehydrogenase (ACADL) [10,11,12,13]

  • We identified DEGs and Differentially expressed proteins (DEPs) associated with hepatic lipid metabolism at embryonic stages between the two chicken lines, which could help explain the striking differences of post-hatch abdominal fat content

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Summary

Introduction

Liver is the main site of de novo lipogenesis, and hepatic lipid metabolism relates closely to adipose fat deposition. For over half a century, commercial broiler has been selected intensively for growth rate and feed efficiency [1]. Intensive selection on fast growth rate brings along adverse outcomes, such as obesity and related metabolic. Chicken lipogenesis is very limited in the adipose tissue [6], and more than 70% of de novo fatty acid synthesis takes place in the liver instead [7]. Fatty acids synthesized in the liver are incorporated into triacylglycerols, and secreted as very low-density lipoprotein (VLDL). Accumulation of triacylglycerols in adipocytes is closely related to lipid metabolism in the liver [9]

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