Developmental changes in hepatic lipid metabolism of chicks during the embryonic periods and the first week of posthatch

Abstract

The liver is the main site of de novo lipogenesis in poultry, and hepatic lipid metabolism disorder will lead to excessive abdominal fat deposition or fatty liver disease, finally causing huge economic loss. The present study was conducted to investigate developmental changes in hepatic lipid metabolism of chicks from embryonic periods to the first week after hatching. Liver samples were collected from embryonic day 11 (E11) to the age of day 7 posthatch (D7) for lipid metabolism analysis. Hematoxylin-eosin and Oil Red O staining analysis showed that hepatic lipids increased gradually during embryonic period and declined posthatch; The sum of hepatic triglycerides and cholesterol reached the peak at E19 and D1 by ELISA analysis (P < 0.05). Acetyl-CoA carboxylase, fatty acid synthase, and acyl-CoA desaturase 1 mRNA expression in the liver were higher from E17 to D1 with the peak at E19 when compared with those at E13 and E15 (P < 0.05). Hepatic elongase of very long-chain fatty acids 6 and microsomal triglyceride transfer protein mRNA abundance were lower during embryonic periods but reached relative higher level after hatching (P < 0.05). On the contrary, hepatic carbohydrate response element binding protein (ChREBP), carnitine palmitoyltransferase 1, and peroxisome proliferators-activated receptor α expression were higher during embryonic periods but decreased posthatch (P < 0.05). The mRNA abundance of sterol-regulatory element binding protein 1c was the lowest at E13 and E15, then increased gradually from E17 to D1, while decreased from D3 to D7 little by little (P < 0.05). In summary, hepatic lipogenesis genes have different expression patterns during the embryonic periods and the first week of posthatch, which might be activated by ChREBP during embryonic periods; fatty acid oxidation was enhanced around the hatched day but declined posthatch. These findings will broaden the understanding of physiological characteristics and dynamic pattern about hepatic lipid metabolism in chicks.

Keywords: chick; embryonic period; gene expression; hepatic lipid metabolism; posthatch.

Figure 1

Hepatic hematoxylin-eosin staining analysis of chicks from embryonic day 13 to posthatch day 7. White cavities with different sizes all mean fat droplets (magnification:10 × 20), which are located in the cytoplasm. The liver with high lipid contents lost the normal reticular formation, otherwise, hepatic texture is flexible and has clear reticular formations with less fat droplets.

Figure 2

Hepatic Oil Red O staining analysis of chicks from embryonic day 13 to posthatch day 7. Red circle drops are on behalf of fat droplets (magnification:10 × 20).

Figure 3

Developmental changes of embryo or chick growth parameters and hepatic lipid contents. Embryo or chick body weight (A); liver weight of embryo or chick (B); liver index relative to body weight of embryo or chick (C); hepatic TC concentration (D); hepatic TG concentration (E); total TC+TG concentration in the liver (F). Data are expressed as mean ± SEM (n =7), and bars with different lowercase letters indicated statistically significant differences (one-way ANOVA, P < 0.05). Abbreviations: TC, total cholesterol; TG, triglycerides.

Figure 4

Developmental changes of genes expression related to lipogenesis and lipolysis in the liver. Results of hepatic ACC, FAS, SCD1, ELOVL6, ChREBP, SREBP-1c, CPT1, PPARα, and MTTP mRNA expression, respectively (A-I). Data are expressed as mean ± SEM (n = 7), and bars with different lowercase letters indicated statistically significant differences (one-way ANOVA, P < 0.05). Abbreviations: ACC, acetyl CoA carboxylase; ChREBP, carbohydrate responsive element binding protein; CPT1, carnitine palmitoyltransferase 1; ELOVL6, elongase of very long chain fatty acids 6; FAS, fatty acid synthase; MTTP, microsomal triglyceride transfer protein; PPAR, peroxisome proliferator-activated receptor; SCD1, stearoyl-CoA desaturase 1; SRRBP, sterol regulatory element binding proteins.