# Effects of hepatic lipid ratio on lipid metabolism indices and hepatic gene expression in late-phase laying hens

## TL;DR

This study explores how liver fat accumulation affects metabolism and gene activity in aging hens, identifying key indicators and biological pathways involved.

## Contribution

The study identifies practical indicators and gene expression changes linked to hepatic lipid accumulation in aging laying hens.

## Key findings

- Hepatic lipid ratio strongly correlates with liver triglycerides and cholesterol in hens.
- Transcriptomic analysis reveals genes and pathways involved in lipid metabolism, inflammation, and antioxidant responses.
- Body weight and plasma lipid metrics are practical indicators of hepatic lipid deposition.

## Abstract

Alleviating hepatic lipid deposition in aging laying hens is critical for maintaining liver health and extending their productive lifespan. This study aimed to identify potential indicators and elucidate the underlying mechanisms associated with liver fat accumulation. Hepatic lipid ratio is a key indicator of the lipid deposition in the liver. A total of 509 healthy G1 line hens at 66 weeks of age were assessed for hepatic lipid ratio and stratified into three groups: low (L, <5%), medium (M, 5–10%), and high (H, >10%). The results revealed that the correlation coefficients of liver triglyceride (TG) and total cholesterol (TC) with the hepatic lipid ratio were 0.907 and 0.870, respectively, indicating a strong and highly significant association. All three metrics differed significantly among the three groups (P < 0.01), validating the grouping approach. Compared with the L group, the M and H groups showed significantly higher body weight, abdominal fat weight, abdominal fat index, plasma TG, TC, and LDL-c (P < 0.05), while plasma HDL-C was significantly lower in group H compared with groups L and M (P < 0.05). Abdominal skinfold thickness differed significantly across all groups (P < 0.05). Transcriptomic analysis revealed 115 up-regulated and 50 down-regulated genes in the H group compared with the L group. We identified: four genes (PCSK9, ABCG8, G6PC2, FOLH1) were associated with lipid metabolism; three (IL1RAPL1, TNIP2, HPSE2) with inflammatory response; five (CCL3, CCL17, CCL20, SAMSN1, ICOS) with immune response; and six (HBA1, HBAD, HBBA, CHAC1, CREG1, DDIT4) with antioxidant function. KEGG pathway analysis highlighted enrichments in lipid metabolism-related pathways such as “ABC transporters” and “Insulin secretion,” as well as in the inflammatory response-related pathway “Cytokine-cytokine receptor interaction.” In conclusion, body weight, abdominal skinfold thickness, plasma TG, TC, LDL-c, and HDL-c may serve as practical indicators for evaluating hepatic lipid deposition in laying hens. Excessive lipid accumulation perturbs hepatic metabolic homeostasis, triggering transcriptional reprogramming associated with both inflammatory and oxidative stress responses, alongside adaptive antioxidant defense and anti-inflammatory responses. However, further studies are required to determine whether these changes reflect a bona fide compensatory protective mechanism in the liver.