Aquaculture Reports (Dec 2024)

Comparative study on the effects of high dietary levels of pectin and soybean oil on liver health and bile acid homeostasis in grass carp (Ctenopharyngodon idellus)

  • Daiyong Wu,
  • Yuantu Ye,
  • Peizhen Xiao,
  • Shengjie Ren,
  • Ye Shi,
  • Baotong Zhang,
  • Chunfang Cai

Journal volume & issue
Vol. 39
p. 102532

Abstract

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Liver disease in farmed grass carp (Ctenopharyngodon idellus) is a major issue with unclear mechanisms. High dietary fiber and fat may contribute. This study employed pectin and soybean oil as dietary fiber and fat sources, respectively, to evaluate their effects on liver disease in grass carp. Three diets (33.0 % crude protein) were made: control (5 % lipid; CON), high pectin (24 % pectin; HPD), high fat (15 % lipid; HFD). Juvenile grass carp (initial weight 24.1 g) were fed for 8 weeks. The HPD diet reduced growth and feed efficiency, whereas the HFD diet enhanced these parameters (P < 0.05). Both HPD and HFD expanded the scope of green in liver and deepened the color of bile. HPD decreased hepatosomatic index and liver lipid content, with atrophy and fibrosis. In contrast, HFD caused hepatocellular hypertrophy and increased lipid deposition. Gallbladder somatic index (GBSI) in both HPD and HFD groups was lower than in the CON group after 6 hours of fasting (P < 0.05). GBSI increased across all groups after 24 hours of fasting (P < 0.05), with the lowest values in the HPD group. In midgut and hindgut digesta, HPD group had higher total bile acid (TBA) content than CON group; HFD group's midgut also had higher TBA content. (P < 0.05). Serum TBA significantly decreased in the HPD group but increased in the liver (P < 0.05). Intestinal transporters asbt and ostα mRNA expression decreased in the HPD group, while asbt expression increased in the HFD group. Liver gene expression of inflammatory markers il-1β and il-8 was upregulated in both HPD and HFD groups (P < 0.05). These findings indicated high level of both pectin and soybean oil induce green liver syndrome and tissue damage, though the mechanisms differ, with HPD primarily causing cholestasis and HFD promoting lipid deposition.

Keywords