Osteocalcin prevents insulin resistance, hepatic inflammation and autophagy associated with high-fat diet induced fatty liver hemorrhagic syndrome in aged laying hens

Authors: WU, X - Southwest University; ZOU, X - Southwest University; ZHANG, M - Southwest University; HU, H - Southwest University; WEI, X - Southwest University; JIN, M - Southwest University; Cheng, Heng-Wei; JIANG, S - Southwest University

Submitted to: Journal of Animal Science and Biotechnology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/7/2020
Publication Date: 10/12/2020
Citation: Wu, X.L., Zou, X.Y., Zhang, M., Hu, H.Q., Wei, X.L., Jin, M.L., Cheng, H., Jiang, S. 2020. Osteocalcin prevents insulin resistance, hepatic inflammation and autophagy associated with high-fat diet induced fatty liver hemorrhagic syndrome in aged laying hens. Journal of Animal Science and Biotechnology. 100(1), 73-83. https://doi.org/10.1016/j.psj.2020.10.022.
DOI: https://doi.org/10.1016/j.psj.2020.10.022

Interpretive Summary: Fatty liver syndrome is a metabolic disorder seen in high-producing laying hens globally. Its pathological characteristics are heavy fat deposition within the liver and abdominal cavity along with liver bleeding, causing sudden death of hens and leading to economic loss. The aim of this study was to investigate the effects of osteocalcin, a bone hormone, on fatty liver syndrome in aged laying hens. Hens at 68-weeks of age were randomly allocated into one of three treatments for 40 days: normal diet, high-fat diet, and high-fat diet plus osteocalcin. The results indicate that osteocalcin prevents the development of fatty liver syndrome in aged laying hens through inhibiting high-fat diet-induced insulin resistance, oxidative damage, and inflammation. The results can be used by producers and scientists for development of a novel management practice for improving chicken health and welfare.

Technical Abstract: The aim of this study was to investigate the effects of osteocalcin (OCN) on fatty liver hemorrhagic syndrome (FLHS) in aged laying hens. Thirty 68-week-old White Plymouth laying hens were randomly assigned into conventional single-bird cages, and the cages were randomly allocated into one of three treatments: normal diet (ND + vehicle, ND+V), high-fat diet (HFD + vehicle, HFD+V), and HFD + OCN (3 µg/bird, 1 time/2 days, i.m.) for 40 days. At day 30, oral glucose tolerance tests (OGTT) and insulin tolerance tests (ITT) were performed. At the end of experiment, the hens were euthanized followed by blood collection. The plasma aspartate transaminase (AST), alkaline phosphatase (ALP), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were measured using an automatic biochemistry analyzer. Pathological changes in the liver were examined under both light and transmission electron microscopes. The plasma inflammatory factors including interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-a) were analyzed by ELISA, and the gene expressions of these inflammatory factors in the liver were analyzed by real-time PCR. The level of oxidative stress was evaluated using malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) assay kits, respectively. The results showed that HFD+V hens had more severe liver haemorrhage and fibrosis than ND+V hens. The ultra-microstructural examination showed that hepatocytes of HFD+V hens exhibited necrotic pyknosis showing great intracellular electron, mitochondrial swelling, shrunk nucleus and absence of autolysosomes. OCN mitigated HFD+V induced pathological changes in aged laying hens. HFD-OCN hens had higher insulin sensitivity; lower liver concentrations of MDA but higher GSH-Px; and lower blood IL-6 and TNF-a concentrations and mRNA expressions compared to HFD+V hens (P < 0.05, respectively). These results suggest OCN functions in preventing the FLHS process in old laying hens through inhibiting excessive dietary energy diet-induced insulin resistance, oxidative damage, and inflammatory reaction.