Effect of precalving body condition score on insulin signaling and hepatic inflammatory state in grazing dairy cattle
- PMID: 33714908
- DOI: 10.1016/j.domaniend.2021.106621
Effect of precalving body condition score on insulin signaling and hepatic inflammatory state in grazing dairy cattle
Abstract
During postpartum, high-production dairy cows show a temporary period of insulin resistance, during which glucose uptake by peripheral tissues is reduced to prioritize milk production. However, this can further increase their negative energy balance by compromising liver function, especially in cows with excessive body condition score (BCS) and a pro-inflammatory state. Based on this, the aim of this study was to evaluate the hepatic expression of proteins of the insulin signaling pathway (PI3K) and of the cytokines TNFα, IL-6 and NF-κB, as well as the plasma concentrations of non-esterified fatty acids (NEFA), beta-hydroxybutyrate, glucose, triglycerides (TAG), insulin and insulin-like growth factor-1, insulin sensitivity indexes, and the hepatic content of TAG during the transition period in cows with different BCS. Sixteen Holstein cows were selected 14 days before the expecting calving date and classified into 2 groups: low BCS (LBCS) ≤ 3.25 (n = 9) and high BCS (HBCS) ≥ 3.5 (n = 7). Blood and liver samples were obtained 14 (±3) days before the expected calving date and 4 (±3), 14 (±3) and 28 (±3) days after calving. The concentration of NEFA was higher in the HBCS group than in the LBCS group. Glucose concentration showed an interaction effect, with a greater concentration on day 28 in HBCS. Insulin concentration showed no changes. While the pAkt/total Akt ratio was lower in the HBCS group, the TNFα protein expression was higher only on day 4 postcalving in the HBCS group. In agreement with these results, the insulin sensitivity indexes RQUICKI and RQUICKIBHBA were lower in the HCBS group. The results suggest an insulin resistance and a pro-inflammatory state in the liver of cows with HBCS.
Keywords: Dairy cattle; Inflammatory state; Insulin signaling; Liver.
Copyright © 2021. Published by Elsevier Inc.
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