Answers are grounded in this paper and cite their sources.
Owing to insufficient energy production and calcium deficiency, postpartum dairy cows are susceptible to metabolic disorders. Despite some evidence of the relationship between energy metabolism and calcium homeostasis, the mechanism by which uncarboxylated osteocalcin (unOCN) regulates hepatic lipid metabolism in postpartum cows remains unknown. Here, the relationship between postpartum calcium and energy metabolism and the mechanism underlying unOCN regulation of hepatic lipid metabolism were investigated. In vivo experiments demonstrated that high‐unOCN cows promoted increased secretion of adiponectin and glucagon like peptide‐1, thereby stimulating insulin secretion and subsequently regulating energy metabolism in postpartum dairy cows. Combined in vivo and in vitro findings, we hypothesized that unOCN activated the hepatic AMPK signaling pathway to reduce hepatic lipid synthesis, while concurrently upregulating the PPAR signaling pathway to promote fatty acid β‐oxidation in the liver, ultimately diminishing lipid accumulation. This study provides a new perspective for alleviating metabolic diseases in postpartum cows.
No takes yet. Share an insight, caveat, or question.
Yang et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: