Abstract: Subclinical ketosis （SCK） is a common metabolic disorder in high-yielding dairy cows during the periparturient period. It is characterized by elevated blood β-hydroxybutyrate （BHBA） levels and decreased blood glucose concentrations, presenting no apparent clinical symptoms but posing insidious detrimental effects. The occurrence of SCK is associated with physiological metabolic changes and feeding management during the periparturient period. SCK can trigger hepatic glucose and lipid metabolism disorders, impair dairy cow health, and reduce production performance, leading to significant economic losses in the livestock industry. Recent studies have indicated that SCK interferes with key processes of hepatic glucose metabolism and disrupts the balance between lipid synthesis and lipolysis. Through multiple signaling pathways, including peroxisome proliferator-activated receptors （PPARs）, nuclear factor-κB （NF-κB）, mechanistic target of rapamycin complex 1/2 （mTORC1/2）, and phosphatidylinositol 3-kinase/protein kinase B （PI₃K/Akt）, as well as key genes such as forkhead box O1 （FOXO1）, SCK regulates transcriptional networks and the activities of key metabolic enzymes, thereby exacerbating insulin resistance （IR）, hepatic steatosis, and oxidative stress. This review systematically summarizes the definitional characteristics and etiologies of SCK, and the effects of SCK on glucose and lipid metabolism and the associated molecular regulatory mechanisms, with the aim of providing a basis for reducing SCK incidence, optimizing farm management, and improving the production performance of dairy cows.

Key words: dairy cow, subclinical ketosis, glucose and lipid metabolism, insulin resistance, signaling pathways