During the transition period, dairy cows exhibit heightened energy requirements to sustain fetal growth and lactogenesis. The mammary gland and the growing fetus increase their demand for glucose, leading to the mobilization of lipids to support the function of tissues that can use fatty acids as energy substrates. These physiological adaptations lead to negative energy balance, metabolic inflammation, and transient insulin resistance (IR), processes that are part of the normal homeorhetic adaptations related to parturition and subsequent lactation. Insulin resistance is characterized by a reduced biological response of insulin-sensitive tissues to normal physiological concentrations of insulin. Metabolic inflammation is characterized by a chronic, low-level inflammatory state that is strongly associated with metabolic disorders. The relationship between IR and metabolic inflammation in transitioning cows is intricate and mutually influential. On one hand, IR may play a role in the initiation of metabolic inflammation by promoting lipolysis in adipose tissue and increasing the release of free fatty acids. Metabolic inflammation, conversely, triggers inflammatory signaling pathways by pro-inflammatory cytokines, thereby leading to impaired insulin signaling. The interaction of these factors results in a harmful cycle in which IR and metabolic inflammation mutually reinforce each other. This article offers a comprehensive review of recent advancements in the research on IR, metabolic inflammation, and their intricate interrelationship. The text delves into multiple facets of physiological regulation, pathogenesis, and their consequent impacts.

Objective: To investigate whether (+)-catechin, a strong antioxidant, can prevent methylglyoxal (MGO)-induced cytotoxicity and its mechanism. Methods: Cytotoxicity, apoptosis, reactive oxygen species (ROS) generation, hydrogen peroxide (H₂O₂) formation, mitochondrial membrane potential (MMP) and mitochondrial morphology were measured in EA.hy926 cells. Result: MGO (4 mM)-induced cytotoxicity was markedly inhibited by (+)-catechin (0.1–4 mM) in 24 h. 1 mM MGO-induced apoptotic cell death (44.7%) was significantly inhibited by 4 mM (+)-catechin (to 24.4%), 1 mM aminoguanidine (AG) (to 28.8%) or 4 mM N-acetylcysteine (NAC) (to 24.3%). (+)-Catechin (4 mM) or AG (4 mM) can inhibit the decrease of MMP induced by MGO (2–8 mM) in 3 h. (+)-Catechin (4 mM) or AG (4 mM) can inhibit MGO (4 mM)-induced mitochondrial swelling in 3 h. However, MGO (4 mM)-induced ROS and H₂O₂ generation was not prevented by (+)-catechin (4 mM). Conclusions: (+)-Catechin prevents MGO-induced cytotoxicity in EA.Hy926 cells through inhibiting apoptosis and mitochondrial damage.