The Complex Interplay of Insulin Resistance and Metabolic Inflammation in Transition Dairy Cows

Simple Summary This review critically examined the literature on the interaction between insulin resistance (IR) and metabolic inflammation in transition dairy cows. Our review emphasizes how IR and metabolic inflammation mutually influence each other, leading to heightened lipolysis, immune activation, and tissue inflammatory pathways. These processes contribute to a harmful cycle where inflammatory mediators exacerbate IR and metabolic inflammation. While transient IR and metabolic inflammation are natural adaptations in transitioning cows, this review highlights the increased disease risk in over-conditioned cows. Understanding these interactions is crucial for managing metabolic disorders in dairy herds and promoting animal health, welfare, and productivity.Abstract 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.