Immune cell functions such as phagocytosis and synthesis of immunometabolites, as well as immune cell survival, proliferation and differentiation, largely depend on an adequate availability of glucose by immune cells. During inflammation, the glucose demands of the immune system may increase to amounts similar to those required for high milk yields. Similar metabolic pathways are involved in the adaptation to both lactation and inflammation, including changes in the somatotropic axis and glucocorticoid response, as well as adipokine and cytokine release. They affect (i) cell growth, proliferation and activation, which determines the metabolic activity and thus the glucose demand of the respective cells; (ii) the overall availability of glucose through intake, mobilization and gluconeogenesis; and (iii) glucose uptake and utilization by different tissues. Metabolic adaptation to inflammation and milk synthesis is interconnected. An increased demand of one life function has an impact on the supply and utilization of glucose by competing life functions, including glucose receptor expression, blood flow and oxidation characteristics. In cows with high genetic merits for milk production, changes in the somatotropic axis affecting carbohydrate and lipid metabolism as well as immune functions are profound. The ability to cut down milk synthesis during periods when whole-body demand exceeds the supply is limited. Excessive mobilization and allocation of glucose to the mammary gland are likely to contribute considerably to peripartal immune dysfunction.
Keywords: glucose metabolism; immune dysfunction; lactational physiology; production diseases; trade-offs.