Regulation of adipose tissue metabolism in support of lactation.

In the dairy cow, adipose tissue lipid accumulates during pregnancy, and catabolism begins prior to parturition and increases dramatically afterward. After peak lactation, body lipid is replenished. The duration and magnitudes of these adaptations depend on milk energy secretion, net energy intake, genotype, and endocrine environment. Recent research efforts have focused on endocrine, genetic, and biochemical mechanisms underlying metabolic adaptations in cows of high production potential. Adipose tissue lipid synthesis is decreased and lipolysis is increased in early lactation. The magnitude and duration of these adaptations are increased in animals either consuming relatively less energy or producing more milk. Adipose tissue is more responsive to catecholamines in early and midlactation and in animals with higher production. This is more of an increase in maximal response than in sensitivity. In vivo and in vitro rates of adipose tissue lipolysis correlate positively with milk energy secretion, whereas lipid synthesis rates correlate with energy intake. Thus, mammary metabolic activity, within and among lactations, correlates with that in adipose tissue. Likely mechanisms include adaptations in receptors for homeostatic signals and modulation of postreceptor responses. Research is needed into neural, genetic, and hormone regulation of nutrient utilization and body fat use and recovery during lactation. Research should describe mechanistic relationships among nutrients in animals of high production as well as investigate cellular and molecular mechanisms suitable to genetic manipulation.