Lipid metabolism in adipose tissue during lactation: a model of a metabolic control system.
The flux of energy-yielding compounds through the pathways of lipogenesis, esterification into triglycerides and lipolysis in adipose tissue plays a pivotal role in supplying the demands of lactation and maternal health. The critical importance of these pathways is demonstrated by the number of highly coordinated and redundant metabolic control elements that regulate the enzyme activity in these pathways, including protein and several steroid hormones, catecholamines, and blood concentrations of several nutrients. Control on these pathways is exerted by all of these elements during lactation. Insights have been gained recently into the adaptations of these pathway reactions due to genetic propensity for milk production, stage of lactation, and intake of energy-yielding components such as starch, cellulose and triglycerides. The rates of these pathways vary exponentially with the intakes of key substrates and demands for milk precursors. The parameters of equations describing these pathways are not constant, but vary with genotype and with prolonged changes in nutritional and environmental conditions. Two major regulatory systems are critical to alterations of carbon flux during the entire lactational period. One is the interaction of growth hormone and insulin to control lipogenesis; the other is the counter-regulation by norepinephrine and insulin on cyclic AMP-initiated enzyme phosphorylation to regulate lipolysis. Examples of specific control points having a critical impact on lactational success and that are associated with genetic selection for milk production are the activities of acetyl-CoA carboxylase and hormone sensitive lipase. Further insights into the mechanisms of these adaptations will help us to improve the efficiency of metabolic flux during lactation.(ABSTRACT TRUNCATED AT 250 WORDS)
McNamara
J P
JP
Department of Animal Sciences and Nutrition Program, Washington State University, Pullman 99164-6320.
D000273:Adipose Tissue / Q000378:metabolism / Q000502:physiology*; D000818:Animals; D004951:Esterification; D005227:Fatty Acids / Q000096:biosynthesis / Q000378:metabolism; D007774:Lactation / Q000235:genetics / Q000378:metabolism*; D050356:Lipid Metabolism; D008066:Lipolysis; D008954:Models, Biological
D005227:Fatty Acids