Control of fatty acid synthesis in lactation.
Lactation results not only in an increased rate of fatty acid synthesis in the mammary gland but also in a decreased rate of fatty acid synthesis in adipose tissue and, in the rat at least, an increased rate of hepatic fatty acid synthesis. Progesterone (during pregnancy), prolactin and (in ruminants) GH are implicated in the regulation of the reciprocal changes in fatty acid synthesis in mammary gland and adipose tissue. Progesterone and prolactin, at least, appear to influence the rate of fatty acid synthesis by modulating the insulin-binding capacities of the tissues, but it is clear that steps in the mechanism of action of insulin subsequent to its binding to the receptor are also changed in adipose tissue during lactation.
D000273:Adipose Tissue / Q000378:metabolism; D002001:Adipose Tissue, Brown / Q000378:metabolism; D000818:Animals; D005227:Fatty Acids / Q000096:biosynthesis*; D005260:Female; D013006:Growth Hormone / Q000378:metabolism; D007328:Insulin / Q000378:metabolism; D007774:Lactation; D008099:Liver / Q000378:metabolism; D008321:Mammary Glands, Animal / Q000378:metabolism; D011247:Pregnancy; D011374:Progesterone / Q000378:metabolism; D011388:Prolactin / Q000378:metabolism; D011972:Receptor, Insulin / Q000378:metabolism
D005227:Fatty Acids; D007328:Insulin; D011374:Progesterone; D011388:Prolactin; D013006:Growth Hormone; D011972:Receptor, Insulin