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Lactation Biology Symposium: Novel Mechanisms Regulating Milk Secretion and Mammary Involution

The lipid component of milk is an important energy source and a critical nutrient for proper development of the newborn. The lactating mouse secretes her entire body weight in fat during a normal lactation period. Fatty acids in milk triglyceride are blended from preformed sources (dietary and adipose stores), and de novo synthesized fatty acids. Factors that control lipogenic differentiation of mammary epithelial cells have not been identified. Gene expression profiling has identified potential controller genes including SREBP1c, Src, Spot14 (THRSP), Akt1, and the long form of the prolactin receptor. Metabolic genes that increase at parturition include the glucose transporter GLUT1, citrate synthase (CS), malic enzyme 1 (ME1), citrate transporter (SLC25a1), ATP citrate lyase (ACLY), acetyl-CoA carboxylase 1(ACC1), fatty acid synthase (FASN), and stearoyl-CoA desaturase 2 (SCD2). SREBP1c regulates transcription of several of these genes in the liver; however, SREBP1c knockout mice do not display a lactation defect. Mice deficient in SCAP (SREBP Cleavage Activation Protein) have a significant lactation defect characterized by a 25% decrease in de novo synthesized fatty acids in milk and a 50% decrease in pup growth. Expression of FASN, Insig1, SLC25a1, and SCD2 in mammary epithelial cells is reduced, but there is no change in ACC1 and ACLY. This suggests SREBP-dependent and -independent regulation of lipid biosynthetic enzymes in mouse mammary epithelium. To compensate for loss of de novo fatty acid biosynthesis in SCAP null dams, we fed them a high fat diet (45% kCal). Although pup growth improved, lactation competency was not restored completely. Interestingly, the mRNA levels of ACC1, ACLY, FASN, SCD2, and SLC25a1 did not change, but the protein levels of ACC1, ACLY, and FASN were significantly reduced. This implies post-transcriptional regulation of fatty acid biosynthetic enzymes in mammary epithelial cells in response to dietary fat, rather than at the transcriptional level. Current efforts are focused upon understanding aspects of this post-transcriptional regulation in mammary epithelial cells.