Figure 1.

Intertissue flux of vitamin A during lactation. Dietary intake of vitamin A occurs mainly in the form of precursor β-carotene from vegetables and fruits, or retinyl esters (REs) from sources of animal origin. Both molecules are absorbed by enterocytes in the small intestine, although REs must be hydrolyzed into retinol (ROH) within the intestinal lumen by means of hydrolases. Within enterocytes, ROH and β-carotene are metabolized into REs, which in turn are secreted into the lymph in chylomicrons. Circulating chylomicrons, before reaching the liver, are hydrolyzed in tissues with lipoprotein lipase (LPL) activity and REs released into these extrahepatic tissues. During lactation, increased levels of lactogenic hormones regulate LPL activity, inducing it in the mammary tissue, whereas it is reduced in white adipose tissue. The effect of these hormones redirects REs into the mammary epithelial cells during lactation. Finally, chylomicron remnants are taken up by hepatocytes, where REs are hydrolyzed into ROH, stored, or oxidized to retinoic acid (RA). When needed, ROH is released from hepatic cells into plasma bound to retinol-binding protein (RBP4). Once in plasma, it associates with the stabilizing protein transthyretin (TTR), which decreases the renal clearance of vitamin A [49,50,51,52,53,54,55].