In plain words
Lactocytes are the cells in the breast that make milk. They line the alveoli, which are small sacs at the ends of the milk ducts. Blood brings nutrients to these cells, and the cells turn those nutrients into milk. Lactocytes start to change during pregnancy, so the breasts are ready to make milk after birth. They keep doing this work for as long as you breastfeed or pump. Milk that is not fully removed can build up in the sacs and ducts, which is one reason for and blocked ducts. Medicines and some illnesses can affect how these cells work. The idea is a cell-level one, and you cannot feel individual cells. Knowing they exist helps explain why milk supply responds to how often milk is removed.
The deeper version
Lactocytes are polarized secretory epithelial cells of the mammary alveolus, with apical secretory granules and basolateral uptake of plasma nutrients. During , under estrogen, progesterone, , , cortisol, and insulin, they differentiate and acquire secretory capacity. After birth, prolactin and milk removal sustain secretion. between lactocytes regulate paracellular transport, and their closure at shifts milk composition. Lactocyte activity is also regulated by local feedback inhibitors that accumulate in milk stasis, which underlies supply regulation by removal. Direct study of human lactocytes is limited by tissue access, so much knowledge comes from animal models and milk composition studies (Neville et al., 2001).
Where it comes up
- How breastfeeding works: supply and demandFeeding Your Baby
- When your milk comes inFeeding Your Baby
- Weaning: gradual, abrupt, and baby-ledFeeding Your Baby
- Medications and breastfeeding: how to checkFeeding Your Baby
- Clogged ducts and mastitisPostpartum: Your Body
What mothers here say about lactocyte
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Sources
- Neville MC, Morton J, Umemura S — Lactogenesis: the transition from pregnancy to lactation. Pediatric Clinics of North America, 2001
- Neville MC, Morton J — Physiology and endocrine changes underlying human lactogenesis II. Journal of Nutrition, 2001