Lactocyte
| Lactocyte | |
|---|---|
| Details | |
| System | Exocrine system |
| Location | Mammary gland |
| Shape | Cuboidal |
| Function | Milk secretion |
| Identifiers | |
| TA | Lua error in Module:Wikidata at line 744: attempt to index field 'wikibase' (a nil value). |
| TH | {{#property:P1694}} |
| TE | {{#property:P1693}} |
| FMA | {{#property:P1402}} |
| Anatomical terms of microanatomy [[[d:Lua error in Module:Wikidata at line 863: attempt to index field 'wikibase' (a nil value).|edit on Wikidata]]] | |
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Lactocytes are cells that synthesize and secrete milk within the mammary glands of lactating mammals.[1][2] In preparation of lactation, lactocytes differentiate from luminal adaptive secretory precursor (LASP) cells found in the resting mammary gland.[3]
Milk synthesis
Many of these processes are still under investigation. It is thought that nutrients are transported to mammary alveoli by transport proteins on the membranes of mammary epithelial cells. Milk proteins are synthesized in the endoplasmic reticulum and packaged into secretory vesicles, alveolar cells add nutrients such as calcium, zinc, phosphate, lactose, and citrate, and the milk is transported from the lactocyte via exocytosis. Lipids are wrapped in a membrane and secreted as milk fat globules. Other transport proteins uptake nutrients from the blood and from interstitial fluid.[4]
Structure
The primary secreting components of the mammary gland are the alveoli, which are small cavities surround by cells. In lactating mammals, a bulb-like lumen (cavity) is lined by lactocytes, which secrete milk into the lumen. The lactocytes are surrounded by a second layer of cells, called basal-myoepithelial (B-myo) cells, which function like muscle cells to squeeze milk out of the lobules (groups of alveoli) and into the milk ducts during suckling.[3][5]
Origin and stages
Before pregnancy, the innermost (luminal) layer of mammary ductal tissue consists of two types of epithelial cell: the luminal hormone sensing (LHS) cells and the luminal adaptive secretory precursor (LASP) cells.[3] During pregnancy, the LHS cells receive signals from hormones (especially estrogen, progesterone, prolactin, and human placental lactogen) and pass these signals onto nearby LASP cells, which subsequently differentiate into lactocytes.[3]
Following secretory differentiation, pregnancy hormones suppress the lactocytes, reducing their size and function. Upon delivery of the placenta, the resulting significant drop in progesterone allows prolactin to stimulate milk synthesis and secretion in the alveoli. Initially, there are large intercellular gaps between lactocytes, allowing high transfer of maternal plasma components to enter the milk, and colostrum - the initial, immature, and highly beneficial milk - is produced. As the intercellular gaps are bridged by an apical junctional complex and the number of lactocytes increase, they begin to produce "mature" breast milk.[6][7]
Milk secretion and regulation
Lactocytes secrete milk in a slow but mostly continuous fashion.[2] However, suckling triggers a spike in the release of the hormone prolactin from the pituitary gland, which stimulates the lactocytes to increase their production of milk to prepare for the next feeding.[5]
The mechanisms that pause milk production and control the amount of milk produced remain poorly understood. Some have hypothesized the existence of a protein (or multiple proteins), they term "feedback inhibitor of lactation", which accumulates and stops milk production. The existence and identity of this protein have yet to be definitively proven, but recently some have suggested that serotonin may be part of this.[8]
As the lactocytes produce milk globules within the alveoli, intra-alveolar pressure stretches the lactocytes which prevents the cells from producing and "pinching off" fatty globule membranes, causing a reduced fat content. As the milk is removed, pressure reduces, and the fat content of the milk increases.[9]
References
- ↑ "Endosymbiont". www.endosymbiont.com. Retrieved 2026-09-11.
- ↑ 2.0 2.1 Pang, Wei Wei; Hartmann, Peter E. (2007-12-01). "Initiation of Human Lactation: Secretory Differentiation and Secretory Activation". Journal of Mammary Gland Biology and Neoplasia. 12 (4): 211–221. doi:10.1007/s10911-007-9054-4. ISSN 1573-7039. PMID 18027076.
- ↑ 3.0 3.1 3.2 3.3 Gray GK, Carlson EG, Lev T, Marshall B, Reed AD, Sánchez-Covarrubias AP, Twigger AJ, Puig-Barbe A, Thennavan A, Omotoso A, Murrow LM (2025-09-08). "Defining breast epithelial cell types in the single-cell era". Developmental cell. 60 (17): 2218–36. doi:10.1016/j.devcel.2025.06.032.
- ↑ Montalbetti, Nicolas; Dalghi, Marianela G.; Albrecht, Christiane; Hediger, Matthias A. (March 2014). "Nutrient Transport in the Mammary Gland: Calcium, Trace Minerals and Water Soluble Vitamins". Journal of Mammary Gland Biology and Neoplasia. 19 (1): 73–90. doi:10.1007/s10911-014-9317-9. ISSN 1083-3021. PMID 24567109.
- ↑ 5.0 5.1 "Lactation | Anatomy and Physiology II". courses.lumenlearning.com. Retrieved 2026-09-11.
- ↑ Physiology, Fetal and Neonatal (2024-03-22). "Drug Transfer During Breastfeeding". Clinical Tree. Retrieved 2026-09-11.
- ↑ "NDC | Lactogenesis: secretory differentiation and activation of the human mammary gland". ndcinstitute.au. Retrieved 2026-09-11.
- ↑ Anderson SM, MacLean PS, McManaman JL, Neville MC (2015). "Lactation and its hormonal control". Knobil and Neill’s Physiology of reproduction (4 ed.). pp. 2055–105. ISBN 9780123977694. Search this book on
- ↑ "NDC | Limitations of the bioactive factors Feedback Inhibitor of Lactation model". ndcinstitute.au. Retrieved 2026-09-11.
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