title: Late gestational hyperprolactinemia accelerates mammary epithelial cell differentiation that leads to increased milk yield.
abstract: The growth rate of piglets is limited by sow milk yield, which reflects the extent of epithelial growth and differentiation in the mammary glands (MG) during pregnancy. Prolactin (PRL) promotes both the growth and differentiation of the mammary epithelium, where the lactational success of pigs is absolutely dependent on PRL exposure during late gestation. We hypothesized that inducing hyperprolactinemia in primiparous gilts during late gestation by administering the dopamine antagonist domperidone (DOM) would increase MG epithelial cell proliferation and differentiation, subsequent milk yield, and piglet growth. A total of 19 Yorkshire-Hampshire gilts were assigned to receive either no treatment (CON, n = 9) or DOM (n = 10) twice daily from gestation d 90 to 110. Serial blood sampling during the treatment period and subsequent lactation confirmed that plasma PRL concentrations were increased in DOM gilts on gestation d 91 and 96 (P < 0.001). Piglets reared by DOM-treated gilts gained 21% more BW during lactation than controls (P = 0.03) because of increased milk production by these same gilts on d 14 (24%, P = 0.02) and 21 (32%, P < 0.001) of lactation. Milk composition did not differ between the 2 groups on d 1 or 20 of lactation. Alveolar volume within the MG of DOM-treated gilts was increased during the treatment period (P < 0.001), whereas epithelial proliferation was unaffected by treatment. Exposure to DOM during late gestation augmented the postpartum increase in mRNA expression within the MG for β-casein (P < 0.03), acetyl CoA carboxylase-α (P < 0.01), lipoprotein lipase (P < 0.06), α-lactalbumin (P < 0.08), and glucose transporter 1 (P < 0.06). These findings demonstrate that late gestational hyperprolactinemia enhances lactogenesis within the porcine MG and increases milk production in the subsequent lactation.
authors.affiliation: Department of Animal Science, University of California, Davis 95616, USA.
authors.forename: M K
authors.initials: MK
authors.lastname: Vanklompenberg
authors.forename: R
authors.initials: R
authors.lastname: Manjarin
authors.forename: J F
authors.initials: JF
authors.lastname: Trott
authors.forename: H F
authors.initials: HF
authors.lastname: McMicking
authors.forename: R C
authors.initials: RC
authors.lastname: Hovey
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D049109:Cell Proliferation; D004294:Domperidone / Q000008:administration & dosage; D018492:Dopamine Antagonists / Q000008:administration & dosage; D004847:Epithelial Cells / Q000166:cytology; D005260:Female; D006966:Hyperprolactinemia / Q000139:chemically induced / Q000503:physiopathology / Q000662:veterinary*; D007774:Lactation; D008321:Mammary Glands, Animal / Q000166:cytology* / Q000254:growth & development*; D008892:Milk / Q000378:metabolism*; D010298:Parity; D011247:Pregnancy; D011388:Prolactin / Q000097:blood; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000662:veterinary; D013552:Swine / Q000254:growth & development / Q000502:physiology*; D013553:Swine Diseases / Q000139:chemically induced / Q000503:physiopathology*
chemical_list: D018492:Dopamine Antagonists; D012333:RNA, Messenger; D004294:Domperidone; D011388:Prolactin