Late gestational hyperprolactinemia accelerates mammary epithelial cell differentiation that leads to increased milk yield1

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.

Study on effects of microbial fermented soyabean meal on production performances of sows and suckling piglets and its acting mechanism

“…Prolactin promotes both the growth and differentiation of the mammary epithelium for milk excretion, so higher blood serum prolactin concentration of sows may increase milk production and piglet growth (Vanklompenberg et al, 2013). This study showed a higher serum prolactin concentration in the lactating sows fed diet containing 5 -15% FSBM, inferring that milk excretion would be improved to increase growth and weaning survival rates for suckling piglets.…”

Relative prolactin-to-progesterone concentrations around farrowing influence colostrum yield in primiparous sows

“…Thus, the total output of colostrum constituents was greater in high PRL/P4 than in low PRL/P4 sows. In sows, there is evidence that PRL stimulates lactose, protein, and lipid synthesis in lacteal secretions [15][16][17]. Furthermore, the number of PRL receptors in the mammary gland may be a limiting factor for PRL action.…”

Alcohol intake stimulates epithelial proliferation in an authentic model of the human breast

“…Immunohistochemistry for phosphorylated histone H3 (PH3), phosphorylated STAT5 (P-STAT5) and progesterone receptor (PR) was performed using procedures outlined by VanKlompenberg et al [23]. Sections of MG2, 3 and 5 (cranial to caudal) from each female were analyzed for PH3 and P-STAT5, while one section from MG3 was analyzed for PR.…”

“…Primers were synthesized by Sigma Life Science (St. Louis, MO) and PCR products sequence verified. Quantitative PCR reactions were performed using Fast SYBR Green master mix (Applied Biosystems, Foster City, CA), 200 nM of each primer and 0.4 L of cDNA, in duplicate, on a 7500 Fast Real-Time PCR System (Applied Biosystems) as previously described [23] with the following modifications. The annealing and extension temperatures used for each primer set are in Table 1.…”

“…Total RNA was extracted from one MG from each pig, treated with DNase and reverse transcribed as described [23]. Primers used for reference and target genes are presented in Table 1.…”