Maternal Progesterone Treatment Rescues the Mammary Impairment Following Uteroplacental Insufficiency and Improves Postnatal Pup Growth in the Rat

Abstract

Uteroplacental insufficiency in the rat reduces maternal progesterone and impairs mammary function and pup milk intake, compromising postnatal growth. We determined whether progesterone administration to rat dams progesterone-deficient following uteroplacental insufficiency improves lactation and pup growth. Uteroplacental insufficiency (Restriction) or sham surgery (Control) was performed on day 18 of pregnancy in WKY rats. Pregnant dams were injected with progesterone or vehicle, and Control mothers with vehicle for three days and killed on day 20 of pregnancy or day 6 of lactation. Progesterone treatment in the Restricted group restored maternal progesterone with no effect on mammary Pgr mRNA expression. Uteroplacental insufficiency triggered early lactogenesis, with increased mammary Csn2, Lalba and Wap mRNA. Progesterone treatment following uteroplacental insufficiency increased mammary alveolar number and area. Pups from progesterone treated mothers had increased body weight when compared to Controls. Overall, maternal progesterone treatment following uteroplacental insufficiency improved postnatal growth by rescuing the mammary impairment.

Uteroplacental insufficiency reduces rat plasma leptin concentrations and alters placental leptin transporters: ameliorated with enhanced milk intake and nutrition

“…Total calcium concentrations were determined using colorimetric spectrometry using the Synchron CX‐5 Clinical System (Beckman Coulter; Lane Cove, NSW, Australia) and ionic calcium (active or free calcium; regulated by PTHrP), sodium and potassium concentrations were determined using ion selective electrodes correcting for pH (Ciba‐Corning model 644; Cambridge, MA, USA) from milk as well as from pup and maternal plasma (Wlodek et al . , ). Total calcium concentration in the pup body was determined after ashing using the CX‐5 Analyser (Wlodek et al .…”

The effect of low-to-moderate-dose ethanol consumption on rat mammary gland structure and function and early postnatal growth of offspring

“…Progesterone withdrawal at the end of pregnancy is necessary to initiate lactation (37,28), and suckling-induced prolactin (2) and oxytocin (5) release, in combination with milk removal, are responsible for the maintenance of lactation. In the rat, uteroplacental insufficiency has been shown to induce premature withdrawal of progesterone in late gestation, thereby stimulating early onset milk production (55). In our model of low-to-moderate EtOH consumption, circulating levels of progesterone and prolactin were unaltered, suggesting that the initiation and maintenance of lactation was not disrupted by EtOH.…”

“…Secretory differentiation of the mammary gland can be altered by a number of insults. Animal models have shown that secretory differentiation is disrupted by maternal: uteroplacental insufficiency (55), undernutrition (46), obesity (17), hypertension (56), and vitamin A deficiency (8). Most of these insults result in decreased mammary alveolar development.…”

Prenatal Programming of Hypertension in the Rat: Effect of Postnatal Rearing

“…Prenatal maternal insults can affect postnatal rearing and/or lactation resulting in poor postnatal weight gain of neonates [23, 23, 46, 47]. Mothers that have uteroplacental insufficiency, created by prenatal ligation of the uterine artery on day 18 of gestation, produce less milk with altered composition, including less calcium, compared to control rats [23].…”