Effects of prolactin, progesterone and ovariectomy on metabolic activities and insulin receptors in the mammary gland and adipose tissue during extended lactation in the rat

Abstract

Prolactin implants prevented the decline in milk yield and the resumption of oestrous cycles which occurred between days 22 and 28 in untreated lactating rats. Ovariectomy and progesterone implants only partially prevented the decline in milk yield despite preventing the occurrence of oestrous cycles. All three treatments increased total RNA content of the mammary gland compared with controls. In untreated rats there were no changes in mammary DNA content or the number of insulin receptors whereas lipoprotein lipase (LPL) activity decreased significantly during the declining phase of lactation. In contrast, the number of insulin receptors, LPL activity and glucose incorporation into lipid increased in adipose tissue. Prolactin prevented the increase in insulin receptors and lipid synthesis and significantly decreased LPL activity in adipose tissue. Progesterone stimulated LPL activity in the mammary gland and also prevented the increase in lipid synthesis and insulin receptors in adipose tissue but was without effect on LPL activity whereas ovariectomy stimulated LPL activity in the mammary gland but prevented only the increase in the number of insulin receptors in adipose tissue. The results show that raising the serum prolactin concentration can prevent the decline in milk yield during extended lactation and whilst part of this effect may be due to a direct effect on the mammary gland and an indirect effect due to inhibition of oestrous cycles, prolactin may also produce part of its effect on milk synthesis by inhibiting competitive metabolic processes in tissues such as adipose tissue.

Enhancement of maternal lactation performance during prolonged lactation in the mouse by mouse GH and long-R3-IGF-I is linked to changes in mammary signaling and gene expression

“…Numerous studies have examined the impact of PRL, GH, and IGF-I on milk production in lactating cows, goats, and rats respectively (Tucker 1974, Flint et al 1984, Plaut et al 1987, Davis et al 1989, Prosser et al 1990 Figure 5 Exogenous administration of IGF-I, GH, and prolactin differentially affect mammary gland expression of SOCS genes and TPH1 during prolonged lactation. Total RNA from mammary tissue of lactating dams injected with either saline, LR3, GH, or prolactin was collected on day 37 post partum and analyzed for (A) SOCS1, (B) SOCS2, (C) SOCS3, (D) CIS, and (E) TPH1 by real-time RT-PCR.…”

“…The effects of PRL on milk production in normal lactating rats as well as in dairy cows have been largely negative with the exception of one study on prolonged lactation (Flint et al 1984). Both PRL and GH have been demonstrated to support lactogenesis in hypophysectomized mice (Nandi 1958a,b) and both factors also stimulate milk production in lactating rats that have been treated with anti-GH antiserum and bromocryptine .…”

Influence of glucogenic dietary supplementation and reproductive state of dairy cows on the composition of lipids in milk

“…In general, milk polar lipid composition and concentration are altered when systemic or local -within the mammary gland -changes in lipid metabolism are induced. Two factors with a known effect on whole-body lipid metabolism are insulin and progesterone (Bauman and Currie, 1980;Flint et al, 1984;Li et al, 2007). Although the concentrations of both hormones are frequently altered by glucogenic dietary supplementation in dairy cows and during the animal's estrous cycle, respectively, information about their individual and combined effects on lipid composition in milk is still scarce.…”

“…Progesterone has been shown to modulate the partitioning of lipid precursors between mammary gland and adipose tissue, primarily by inducing opposing changes in lipoprotein lipase (LPL) activity and expression in these two tissues (Bauman and Currie, 1980;Flint et al,1984). LPL hydrolyzes lipoprotein triglycerides, releasing fatty acids, which are utilized by the mammary gland as preformed fatty acids.…”

Revue bibliographique : Variations quantitatives et métabolisme des lipides dans les tissus adipeux et le foie au cours du cycle gestation-lactation. 1re partie : chez la ratte

“…5 ; Agius et Williamson, 1980a, b ;Burnol et al, 1983). Elle s'accroît aussi en fin de lactation (28 e jour) (Flint et al, 1984a (Farid et al, 1978 ;Sinnet-Smith et al, 1979Flint et al, 1981) alors que les activités des déshydrogénases produisant du NADPH ne semblent pas varier aussi largement (Smith, 1973a ;Baldwin et al, 1973 ;Farid et al, 19781. Les variations de l'activité de la synthétase des acides gras, mesurées par immunotitration, sont dues à des variations de la quantité d'enzyme reflétant une régulation à long terme.…”