Prolactin Receptor Gene Expression and Foetal Adipose Tissue

161

113

In the fetus, adipose tissue comprises both brown and white adipocytes for which brown fat is characterised as possessing the unique uncoupling protein (UCP)1. The dual characteristics of fetal fat reflect its critical role at birth in providing lipid that is mobilised rapidly following activation of UCP1 upon cold exposure to the extrauterine environment. A key stage in the maturation of fetal fat is the gradual rise in the abundance of UCP1. For species with a mature hypothalamic-pituitary axis at birth there is a gradual increase in the amount and activity of UCP1 during late gestation, in conjunction with an increase in the plasma concentrations of catecholamines, thyroid hormones, cortisol, leptin and prolactin. These may act individually, or in combination, to promote UCP1 expression and, following the post-partum surge in each hormone, UCP1 abundance attains maximal amounts.Adipose tissue grows in the fetus at a much lower rate than in the postnatal period. However, its growth is under marked nutritional constraints and, in contrast to many other fetal organs that are unaffected by nutritional manipulation, fat mass can be significantly altered by changes in maternal and, therefore, fetal nutrition. Fat deposition in the fetus is enhanced during late gestation following a previous period of nutrient restriction up to mid gestation. This is accompanied by increased mRNA abundance for the receptors of IGF-I and IGF-II. In contrast, increasing maternal nutrition in late gestation results in less adipose tissue deposition but enhanced UCP1 abundance. The pronounced nutritional sensitivity of fetal adipose tissue to both increased and decreased maternal nutrition may explain why the consequences of an adverse nutritional environment persist into later life.

“…Increase in plasma prolactin (Houghton et al 1995) and prolactin receptor abundance (Symonds et al 1998) that may directly stimulate further expression of UCP1.…”

Section: Ontogeny Of Fetal Adipose Tissuementioning

confidence: 99%

Section: Nutritional Regulation Of Fetal Adipose Tissue Depositionmentioning

confidence: 99%

Endocrine and nutritional regulation of fetal adipose tissue development

Symonds¹,

Mostyn²,

Pearce³

et al. 2003

161

113

“…Although it is speculated that the short form of the PRL-R plays a role in such functions as reproduction and lactation in the ewe (Cassy et al 1998, Symonds et al 1998) and the rat (Telleria et al 1997, Feng et al 1998, no studies done to date have found a specific role for the short form of the receptor in the bovine. However, the present study identifies shifts in short form that occur in the same trend as the long form of the receptor, potentially indicating a role for the short form PRL-R in the bovine.…”

Section: Figurementioning

confidence: 99%

Photoperiod and bromocriptine treatment effects on expression of prolactin receptor mRNA in bovine liver, mammary gland and peripheral blood lymphocytes

Auchtung

Kendall

Salak‐Johnson

et al. 2003

Recent evidence suggests that photoperiod influences immune function. Interestingly, photoperiod has profound effects on concentrations of prolactin (PRL), a hormone also known to be involved in fluctuations of the immune system. However, the impact of photoperiod on PRL receptor (PRL-R) expression is poorly understood, particularly in tissues of the immune system. Two experiments were performed to increase the general understanding of how photoperiod interacts with the immune system. Our first objective was to determine the effects of photoperiod on PRL-R mRNA expression and cellular immune function. Lymphocytes were isolated from blood collected from calves (n=10) and PRL-R mRNA expression of both long and short forms was quantified using real-time PCR. Lymphocytes expressed PRL-R mRNA, suggesting that PRL could act directly on these cells. To determine the relationship between photoperiod and PRL-R mRNA expression in other tissues, hepatic and mammary biopsies were collected after calves were exposed to long days (LDPP; 16 h light:8 h darkness) or short days (SDPP; 8 h light:16 h darkness). Relative to LDPP, SDPP decreased circulating PRL, but increased expression of both forms of PRL-R mRNA in liver, mammary gland and lymphocytes. Short days also increased lymphocyte proliferation compared with long days. Reversal of photoperiodic treatments reversed the effects on circulating PRL, PRL-R mRNA expression and lymphocyte proliferation. Our second objective was to manipulate PRL concentration in photoperiod-treated animals, using bromocriptine. Concentrations of PRL in LDPP animals injected daily with bromocriptine for 1 week were decreased compared with LDPP controls, to a level similar to SDPP animals. Receptor expression was increased in LDPP+bromocriptine-treated animals relative to LDPP controls, as was lymphocyte proliferation. Overall, our results indicate that photoperiodic effects on PRL-R mRNA expression were inverse to those on circulating PRL, with short days stimulating expression of both forms of PRL-R mRNA. Expression of PRL-R mRNA changed in the same direction as lymphocyte proliferation with regard to photoperiod treatment, suggesting a link between photoperiodic effects on PRL sensitivity and immune function. Thus, PRL signaling may mediate photoperiodic effects on immune function.

“…Both mRNA and protein for the PRLRs are highly abundant in fetal and neonatal brown adipose tissue (Symonds et al 1998, Bispham et al 1999. Growth of fetal fat occurs primarily over the second half of gestation when there is a marked rise in abundance of PRLR mRNA (Symonds et al 1998) preceding the rise in the abundance of the brown adipose tissue-specific mitochondrial protein, uncoupling protein (UCP)1 (Clarke et al 1997a) immediately after birth. Rapid activation of UCP1 in the newborn is critical in preventing hypothermia (Clarke et al 1997c).…”

Section: Introductionmentioning

confidence: 99%

Prolactin, the prolactin receptor and uncoupling protein abundance and function in adipose tissue during development in young sheep

Pearce¹,

Budge²,

Mostyn³

et al. 2005

A primary role of the prolactin receptor (PRLR) during fetal and postnatal development has been suggested to be the regulation of uncoupling protein (UCP) expression. We, therefore, determined whether: (1) the rate of loss of UCP1 from brown adipose tissue after birth was paralleled by the disappearance of PRLR; and (2) administration of either pituitary extract prolactin (PRL) containing a mixture of posttranslationally modified forms or its pseudophosphorylated form (S179D PRL) improved thermoregulation and UCP1 function over the first week of neonatal life. PRLR abundance was greatest in adipose tissue 6 h after birth before declining up to 30 days of age, a trend mirrored by first a gain and then a loss of UCP1. In contrast, in the liver -which does not possess UCPsa postnatal decline in PRLR was not observed. Administration of PRL resulted in an acute increase in colonic temperature in conjunction with increased plasma concentrations of non-esterified fatty acids and, as a result, the normal postnatal decline in body temperature was delayed. S179D PRL at lower concentrations resulted in a transient rise in colonic temperature at both 2 and 6 days of age. In conclusion, we have demonstrated a close relationship between the ontogeny of UCP1 and the PRLR. Exogenous PRL administration elicits a thermogenic effect suggesting an important role for the PRLR in regulating UCP1 function.