Differential Effects of Age and Sex on the Postnatal Responsiveness of Brown Adipose Tissue to Prolactin Administration in Rats

Pearce, Sarah; Diéguez, Carlos; Gualillo, Oreste; Symonds, Michael; Stephenson, Terence

doi:10.1113/eph8802575

Cited by 14 publications

(20 citation statements)

References 28 publications

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“…In addition, the high levels of circulating prolactin are correlated with increased milk production more by downregulation of BAT activity than by BATindependent processes (Fig.5). The link between prolactin and BAT E. Król and others activity is consistent with the administration of exogenous prolactin (Pearce et al, 2003) and pharmacological stimulation of endogenous prolactin secretion (Chan and Swaminathan, 1990) in non-breeding rats promoting the loss of UCP1. These effects are likely to be mediated via prolactin receptors on brown adipocytes (Pearce et al, 2003).…”

Section: Leptin and Prolactin As Correlates Of Milk Productionmentioning

confidence: 76%

“…Both suppression of leptin and induction of prolactin have been suggested to contribute to lactational hyperphagia, facilitating milk production (Crowley et al, 2004;Naef and Woodside, 2007;Woodside, 2007;Smith et al, 2010). Importantly, both of these hormones have also been demonstrated to modify the gene and protein expression of UCP1 in BAT (Chan and Swaminathan, 1990;Pearce et al, 2003;Cannon and Nedergaard, 2004;Xiao et al, 2004;Cui et al, 2011). These hormones may therefore influence milk production via BAT-mediated and BATindependent effects.…”

Section: Leptin and Prolactin As Correlates Of Milk Productionmentioning

confidence: 99%

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Negative correlation between milk production and brown adipose tissue gene expression in lactating mice

Król

Martín

Huhtaniemi

et al. 2011

Journal of Experimental Biology

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SUMMARYIt has been proposed that the performance of lactating animals is limited by the capacity of the female to dissipate body heatthe heat dissipation limit (HDL) theory. This theory predicts that milk production might be constrained not by intrinsic properties of the mammary glands but rather by competitive heat production such as thermogenesis in brown adipose tissue (BAT). To test this prediction, we measured the expression of genes linked to thermogenesis in BAT of lactating laboratory mice. The applicability of BAT gene expression to reflect thermogenic activity of BAT was confirmed by a positive relationship between expression levels of several BAT genes (summarised by the first principal component following principal component analysis) and daily energy expenditure in virgin mice. Milk production at peak lactation was strongly and negatively associated with the expression of thermogenic genes in BAT. Downregulation of these genes during lactation was correlated with low levels of circulating leptin and high levels of circulating prolactin. Our results are consistent with the HDL theory. However, we cannot discount the converse interpretation that milk production may reduce BAT activity. If the reduction in BAT activity does facilitate increased milk production, then reducing the heat generated by competitive processes may be a more productive route to increase lactational performance than attempts to improve mammary gland performance in isolation from the other body systems. Supplementary material available online at

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Section: Leptin and Prolactin As Correlates Of Milk Productionmentioning

confidence: 76%

Section: Leptin and Prolactin As Correlates Of Milk Productionmentioning

confidence: 99%

Negative correlation between milk production and brown adipose tissue gene expression in lactating mice

Król

Martín

Huhtaniemi

et al. 2011

Journal of Experimental Biology

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“…Despite high levels of PRLR transcripts in BAT, the precise role of PRL in this tissue is still unclear. Indeed, a recent study reported that infusion of PRL to pregnant rats induced an increase in UCP1 protein expression in the BAT of fetuses (Budge et al 2002), while the same authors reported that PRL caused a reduction in UCP1 abundance only in females and not in males (Pearce et al 2003). These observations suggested a potential involvement of PRL in thermoregulation.…”

Section: Introductionmentioning

confidence: 80%

“…a direct target of PRL but rather should be regulated mostly by a sympathetic pathway. However, we cannot exclude that in vivo PRL might modulate UCP1 expression, which also depends on the hormonal and metabolic environment in a developmental-stage manner (Pearce et al 2003, Xiao et al 2004.…”

Section: Discussionmentioning

confidence: 99%

Prolactin potentiates insulin-stimulated leptin expression and release from differentiated brown adipocytes

Viengchareun

Bouzinba-Ségard²,

Jp³

et al. 2004

Journal of Molecular Endocrinology

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The pituitary hormone prolactin (PRL) exerts pleiotropic effects, which are mediated by a membrane receptor (PRLR) present in numerous cell types including adipocytes. Brown adipose tissue (BAT) expresses uncoupling proteins (UCPs), involved in thermogenesis, but also secretes leptin, a key hormone involved in the control of body weight. To investigate PRL effects on BAT, we used the T37i brown adipose cell line, and demonstrated that PRLRs are expressed as a function of cell differentiation. Addition of PRL leads to activation of the JAK/STAT and MAP kinase signaling pathways, demonstrating that PRLRs are functional in these cells. Basal and catecholamine-induced UCP1 expression were not affected by PRL. However, PRL combined with insulin significantly increases leptin expression and release, indicating that PRL potentiates the stimulatory effect of insulin as revealed by the recruitment of insulin receptor substrates and the activation of phosphatidylinositol 3-kinase. To explore the in vivo physiological relevance of PRL action in BAT, we showed that leptin content was significantly increased in BAT of PRLR-null mice compared with wild-type mice, highlighting the involvement of PRL in the leptin secretion process. This study provides the first evidence for a functional link between PRL and energy balance via a cross-talk between insulin and PRL signaling pathways in brown adipocytes.

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“…For example, in the juvenile and adult rat, prolactin administration downregulates UCP1 abundance (Chan & Swaminathan 1990, Pearce et al 2003a) compared with up-regulation in the fetus (Budge et al 2002). This distinct difference is likely to reflect the critical role of adipose tissue in the neonatal period as the newborn is subjected to physical and environmental stresses of an intensity seldom encountered again through life.…”

Section: Ontogeny Of Fetal Adipose Tissuementioning

confidence: 99%

Endocrine and nutritional regulation of fetal adipose tissue development

Symonds¹,

Mostyn²,

Pearce³

et al. 2003

Journal of Endocrinology

162

113

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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.

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Differential Effects of Age and Sex on the Postnatal Responsiveness of Brown Adipose Tissue to Prolactin Administration in Rats

Cited by 14 publications

References 28 publications

Negative correlation between milk production and brown adipose tissue gene expression in lactating mice

Negative correlation between milk production and brown adipose tissue gene expression in lactating mice

Prolactin potentiates insulin-stimulated leptin expression and release from differentiated brown adipocytes

Endocrine and nutritional regulation of fetal adipose tissue development

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