Adipocyte prolactin: regulation of release and putative functions

Brandebourg, Terry D.; Hugo, Eric R.; Ben‐Jonathan, Nira

doi:10.1111/j.1463-1326.2006.00671.x

Cited by 122 publications

(105 citation statements)

References 91 publications

(125 reference statements)

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“…In this study, both receptor isoforms were dramatically induced in epididymal preadipocytes during adipogenesis. A marked increase in total PRLR expression during adipocyte differentiation was also observed by others [14,15,16]. Regardless of the expression level of the PRLR, PRL further increased the expression of both isoforms (Fig 2).…”

Section: Discussionsupporting

confidence: 81%

Prolactin upregulates its receptors and inhibits lipolysis and leptin release in male rat adipose tissue

Brandebourg

Bown

Ben‐Jonathan

2007

Biochemical and Biophysical Research Communications

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Prolactin (PRL) is recognized as a metabolic regulator during lactation, but little information exists on its actions in male adipose tissue. We examined whether PRL affects the expression of its receptors (PRLR), lipolysis and adipokine secretion in male rats. Both long and short PRLR isoforms were induced 40 to 50-fold during differentiation of epididymal preadipocytes, with a 10 fold higher expression of the long isoform. PRL upregulated both isoforms before and after differentiation. PRL suppressed lipolysis in epididymal explants and mature adipocytes in a dose-and time-dependent manner, which was reversed by a Jak2 inhibitor. PRL also inhibited leptin, but not adiponectin, release. We conclude that PRL inhibits lipolysis and leptin release by acting directly on adipocytes via interaction with either of its receptors and activation of a Jak2-dependent signaling pathway(s). This is the first demonstration of substantial effects of PRL on male adipocytes.

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Section: Discussionsupporting

confidence: 81%

Prolactin upregulates its receptors and inhibits lipolysis and leptin release in male rat adipose tissue

Brandebourg

Bown

Ben‐Jonathan

2007

Biochemical and Biophysical Research Communications

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“…Hyperprolactinemia adversely affects the fertility potential by impairing pulsatile secretion of GnRH and hence interfering with ovulation [10,13]. Recent studies have shown that prolactin may also be secreted from adipose tissue thus providing a link between obesity and hyperprolactinemia [14].…”

Section: Introductionmentioning

confidence: 99%

Association of Obesity with Hormonal Imbalance in Infertility: A Cross-Sectional Study in North Indian Women

2013

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Hormones play an important role in the development and regulation of reproductive function and the menstrual cycle of women. Extremes of body weight tend to affect the homeostasis of the hypothalamo-pituitary-gonadal axis. This cross-sectional study was carried out in 113 women (57 with primary infertility and 56 with secondary infertility) in the age group 20-35 years, presenting for hormonal evaluation of infertility in a tertiary care hospital. After preliminary clinical evaluation, anthropometric indices (height, weight, BMI, waist circumference and waist hip ratio) were measured in all subjects. Fasting blood sample drawn on second/third day of menstrual cycle was analysed for serum luteinizing hormone, follicle stimulating hormone (FSH), prolactin and thyroid stimulating hormone (TSH). Serum FSH levels showed a significant positive correlation with indicators of central obesity (waist circumference and waist hip ratio in both the study groups). In primary infertility, significant positive correlation was also observed between serum FSH levels and other markers of obesity like body weight, hip circumference and BMI. In secondary infertility, serum prolactin and serum TSH levels demonstrated a significant positive correlation with body weight and BMI. Obesity is associated with hormonal derangements which are responsible for infertility. In overweight women with infertility, weight loss should be considered as a first line treatment.

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“…We suggest that the increase of Pck1 activity for the Lobato studies was due to changes in adipocyte expression of Pck1 , because in our studies, we found prolactin increased Pck1 mRNA expression in isolated adipocytes from the mammary gland after prolactin administration. Prolactin has been shown not only to regulate lactation in the mammary gland, but also to regulate adipocyte metabolism ( 46 ). In WAT, Pck1 is increased during fasting to reesterify FA back to triglycerides after lipolysis.…”

Section: Discussionmentioning

confidence: 99%

Function of phosphoenolpyruvate carboxykinase in mammary gland epithelial cells

Hsieh¹,

Huang²,

Bederman

et al. 2011

Journal of Lipid Research

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This article is available online at http://www.jlr.org tissues during lactation, promoting lipogenesis over esterifi cation in the adipose tissue ( 2,3,7,8 ). These changes cause mobilization of lipid stores in adipose tissues to support milk production in the mammary gland.One gene that is present in both adipocytes and epithelial cells of the mammary gland is the phosphoenolpyruvate carboxykinase gene Pck1 . The role of Pck1 in adipocytes of white adipose tissue (WAT) has been clearly defi ned as glyceroneogenic. Over 30 years ago, Ballard, Hanson, and Leveille ( 9 ) and Reshef, Niv, and Shapiro ( 10, 11 ) demonstrated that in vitro incubation of rat epididymal fat pad with pyruvate reduced the amount of FFAs released by 65% ( 10, 11 ). However, the rate of lipolysis remained unaffected. In WAT, glycerol is released during lipolysis, but it cannot be phosphorylated in preparation for triglyceride synthesis because the tissue manifests negligible glycerol kinase activity. Ballard and Hanson ( 12 ) and Reshef, Hanson, and Ballard ( 13 ) determined that during fasting, gluconeogenic precursors such as pyruvate and alanine are converted into the glycerol backbone of triglycerides through the glyceroneogenic pathway. Support for a glyceroneogenic role for Pck1 in the mammary gland was established by Jimenez et al. ( 14 ), who established incorporation of labeled oleate into glycerol-3-phosphate in isolated acini from lactating Wistar rats. However, they suggested that the last steps of gluconeogenesis between triose-phosphate and glucose-6-phosphate are not operative in rat mammary gland acinar cells ( 14 ).Abstract Previously, we have shown that Pck1 expression in mammary gland adipocytes and white adipose tissue maintains triglyceride stores through glyceroneogenesis, and these lipids were used for synthesis of milk triglycerides during lactation. Reduced milk triglycerides during lactation resulted in patterning of the newborn for insulin resistance. In this study, the role of Pck1 in mammary gland epithelial cells was analyzed. The developmental expression of Pck1 decreased in isolated mouse mammary gland epithelial cells through development and during lactation. Using HC11, a clonal mammary epithelial cell line, we found that both Janus kinase 2 signal transducers and activators of transcription 5 and the AKT pathways contributed to the repression of Pck1 mRNA by prolactin. These pathways necessitate three accessory factor regions of the Pck1 promoter for repression by prolactin. Using [U- During lactation, there are profound modifi cations in the intermediary metabolism of different tissues to adequately supply nutrients for milk production ( 1, 2 ). There are decreases in both lipogenic capacity and activities of several lipogenic enzymes in adipose tissue ( 3-7 ). Prolactin is one of the key signals that integrates metabolism of

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Adipocyte prolactin: regulation of release and putative functions

Cited by 122 publications

References 91 publications

Prolactin upregulates its receptors and inhibits lipolysis and leptin release in male rat adipose tissue

Prolactin upregulates its receptors and inhibits lipolysis and leptin release in male rat adipose tissue

Association of Obesity with Hormonal Imbalance in Infertility: A Cross-Sectional Study in North Indian Women

Function of phosphoenolpyruvate carboxykinase in mammary gland epithelial cells

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