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

Brandebourg, Terry D.; Bown, Jenna L.; Ben‐Jonathan, Nira

doi:10.1016/j.bbrc.2007.03.168

Cited by 50 publications

(43 citation statements)

References 35 publications

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“…However, results of recent studies suggest that the response is reciprocal in both directions, since on the one hand it has been found that leptin regulates DA in response to sustained stress and eating behavior in humans, implicating involvement of DAergic pathways in this response, 34,35 and on the other hand a study in an experimental model showed that prolactin inhibits lipolysis and leptin release. 36 These discrepancies may be due to several factors, such as doses of DA and prolactin, experimental design, species, or sex. …”

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confidence: 99%

Effects of dopamine on leptin release and leptin gene (OB) expression in adipocytes from obese and hypertensive patients

Álvarez-Aguilar¹,

Alvarez-Paredes²,

Lindholm³

et al. 2013

IJNRD

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Background A reduction of dopaminergic (DAergic) activity with increased prolactin levels has been found in obese and hypertensive patients, suggesting its involvement as a pathophysiological mechanism promoting hypertension. Similarly, leptin action increasing sympathetic activity has been proposed to be involved in mechanisms of hypertension. The aim of this study was to analyze the effects of DA, norepinephrine (NE), and prolactin on leptin release and leptin gene ( OB ) expression in adipocytes from obese and hypertensive patients. Methods Leptin release and OB gene expression were analyzed in cultured adipocytes from 16 obese and hypertensive patients treated with DA (0.001, 0.01, 0.1, and 1.0 μmol/L), NE (1.0 μmol/L), insulin (0.1 μmol/L), and prolactin (1.0 μmol/L), and from five nonobese and normotensive controls treated with DA (1 μmol/L), NE (1 μmol/L), insulin (0.1 μmol/L), and prolactin (1.0 μmol/L). Results A dose-related reduction of leptin release and OB gene messenger ribonucleic acid expression under different doses of DA was observed in adipocytes from obese hypertensive patients. Whereas prolactin treatment elicited a significant increase of both leptin release and OB gene expression, NE reduced these parameters. Although similar effects of DA and NE were observed in adipocytes from controls, baseline values in controls were reduced to 20% of the value in adipocytes from obese hypertensive patients. Conclusion These results suggest that DAergic deficiency contributes to metabolic disorders linked to hyperleptinemia in obese and hypertensive patients.

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confidence: 99%

Effects of dopamine on leptin release and leptin gene (OB) expression in adipocytes from obese and hypertensive patients

Álvarez-Aguilar¹,

Alvarez-Paredes²,

Lindholm³

et al. 2013

IJNRD

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“…In all, our data suggest that hypophysectomy-induced effects on Rab18 mRNA expression may be mediated by the decrease in circulating thyroid hormones resulting from the lack of pituitary TSH. Nonetheless, we cannot exclude the possibility that other pituitary hormones (or lack thereof) not investigated in this study and known to act on adipose tissue, such as PRL (Brandebourg et al 2007), might also be responsible, at least in part, for the effects observed in hypophysectomized animals.…”

Section: Discussionmentioning

confidence: 87%

Nutritional, hormonal, and depot-dependent regulation of the expression of the small GTPase Rab18 in rodent adipose tissue

Pulido

Almabouada

Díaz‐Ruiz

et al. 2012

Journal of Molecular Endocrinology

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There is increasing evidence that proteins associated with lipid droplets (LDs) play a key role in the coordination of lipid storage and mobilization in adipocytes. The small GTPase, RAB18, has been recently identified as a novel component of the protein coat of LDs and proposed to play a role in both b-adrenergic stimulation of lipolysis and insulin-induced lipogenesis in 3T3-L1 adipocytes. In order to better understand the role of Rab18 in the regulation of lipid metabolism in adipocytes, we evaluated the effects of age, fat location, metabolic status, and hormonal milieu on Rab18 expression in rodent white adipose tissue (WAT). Rab18 mRNA was undetectable at postnatal day 15 (P15), but reached adult levels by P45, in both male and female rats. In adult rats, Rab18 immunolocalized around LDs, as well as within the cytoplasm of mature adipocytes. A weak Rab18 signal was also detected in the stromal-vascular fraction of WAT. In mice, fasting significantly increased, though with a distinct time-course pattern, Rab18 mRNA and protein levels in visceral and subcutaneous WAT. The expression of Rab18 was also increased in visceral and subcutaneous WAT of obese mice (diet-induced, ob/ob, and New Zealand obese mice) compared with lean controls. Rab18 expression in rats was unaltered by castration, adrenalectomy, or GH deficiency but was increased by hypophysectomy, as well as hypothyroidism. When viewed together, our results suggest the participation of Rab18 in the regulation of lipid processing in adipose tissue under both normal and pathological conditions.

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“…Although the majority of experimental studies have demonstrated the effect of prolactin in increasing leptin expression and secretion [36,37], data regarding an influence of leptin on prolactin production have been lacking. Therefore, future research is necessary to clarify the relationship between prolactin and leptin serum levels in euprolactinemic subjects.…”

Section: Discussionmentioning

confidence: 99%

Is prolactin the missing link in adipose tissue dysfunction of polycystic ovary syndrome patients?

Albu

Florea²,

Fica

2015

Endocrine

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The aims of the study were to evaluate whether adiposity was among the determinants of circulating prolactin levels and to determine whether serum prolactin independently predicted metabolic abnormalities in patients with polycystic ovary syndrome (PCOS). A total of 322 PCOS patients with normal serum prolactin levels were recruited between January 2007 and January 2014. Anthropometric, metabolic, and hormonal parameters were measured in all of the patients. HOMA-IR was calculated as an index of insulin resistance. Serum prolactin was negatively correlated with age (p < 0.0001), all the adiposity indices [body mass index p < 0.0001; waist circumference p < 0.0001; waist-hip ratio (WHR) p < 0.0001], visceral adiposity index (VAI, p = 0.043), fasting insulinemia (p = 0.002), and HOMA-IR (p = 0.002), and was positively correlated with serum adiponectin (p = 0.034), but not with circulating androgens or serum leptin levels. Serum adiponectin, but not HOMA-IR or fasting insulinemia, was independently associated with serum prolactin after adjustment for age, leptin, and anthropometrical adiposity parameters. Of the adiposity parameters, only WHR and VAI were independent predictors of serum prolactin after adjustment for adiponectin. Circulating prolactin was also negatively correlated with fasting glycemia (only in patients with normal glucose metabolism, p = 0.037) and was inversely correlated with the presence of metabolic syndrome (p < 0.001), but this association was not maintained after adjustment for possible confounders. In PCOS patients, serum prolactin level was related to adipose tissue quantity and function, and adiponectin was a possible mediator of this relationship. Low serum prolactin levels were associated with an unfavorable metabolic profile, but this association seemed to be due to the complex interplay among prolactin, adiposity, and insulin resistance rather than to a direct metabolic effect of prolactin.

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

Cited by 50 publications

References 35 publications

Effects of dopamine on leptin release and leptin gene (OB) expression in adipocytes from obese and hypertensive patients

Effects of dopamine on leptin release and leptin gene (OB) expression in adipocytes from obese and hypertensive patients

Nutritional, hormonal, and depot-dependent regulation of the expression of the small GTPase Rab18 in rodent adipose tissue

Is prolactin the missing link in adipose tissue dysfunction of polycystic ovary syndrome patients?

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