Inhibition of Uncoupling Protein Expression during Lactation: Role of Leptin

Xiao, Xiaoqiu; Grove, Kevin L.; Grayson, Bernadette E.; Smith, M. Susan

doi:10.1210/en.2003-0836

Cited by 62 publications

(46 citation statements)

References 52 publications

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“…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: 96%

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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Section: Discussionmentioning

confidence: 96%

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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“…Alternatively, OLETF rats may not reduce uncoupled proteins (UCPs) in this tissue (an energy-saving strategy characteristic of lactation). 9 During lactation, hypothalamic NPY/AGRP increases. 8,46 DMH NPY has been shown to be important in modulating lactation-associated hyperphagia.…”

Section: Discussionmentioning

confidence: 99%

“…7 Hyperphagia in lactating female rats is associated with decreased sensitivity to the satiety effects of CCK, 1 and with reduced blood leptin levels relative to nonlactating rats. [8][9][10][11] Although the hypoleptinemia should facilitate the hyperphagia of lactation, other orexigenic signals must also be involved. 12,13 During lactation, the amount of hypothalamic neuropeptide Y (NPY) increases 8 mainly in the DMH.…”

Section: Introductionmentioning

confidence: 99%

Adaptation to lactation in OLETF rats lacking CCK-1 receptors: body weight, fat tissues, leptin and oxytocin

et al. 2008

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Objective: To understand the adaptation to lactation of obese rats, by studying the interplay among the gut hormone cholecystokinin (CCK), the adiposity hormone leptin and the affiliation hormone oxytocin in modulating body mass and fat storage. Design: Strain differences were examined between Otsuka Long Evans Tokushima Fatty (OLETF) rats lacking expression of functional CCK-1 receptors and Long Evans Tokushima Otsuka (LETO) controls, tested as nulliparous dams, at the 7 and 15th lactation day, at weaning (lactation day 22) or 8 weeks postweaning. Measurements: We measured body mass, fat pads (brown, retroperitoneal and inguinal) and inguinal adipocytes. Plasma levels of leptin and oxytocin were determined. Results: Fat depots of LETO female rats were larger during lactation compared to the levels found in postweaning and nulliparous female rats. LETO female rats gained weight and accumulated fat during pregnancy and lactation, returning to their normal fat levels postweaning. In contrast, OLETF female rats presented lower body weight and fat depots during the lactation period than nulliparous dams, and regained the weight and fat postweaning. Plasma leptin and oxytocin were highly correlated and followed the same pattern. OLETF leptin levels were highly correlated with fat depot and inguinal cell surface. No significant correlation was found for LETO parameters. Conclusions: Pregnancy and lactation are energy-consuming events, which naturally induce female rats to increase food intake and accumulate fat. When challenged by the demands of rapidly growing preobese OLETF pups, OLETF dams' fat stores are reduced to lean, LETO levels. During lactation, sensitivity of the oxytocinergic neurons descending from the paraventricular nuclei to the nucleus of the solitary tract to CCK is reduced. We theorized that this pathway is not available to OLETF female rats that lack functional CCK-1 receptors to mediate the signal. The current study contributes to the understanding of the female body's adaptation to lactation.

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“…SYBR Green primers were designed using Primer Express Software from Applied Biosystems and the sequences are available upon request. Quantitative real-time PCR was performed as described previously, but with an additional dissociation step for SYBR Green analysis (Xiao et al 2004). All transcriptional levels were normalized to GAPDH and expressed as the fold change compared with CTR-LFD group.…”

Section: Rna Isolation and Real-time Rt-pcrmentioning

confidence: 99%

Neonatal overnutrition in mice exacerbates high-fat diet-induced metabolic perturbations

Liu¹,

Lim²,

Su³

et al. 2013

Journal of Endocrinology

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Neonatal overnutrition results in accelerated development of high-fat diet (HFD)-induced metabolic defects in adulthood. To understand whether the increased susceptibility was associated with aggravated inflammation and dysregulated lipid metabolism, we studied metabolic changes and insulin signaling in a chronic postnatal overnutrition (CPO) mouse model. Male Swiss Webster pups were raised with either three pups per litter to induce CPO or ten pups per litter as control (CTR) and weaned to either low-fat diet (LFD) or HFD. All animals were killed on the postnatal day 150 (P150) except for a subset of mice killed on P15 for the measurement of stomach weight and milk composition. CPO mice exhibited accelerated body weight gain and increased body fat mass prior to weaning and the difference persisted into adulthood under conditions of both LFD and HFD. As adults, insulin signaling was more severely impaired in epididymal white adipose tissue (WAT) from HFD-fed CPO (CPO-HFD) mice. In addition, HFD-induced upregulation of pro-inflammatory cytokines was exaggerated in CPO-HFD mice. Consistent with greater inflammation, CPO-HFD mice showed more severe macrophage infiltration than HFD-fed CTR (CTR-HFD) mice. Furthermore, when compared with CTR-HFD mice, CPO-HFD mice exhibited reduced levels of several lipogenic enzymes in WAT and excess intramyocellular lipid accumulation. These data indicate that neonatal overnutrition accelerates the development of insulin resistance and exacerbates HFD-induced metabolic defects, possibly by worsening HFD-induced inflammatory response and impaired lipid metabolism.

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Inhibition of Uncoupling Protein Expression during Lactation: Role of Leptin

Cited by 62 publications

References 52 publications

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

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

Adaptation to lactation in OLETF rats lacking CCK-1 receptors: body weight, fat tissues, leptin and oxytocin

Neonatal overnutrition in mice exacerbates high-fat diet-induced metabolic perturbations

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