Effects of pain controlling neuropeptides on human fat cell lipolysis

Harmelen, Vanessa van; Dicker, Andrea; Sjölin, Eva; Blomqvist, Lennart; Wirén, Mikael; Hoffstedt, Johan; Rydén, Mikael

doi:10.1038/ijo.2010.46

Cited by 15 publications

(12 citation statements)

References 31 publications

(53 reference statements)

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“…NPFF increases AGMO expression through NPFF receptor 2 (NPFFR2) by sustaining IL-4/STAT6 signaling (62). NPFFR2 is the main receptor for NPFF in AT (70,71), and its expression is restricted to ATMs (62). We found that the plasma concentration of NPFF in neonate mice was negligible and increased at weaning ( Figure 7D).…”

Section: Discussionmentioning

confidence: 87%

Breast milk alkylglycerols sustain beige adipocytes through adipose tissue macrophages

Yu¹,

Dilbaz²,

Coßmann³

et al. 2019

Journal of Clinical Investigation

164

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Section: Discussionmentioning

confidence: 87%

Breast milk alkylglycerols sustain beige adipocytes through adipose tissue macrophages

Yu¹,

Dilbaz²,

Coßmann³

et al. 2019

Journal of Clinical Investigation

164

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“…Appetite control is key in obesity development, and in vitro studies have shown that NPFF inhibits both human and murine adipocyte development (8,9). Peripheral tissues have negligible NPFF receptor expression, with the exception of AT, in which NPFF receptor 2 (NPFFR2, also known as GPR74, HG31, and NPFF2) is expressed (10,11). Genetic variance of NPFFR2 is closely associated with obesity status (12).…”

Section: Introductionmentioning

confidence: 99%

“…Genetic variance of NPFFR2 is closely associated with obesity status (12). Human plasma contains NPFF (13), and it is postulated that NPFF may be released from nerve endings in AT (11). However, the in vivo role of NPFF in AT function is unknown.…”

Section: Introductionmentioning

confidence: 99%

Neuropeptide FF increases M2 activation and self-renewal of adipose tissue macrophages

Waqas¹,

Hoang²,

Lin³

et al. 2017

Journal of Clinical Investigation

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The quantity and activation state of adipose tissue macrophages (ATMs) impact the development of obesity-induced metabolic diseases. Appetite-controlling hormones play key roles in obesity; however, our understanding of their effects on ATMs is limited. Here, we have shown that human and mouse ATMs express NPFFR2, a receptor for the appetite-reducing neuropeptide FF (NPFF), and that NPFFR2 expression is upregulated by IL-4, an M2-polarizing cytokine. Plasma levels of NPFF decreased in obese patients and high-fat diet-fed mice and increased following caloric restriction. NPFF promoted M2 activation and increased the proliferation of murine and human ATMs. Both M2 activation and increased ATM proliferation were abolished in NPFFR2-deficient ATMs. Mechanistically, the effects of NPFF involved the suppression of E3 ubiquitin ligase RNF128 expression, resulting in enhanced stability of phosphorylated STAT6 and increased transcription of the M2 macrophage-associated genes IL-4 receptor α (Il4ra), arginase 1 (Arg1), IL-10 (Il10), and alkylglycerol monooxygenase (Agmo). NPFF induced ATM proliferation concomitantly with the increase in N-Myc downstream-regulated gene 2 (Ndrg2) expression and suppressed the transcription of Ifi200 cell-cycle inhibitor family members and MAF bZIP transcription factor B (Mafb), a negative regulator of macrophage proliferation. NPFF thus plays an important role in supporting healthy adipose tissue via the maintenance of metabolically beneficial ATMs.

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“…These findings are in agreement with earlier observations in chicks and rat ( 32 , 43 ) and suggest that GnIH is one of the orexigenic peptide in mammals. An earlier study has demonstrated the presence of RFRP-3 receptor (GPR147) in the adipose tissue ( 44 ). The GnIH containing neurons was shown in contact with the neurons containing neuropeptides, such as neuropeptideY, pro-opio melanocortin, orexin, and melanopeptide, which are known modulators of nutritional changes ( 28 , 45 , 46 ).…”

Section: Discussionmentioning

confidence: 99%

Possible Role of GnIH as a Mediator between Adiposity and Impaired Testicular Function

2016

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The aim of the present study was to evaluate the roles of gonadotropin-inhibitory hormone (GnIH) as an endocrine link between increasing adiposity and impaired testicular function in mice. To achieve this, the effect of GnIH on changes in nutrients uptake and hormonal synthesis/action in the adipose tissue and testis was investigated simultaneously by in vivo study and separately by in vitro study. Mice were treated in vivo with different doses of GnIH for 8 days. In the in vitro study, adipose tissue and testes of mice were cultured with different doses of GnIH with or without insulin or LH for 24 h at 37°C. The GnIH treatment in vivo showed increased food intake, upregulation of glucose transporter 4 (GLUT4), and increased uptake of triglycerides (TGs) in the adipose tissue. These changes may be responsible for increased accumulation of fat in white adipose tissue, resulting in increase in the body mass. Contrary to the adipose tissue, treatment with GnIH both in vivo and in vitro showed decreased uptake of glucose by downregulation of glucose transporter 8 (GLUT8) expressions in the testis, which in turn resulted in the decreased synthesis of testosterone. The GnIH treatment in vivo also showed the decreased expression of insulin receptor protein in the testis, which may also be responsible for the decreased testicular activity in the mice. These findings thus suggest that GnIH increases the uptake of glucose and TGs in the adipose tissue, resulting in increased accumulation of fat, whereas simultaneously in the testis, GnIH suppressed the GLUT8-mediated glucose uptake, which in turn may be responsible for decreased testosterone synthesis. This study thus demonstrates GnIH as mediator of increasing adiposity and impaired testicular function in mice.

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Effects of pain controlling neuropeptides on human fat cell lipolysis

Cited by 15 publications

References 31 publications

Breast milk alkylglycerols sustain beige adipocytes through adipose tissue macrophages

Breast milk alkylglycerols sustain beige adipocytes through adipose tissue macrophages

Neuropeptide FF increases M2 activation and self-renewal of adipose tissue macrophages

Possible Role of GnIH as a Mediator between Adiposity and Impaired Testicular Function

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