Modulation of food intake by mTOR signalling in the dorsal motor nucleus of the vagus in male rats: focus on ghrelin and nesfatin‐1

Zhang, Weizhen; Zhang, Chao; Fritze, Danielle; Chai, Biaoxin; Li, Jiyao; Mulholland, Michael W.

doi:10.1113/expphysiol.2013.074930

Cited by 30 publications

(25 citation statements)

References 29 publications

(50 reference statements)

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“…Therefore, reduction in mTOR signaling may contribute to the stimulatory action of nesfatin-1 on brown adipocyte differentiation. Consistent with this observation, nesfatin-1 has been demonstrated to inhibit mTOR signaling in the dorsal motor nucleus of the vagus33 and to activate AMPK signaling in hepatocytes17. Activation of AMPK is well recognized to inhibit mTOR signaling in a variety of cell type34.…”

Section: Discussionmentioning

confidence: 57%

Nesfatin-1 promotes brown adipocyte phenotype

Wang

Zhang

et al. 2016

Sci Rep

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Nesfatin-1, an 82 amino acid gastric peptide, is involved in regulation of food uptake and in multiple metabolic activities. Whether nesfatin-1 modulates the differentiation and lipid metabolism of brown adipocytes remains unknown. In the present study, we found that nesfatin-1 mRNA and protein were detectable in isolated brown adipocytes and gradually decreased during differentiation (95% CI 0.6057 to 1.034, p = 0.0001). The decrease in nesfatin-1 was associated with a significant reduction in p-S6. Exposure to nesfatin-1 promoted differentiation of brown adipocytes as revealed by a significant increase in UCP1 mRNA (p = 0.03) and lipolysis-related ATGL mRNA (p = 0.04). Nesfatin-1 attenuated phosphorylation of S6K and S6 during brown adipocyte differentiation. Activation of mTOR by leucine or deletion of TSC1 decreased expression of brown adipocyte-related genes UCP1, UCP3, PGC1α and PRDM16, as well as COX8B and ATP5B. Both leucine and TSC1 deletion blocked nesfatin-1-induced up-regulation of UCP1, PGC1α, COX8B and ATP5B in differentiated brown adipocytes. In conclusion, nesfatin-1 promotes the differentiation of brown adipocytes likely through the mTOR dependent mechanism.

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Section: Discussionmentioning

confidence: 57%

Nesfatin-1 promotes brown adipocyte phenotype

Wang

Zhang

et al. 2016

Sci Rep

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“…We also detected signal in the dorsal part of the dorsal motor nucleus of the vagus nerve (DMX; Fig. B), which is involved in the control of food intake (Williams et al, ; Zhang et al, ) and in gastric function (Washabau et al, ; Krowicki et al, ). Finally, we detected Hoxa5 labeling in the gracile nucleus (GR) as well as in its counterpart in the somatosensory system, the cuneate nucleus, carrying proprioceptive and touch sensation from the upper and lower body, respectively (Fig.…”

Section: Resultsmentioning

confidence: 89%

HOXA5 localization in postnatal and adult mouse brain is suggestive of regulatory roles in postmitotic neurons

Lizen

Hutlet

Bissen

et al. 2016

J of Comparative Neurology

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Hoxa5 is a member of the Hox gene family, which plays critical roles in successive steps of the central nervous system formation during embryonic and fetal development. Hoxa5 expression in the adult mouse brain has been reported, suggesting that this gene may be functionally required in the brain after birth. To provide further insight into the Hoxa5 expression pattern and potential functions in the brain, we have characterized its neuroanatomical profile from embryonic stages to adulthood. While most Hox mapping studies have been based solely on transcript analysis, we extended our analysis to HOXA5 protein localization in adulthood using specific antibodies. Our results show that Hoxa5 expression appears in the most caudal part of the hindbrain at fetal stages, where it is maintained until adulthood. In the medulla oblongata and pons, we detected Hoxa5 expression in many precerebellar neurons and in several nuclei implicated in the control of autonomic functions. In these territories, the HOXA5 protein is present solely in neurons, specifically in γ-aminobutyric acid (GABA)ergic, glutamatergic, and catecholaminergic neurons. Finally, we also detected Hoxa5 transcripts, but not the HOXA5 protein, in the thalamus and the cortex, from postnatal stages to adult stages, and in the cerebellum at adulthood. We provide evidence that some larger variants of Hoxa5 transcripts are present in these territories. Our mapping analysis allowed us to build hypotheses regarding HOXA5 functions in the nervous system after birth, such as a potential role in the establishment and refinement/plasticity of precerebellar circuits during postnatal and adult life. J. Comp. Neurol. 525:1155-1175, 2017. © 2016 Wiley Periodicals, Inc.

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“…mTOR had been shown to integrate immune microenvironment with the differentiation of T cells [ 20 ]. Ghrelin, which plays an important role in energy homeostasis, has been reported to regulate mTOR signaling [ 25 , 26 , 27 ]. We therefore analyzed the phosphorylation of S6, the downstream molecule of mTOR, in GHSR1a -/- T cells.…”

Section: Resultsmentioning

confidence: 99%

Ghrelin Inhibits the Differentiation of T Helper 17 Cells through mTOR/STAT3 Signaling Pathway

Yin

et al. 2015

PLoS ONE

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Enhanced activity of interleukin 17 (IL-17) producing T helper 17 (Th17) cells plays an important role in autoimmune and inflammatory diseases. Significant loss of body weight and appetite is associated with chronic inflammation and immune activation, suggesting the cross talk between immune and neuroendocrine systems. Ghrelin has been shown to regulate the organism immune function. However, the effects of ghrelin on the differentiation of Th17 cells remain elusive. In the present study, we observed the enhanced differentiation of Th17 cells in spleens of growth hormone secretagogue receptor 1a (GHSR1a)-/- mice. Treatment of ghrelin repressed Th17 cell differentiation in a time- and concentration-dependent manner. Phosphorylation of mammalian target of rapamycin (mTOR) and signal transducer and activator of transcription 3 (STAT3) was increased in the spleens of GHSR1a-/- mice. Activation of mTOR signaling by injection of Cre-expressiong adenovirus into tuberous sclerosis complex 1 (TSC1) loxp/loxp mice increased the differentiation of Th17 cells in spleen, which was associated with an increment in the phosphorylation of STAT3. Activation of mTOR signaling by leucine or overexpression of p70 ribosome protein subunit 6 kinase 1 (S6K1) activated mTOR signaling in isolated T cells, while reversed the ghrelin-induced inhibition of iTh17 cell differentiation. In conclusion, mTOR mediates the inhibitory effect of ghrelin on the differentiation of Th17 cells by interacting with STAT3.

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Modulation of food intake by mTOR signalling in the dorsal motor nucleus of the vagus in male rats: focus on ghrelin and nesfatin‐1

Cited by 30 publications

References 29 publications

Nesfatin-1 promotes brown adipocyte phenotype

Nesfatin-1 promotes brown adipocyte phenotype

HOXA5 localization in postnatal and adult mouse brain is suggestive of regulatory roles in postmitotic neurons

Ghrelin Inhibits the Differentiation of T Helper 17 Cells through mTOR/STAT3 Signaling Pathway

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