Nesfatin-1 promotes brown adipocyte phenotype

Wang, Yuexin; Li, Ziru; Zhang, Xinyu; Xiang, Xinxin; Li, Yin; Mulholland, Michael W.; Zhang, Weizhen

doi:10.1038/srep34747

Cited by 24 publications

(18 citation statements)

References 43 publications

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“…Compatible with these findings, nesfatin-1 treatment promotes Atgl as well as Ucp1 and Pgc1a mRNA expression in brown adipocytes in vitro (Wang et al 2016), thus implying that nesfatin-1 can also act peripherally to control lipid utilization and iBAT thermogenesis. Interestingly, it was also reported in the same study that nesfatin-1 is produced by brown adipocytes, suggesting autocrine regulation (Wang et al 2016). However, to what extent locally produced or circulating nesfatin-1 contributes to iBAT thermogenesis remains to be investigated.…”

Section: :2supporting

confidence: 58%

“…However, the latter can be induced by peripheral nesfatin-1 administration, as it was inferred from a decrease in the respiratory quotient in indirect calorimetry (Mortazavi et al 2015). Compatible with these findings, nesfatin-1 treatment promotes Atgl as well as Ucp1 and Pgc1a mRNA expression in brown adipocytes in vitro (Wang et al 2016), thus implying that nesfatin-1 can also act peripherally to control lipid utilization and iBAT thermogenesis. Interestingly, it was also reported in the same study that nesfatin-1 is produced by brown adipocytes, suggesting autocrine regulation (Wang et al 2016).…”

Section: :2mentioning

confidence: 74%

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The thermogenic effect of nesfatin-1 requires recruitment of the melanocortin system

Dore

Levata

Gachkar

et al. 2017

Journal of Endocrinology

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Nesfatin-1 is a bioactive polypeptide expressed both in the brain and peripheral tissues and involved in the control of energy balance by reducing food intake. Central administration of nesfatin-1 significantly increases energy expenditure, as demonstrated by a higher dry heat loss; yet, the mechanisms underlying the thermogenic effect of central nesfatin-1 remain unknown. Therefore, in this study, we sought to investigate whether the increase in energy expenditure induced by nesfatin-1 is mediated by the central melanocortin pathway, which was previously reported to mediate central nesfatin-1´s effects on feeding and numerous other physiological functions. With the application of direct calorimetry, we found that intracerebroventricular nesfatin-1 (25 pmol) treatment increased dry heat loss and that this effect was fully blocked by simultaneous administration of an equimolar dose of the melanocortin 3/4 receptor antagonist, SHU9119. Interestingly, the nesfatin-1-induced increase in dry heat loss was positively correlated with body weight loss. In addition, as assessed with thermal imaging, intracerebroventricular nesfatin-1 (100 pmol) increased interscapular brown adipose tissue (iBAT) as well as tail temperature, suggesting increased heat production in the iBAT and heat dissipation over the tail surface. Finally, nesfatin-1 upregulated pro-opiomelanocortin and melanocortin 3 receptor mRNA expression in the hypothalamus, accompanied by a significant increase in iodothyronine deiodinase 2 and by a nonsignificant increase in uncoupling protein 1 and peroxisome proliferator-activated receptor gamma coactivator-1 alpha mRNA in the iBAT. Overall, we clearly demonstrate that nesfatin-1 requires the activation of the central melanocortin system to increase iBAT thermogenesis and, in turn, overall energy expenditure.

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Section: :2supporting

confidence: 58%

Section: :2mentioning

confidence: 74%

The thermogenic effect of nesfatin-1 requires recruitment of the melanocortin system

Dore

Levata

Gachkar

et al. 2017

Journal of Endocrinology

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“…Consistently, increase of nesfatin‐1 has been detected in TG mice in which mTOR signaling is activated specifically in X/A‐like cells (data not shown). In addition, we have demonstrated that nesfatin‐1 promotes the differentiation of brown adipocytes . However, until the receptor for nesfatin‐1 is characterized, it is not possible to efficiently block the action of nesfatin‐1, and therefore to confirm that increase of nesfatin‐1 in TG mice contributes to metabolic effects in TG mice.…”

Section: Discussionmentioning

confidence: 96%

mTOR Signaling in X/A‐Like Cells Contributes to Lipid Homeostasis in Mice

Yin

et al. 2018

Hepatology

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Gastric mechanistic target of rapamycin (mTOR) signaling is inversely associated with the expression and secretion of ghrelin, a 28-aa peptide hormone produced by gastric X/A-like cells. Ghrelin contributes to obesity and hepatic steatosis. We sought to control global lipid metabolism through manipulating gastric mTOR signaling in X/A-like cells METHODS: We established a ghrl-cre transgene in which the cre enzyme is expressed in X/A-like cells under the control of the ghrelin-promoter. mTOR and TSC1 mice were separately bred with ghrl-cre mice to generate mTOR-ghrl-cre (mG) or TSC1-ghrl-cre (TG) mice, within which mTOR signaling was suppressed or activated respectively. Lipid metabolism in liver and adipose depots was analyzed RESULTS: Under the control of the ghrelin-promoter, cre enzyme is exclusively expressed in stomach X/A-like cells in adult animals. Knockout of mTOR in X/A-like cells increased circulating acyl-ghrelin and promoted hepatic lipogenesis with effects on adipose depots. Activation of mTOR signaling by deletion of its upstream inhibitor, tuberous sclerosis 1 (TSC1), decreased ghrelin expression and secretion, altering lipid metabolism as evidenced by resistance to high fat diet-induced obesity and hepatic steatosis. Both ghrelin administration and rapamycin, an inhibitor of mTOR, altered the phenotypes of TG mice CONCLUSION: Gastric mTOR signaling in X/A-like cells contributes to organism lipid homeostasis by regulating hepatic and adipose lipid metabolism. Gastric mTOR signaling may provide an alternative strategy for intervention in lipid disorders. This article is protected by copyright. All rights reserved.

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“…Activation of mTOR induced by leucine or deletion of TSC1 decreased expression of the brown adipocyterelated genes UCP1, UCP3, PGC-1α and PRDM16, as well as COX8B and ATP5B. Both leucine and TSC1 deletion blocked nesfatin-1-induced up-regulation of UCP1, PGC-1α, COX8B and ATP5B expression in differentiated brown adipocytes (Wang et al, 2016). The results of the present study showed a significant and positive correlation between PGC-1α gene expression and serum levels of nesfatin-1, which is probably because of mTOR activator elements, as mentioned above.…”

Section: Discussionmentioning

confidence: 96%

“…Intracerebroventricular injection of nesfatin-1 inhibits food intake in a dose-dependent manner, resulting in a decrease in total body fat and body mass loss, while anti-nesfatin-1 increases the intake of food in male rats (Oh et al, 2006). It was reported that nesfatin-1 promotes the differentiation of brown adipocytes through PGC-1α (Wang et al, 2016). Hypothalamic resistin seems to be a key regulator of the brain-fat axis which regulates energy homeostasis (Rodríguez et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Eccentric resistance training and β-Hydroxy-β-methylbutyrate free acid affects muscle PGC-1α expression and serum irisin, nesfatin-1 and resistin

Shirvani

Rahmati-Ahmadabad

Broom

et al. 2019

Journal of Experimental Biology

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The hypothalamus controls metabolism and feeding behaviour via several signals with other tissues. Exercise and supplements can change hypothalamic signalling pathways, so the present study investigated the influence of eccentric resistance training and β-hydroxy-β-methylbutyrate free acid supplementation on PGC-1α expression, serum irisin, nesfatin-1 and resistin concentrations. Thirty-two male rats (8 weeks old, 200±17 g body mass) were randomly allocated to control, β-hydroxy-β-methylbutyrate free acid supplementation (HMB), eccentric resistance training (ERT), and β-hydroxy-β-methylbutyrate free acid supplementation plus eccentric resistance training (HMB+ERT) groups. Training groups undertook eccentric resistance training (6 weeks, 3 times a week) and supplement groups consumed β-hydroxy-β-methylbutyrate free acid (HMB-FA) orally (76 mg kg −1 day −1 ). Twenty-four hours after the last training session, serum and triceps brachii muscle samples were collected and sent to the laboratory for analysis. Two-way ANOVA and Pearson correlation were employed (significance level: P<0.05). The results showed that eccentric resistance training increases skeletal muscle PGC-1α gene expression, as well as serum levels of irisin and nesfatin-1 (P=0.001). Eccentric resistance training decreased the serum concentration of resistin (P=0.001). HMB-FA supplementation increased skeletal muscle PGC-1α gene expression (P=0.002), as well as the serum concentration of irisin and nesfatin-1 (P=0.001), but decreased the serum concentration of resistin (P=0.001). Significant correlations were observed between PGC-1α gene expression and serum concentrations of irisin, nesfatin-1 and resistin. HMB-FA supplementation with eccentric resistance training may induce crosstalk between peptide release from other tissues and increases maximal muscle strength. The combination of the two interventions had a more substantial effect than each in isolation.

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Nesfatin-1 promotes brown adipocyte phenotype

Cited by 24 publications

References 43 publications

The thermogenic effect of nesfatin-1 requires recruitment of the melanocortin system

The thermogenic effect of nesfatin-1 requires recruitment of the melanocortin system

mTOR Signaling in X/A‐Like Cells Contributes to Lipid Homeostasis in Mice

Eccentric resistance training and β-Hydroxy-β-methylbutyrate free acid affects muscle PGC-1α expression and serum irisin, nesfatin-1 and resistin

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