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Gastric mechanosensitive channel Piezo1 regulates ghrelin production and food intake

Nature Metabolism volume 6, pages 458–472 (2024)Cite this article

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Abstract

Ghrelin, produced mainly by gastric X/A-like cells, triggers a hunger signal to the central nervous system to stimulate appetite. It remains unclear whether X/A-like cells sense gastric distention and thus regulate ghrelin production. Here we show that PIEZO1 expression in X/A-like cells decreases in patients with obesity when compared to controls, whereas it increases after sleeve gastrectomy. Male and female mice with specific loss of Piezo1 in X/A-like cells exhibit hyperghrelinaemia and hyperphagia and are more susceptible to overweight. These phenotypes are associated with impairment of the gastric CaMKKII/CaMKIV–mTOR signalling pathway. Activation of PIEZO1 by Yoda1 or gastric bead implantation inhibits ghrelin production, decreases energy intake and induces weight loss in mice. Inhibition of ghrelin production by Piezo1 through the CaMKKII/CaMKIV–mTOR pathway can be recapitulated in a ghrelin-producing cell line mHypoE-42. Our study reveals a mechanical regulation of ghrelin production and appetite by PIEZO1 of X/A-like cells, which suggests a promising target for anti-obesity therapy.

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Fig. 1: Expression of Piezo1 in human and mouse gastric mucosa.
Fig. 2: Gastric X/A-like cell-specific Piezo1 knockout mice presented hyperghrelinaemia and body weight gain.
Fig. 3: Ghrl-Piezo1−/− mice are more susceptible to obesity under HFD feeding, which can be blocked by D-Lys-3-GHRP-6.
Fig. 4: Pharmacological stimulation of gastric PIEZO1 inhibits ghrelin production and food intake.
Fig. 5: Inhibition of ghrelin production and ingestive behaviour by gastric bead implantation in both NCD- and HFD-fed mice.
Fig. 6: Yoda1 inhibited, whereas GsMTx4 stimulated ghrelin production in mHypoE-42 cells.
Fig. 7: Genetic and mechanical interference of PIEZO1 regulates ghrelin production in mHypoE-42 cells.
Fig. 8: Modulation of Ghrelin production by CaMKKII/CaMKIV–mTOR signalling in mHypoE-42 cells.

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Data availability

The data that support the findings of this study are available within the paper and Supplementary Information. Source data for Figs. 1–8 and Extended Data Figs. 1–10 are provided with the online version of the paper. Source data are provided with this paper.

References

  1. Hall, K. D. et al. Quantification of the effect of energy imbalance on body weight. Lancet 378, 826–837 (2011).

    Article  PubMed  Google Scholar 

  2. Schwartz, M. W., Woods, S. C., Porte, D., Seeley, R. J. & Baskin, D. G. Central nervous system control of food intake. Nature 404, 661–671 (2000).

    Article  CAS  PubMed  Google Scholar 

  3. De, C. et al. A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans. Diabetes 50, 1714–1719 (2001).

    Article  Google Scholar 

  4. Kojima, M. et al. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature 402, 656–660 (1999).

    Article  CAS  PubMed  Google Scholar 

  5. Cummings, D. E. et al. Elevated plasma ghrelin levels in Prader Willi syndrome. Nat. Med. 8, 643–644 (2002).

    Article  CAS  PubMed  Google Scholar 

  6. Muscogiuri, G. et al. Prader–Willi syndrome: an uptodate on endocrine and metabolic complications. Rev. Endocr. Metab. Disord. 20, 239–250 (2019).

    Article  PubMed  Google Scholar 

  7. Nakazato, M. et al. A role for ghrelin in the central regulation of feeding. Nature 409, 194–198 (2001).

    Article  CAS  PubMed  Google Scholar 

  8. Wren, A. M. et al. Ghrelin enhances appetite and increases food intake in humans. J. Clin. Endocrinol. Metab. 86, 5992 (2001).

    Article  CAS  PubMed  Google Scholar 

  9. Kobelt, P. et al. Anti-ghrelin Spiegelmer NOX-B11 inhibits neurostimulatory and orexigenic effects of peripheral ghrelin in rats. Gut 55, 788–792 (2006).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Altabas, V. & Zjačić-Rotkvić, V. Anti-ghrelin antibodies in appetite suppression: recent advances in obesity pharmacotherapy. ImmunoTargets Ther. 4, 123–130 (2015).

    PubMed  PubMed Central  Google Scholar 

  11. Kojima, M. & Kangawa, K. Ghrelin: structure and function. Physiol. Rev. 85, 495–522 (2005).

  12. Müller, T. D. et al. Ghrelin. Mol. Metab. 4, 437–460 (2015).

    Article  PubMed  PubMed Central  Google Scholar 

  13. Xu, G. et al. Gastric mammalian target of rapamycin signaling regulates ghrelin production and food intake. Endocrinology 150, 3637–3644 (2009).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  14. Camilleri, M. Peripheral mechanisms in appetite regulation. Gastroenterology 148, 1219–1233 (2015).

    Article  CAS  PubMed  Google Scholar 

  15. Coste, B. et al. Piezo proteins are pore-forming subunits of mechanically activated channels. Nature 483, 176–181 (2012).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Wu, J., Lewis, A. H. & Grandl, J. Touch, tension, and transduction: the function and regulation of piezo ion channels. Trends Biochem. Sci. 42, 57–71 (2017).

    Article  PubMed  Google Scholar 

  17. Murthy, S. E., Dubin, A. E. & Patapoutian, A. Piezos thrive under pressure: mechanically activated ion channels in health and disease. Nat. Rev. Mol. Cell Biol. 18, 771–783 (2017).

    Article  CAS  PubMed  Google Scholar 

  18. Min, S. et al. Control of feeding by Piezo-mediated gut mechanosensation in Drosophila. eLife 10, e63049 (2021).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  19. Hughes, K. et al. Distinct mechanoreceptor pezo-1 isoforms modulate food intake in the nematode Caenorhabditis elegans. G3 Bethesda Md 12, jkab429 (2022).

    Article  CAS  PubMed  Google Scholar 

  20. Ye, Y. et al. A critical role of the mechanosensor PIEZO1 in glucose-induced insulin secretion in pancreatic β-cells. Nat. Commun. 13, 4237 (2022).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  21. Sugisawa, E. et al. RNA sensing by gut Piezo1 is essential for systemic serotonin synthesis. Cell 182, 609–624 (2020).

    Article  CAS  PubMed  Google Scholar 

  22. Li, Z. et al. mTOR signaling in X/A-like cells contributes to lipid homeostasis in mice. Hepatology 69, 860–875 (2019).

    Article  CAS  PubMed  Google Scholar 

  23. Ellefsen, K. L. et al. Myosin-II mediated traction forces evoke localized Piezo1-dependent Ca2+ flickers. Commun. Biol. 2, 298 (2019).

    Article  PubMed  PubMed Central  Google Scholar 

  24. Marcelo, K. L., Means, A. R. & York, B. The Ca(2+)/calmodulin/CaMKK2 axis: nature’s metabolic CaMshaft. Trends Endocrinol. Metab. 27, 706–718 (2016).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Tokumitsu, H. & Sakagami, H. Molecular mechanisms underlying Ca2+/calmodulin-dependent protein kinase kinase signal transduction. Int. J. Mol. Sci. 23, 11025 (2022).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  26. Lin, F. et al. The camKK2/camKIV relay is an essential regulator of hepatic cancer. Hepatology 62, 505–520 (2015).

    Article  CAS  PubMed  Google Scholar 

  27. Berthoud, H. R. & Morrison, C. The brain, appetite, and obesity. Annu. Rev. Psychol. 59, 55–92 (2008).

    Article  PubMed  Google Scholar 

  28. Tremblay, A. & Bellisle, F. Nutrients, satiety, and control of energy intake. Appl. Physiol. Nutr. Metab. Physiol. 40, 971–979 (2015).

    Article  Google Scholar 

  29. Wren, A. M. & Bloom, S. R. Gut hormones and appetite control. Gastroenterology 132, 2116–2130 (2007).

    Article  CAS  PubMed  Google Scholar 

  30. Buhmann, H., le Roux, C. W. & Bueter, M. The gut–brain axis in obesity. Best. Pract. Res. Clin. Gastroenterol. 28, 559–571 (2014).

    Article  CAS  PubMed  Google Scholar 

  31. Andrews, Z. B. et al. UCP2 mediates ghrelin’s action on NPY/AgRP neurons by lowering free radicals. Nature 454, 846–851 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  32. Yin, X., Li, Y., Xu, G., An, W. & Zhang, W. Ghrelin fluctuation, what determines its production? Acta Biochim. Biophys. Sin. 41, 188–197 (2009).

    Article  CAS  PubMed  Google Scholar 

  33. Wang, P., Jia, Y., Liu, T., Jan, Y.-N. & Zhang, W. Visceral mechano-sensing neurons control Drosophila feeding by using Piezo as a sensor. Neuron 108, 640–650 (2020).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  34. Gaur, S., Levy, S., Mathus-Vliegen, L. & Chuttani, R. Balancing risk and reward: a critical review of the intragastric balloon for weight loss. Gastrointest. Endosc. 81, 1330–1336 (2015).

    Article  PubMed  Google Scholar 

  35. Anderson, K. A. et al. Hypothalamic CaMKK2 contributes to the regulation of energy balance. Cell Metab. 7, 377–388 (2008).

    Article  CAS  PubMed  Google Scholar 

  36. Xu, G. et al. Ghrelin contributes to derangements of glucose metabolism induced by rapamycin in mice. Diabetologia 55, 1813–1823 (2012).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

Download references

Acknowledgements

We thank J. Guo (The Chinese University of Hong Kong) for providing the Piezo1 plasmid and J. Lyu from Jinan University for providing CaMKKII and CaMKIV plasmids.

This work was supported by grants from the National Natural Science Foundation of China (82170818 and 81770794) and the Fundamental Research Funds for the Central Universities (21620423) to G.X.

Author information

Authors and Affiliations

  1. Department of Physiology, School of Medicine, Jinan University, Guangzhou, China

    Yawen Zhao, Yang Liu, Tian Tao, Jinshan Zhang, Wenying Guo, Handan Deng, Mengxue Han, Haocong Mo, Xiaohan Tong, Song Lin & Geyang Xu

  2. Department of Pathology, School of Basic Medicine, Guangzhou Medical University, Guangzhou, China

    Jie Yang

  3. Endoscopy Center, The First Affiliated Hospital of Jinan University, Guangzhou, China

    Hening Zhai

  4. Biotherapy Center; Cell-gene Therapy Translational Medicine Research Center, the Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China

    Qimeng Wang & Hui Chen

  5. Guangdong-Hongkong-Macau CNS Regeneration Institute of Jinan University, Key Laboratory of CNS Regeneration (Jinan University)-Ministry of Education, Guangzhou, China

    Zhengfang Hu

  6. Department of Physiology and Pathophysiology, Peking University Health Science Center, Beijing, China

    Weizhen Zhang

  7. Key Laboratory of Viral Pathogenesis & Infection Prevention and Control (Jinan University), Ministry of Education, Guangzhou, China

    Geyang Xu

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  1. Yawen Zhao
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Contributions

G.X. and W.Z. designed the research. Y.Z., Y.L., T.T., J.Z., W.G., H.D., M.H., H.M., X.T., S.L., J.Y., H.Z., Q.W., H.C. and Z.H. conducted the study. Y.Z., H.C. and G.X. analysed data. G.X., H.C. and Y.Z. wrote and edited the paper. All authors contributed to the discussion, revised the paper and approved the final versions of the paper. G.X. is responsible for the integrity of the work as a whole.

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Correspondence to Hui Chen or Geyang Xu.

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Nature Metabolism thanks Melanie Kaelberer and the other, anonymous, reviewer(s) for their contribution to the peer review of this work. Primary Handling Editor: Ashley Castellanos-Jankiewicz, in collaboration with the Nature Metabolism team.

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Extended data

Extended Data Fig. 1 Body weight of pubs of control and Ghrl-Piezo1-/- mice.

a, A representative photograph showing 1-week-old Ghrl-Cre, Piezo1fl/fl, and Ghrl-Piezo1-/- mice. b, Genotyping PCR results for control and Ghrl-Piezo1-/- mice. Representative images of three replicates. c, Body weight of control and Ghrl-Piezo1-/- mice at one- and two- week after born (both male and females, n = 6 mice per group). Data are shown as mean values ± SEM, and are representative of six biological replicates, P values were calculated by one-way ANOVA with Tukey post-hoc test.

Source data

Extended Data Fig. 2 Glucose metabolism in male control and Ghrl-Piezo1-/- mice.

a, Intraperitoneal Glucose Tolerance Test (IPGTT) and associated area under the curve (AUC) values of Piezo1fl/fl and Ghrl-Piezo1-/- mice under NCD (n = 5 mice per group). b, Insulin tolerance tests (ITT) and AUC of Piezo1fl/fl and Ghrl-Piezo1-/- mice under NCD (n = 5 mice per group). Data are shown as mean values ± SEM, and are representative of five biological replicates, P values were calculated by two-sided t-tests. *p < 0.05, **p < 0.01, ***p < 0.001. c, IPGTT and AUC values of Piezo1fl/fl and Ghrl-Piezo1-/- mice under HFD (n = 6 mice per group). d, Insulin tolerance tests (ITT) and AUC values of Piezo1fl/fl and Ghrl-Piezo1-/- mice under HFD. Date are expressed as mean values ± SEM. Student’s t-test was used for comparison between two groups (n = 6 mice per group). Data are shown as mean values ± SEM, and are representative of six biological replicates, P values were calculated by two-sided t-tests.

Source data

Extended Data Fig. 3 Double immunofluorescence staining of pCaMKIV and GHRELIN in the mouse gastric mucosa of Piezo1fl/fl and Ghrl-Piezo1-/- mice under NCD.

a, Co-localization of pCaMKIV(red) and GHRELIN (green) in the mouse gastric mucosa of Piezo1fl/fl and Ghrl-Piezo1-/- mice under NCD (n = 6 mice per group). b, Quantitative analysis of pCaMKIV-positive X/A-like cells in the stomach of male mice. 294 Piezo1-positive cells and 177 Ghrelin-positive cells from six control mice, 241 pCaMKIV-positive cells and 295 Ghrelin-positive cells from six Ghrl-Piezo1-/- mice were quantified (n = 6 mice per group). c, Quantitative analysis of ghrelin intensity. Three typical images from each mice (six Piezo1fl/fl and six Ghrl-Piezo1-/- mice) were chose for quantitative analysis of ghrelin intensity (n = 6 mice per group). Data are shown as mean values ± SEM, and are representative of six biological replicates, P values were calculated by two-sided t-tests, *p < 0.05, **p < 0.01, ***p < 0.001,****p < 0.0001.

Source data

Extended Data Fig. 4 Quantitative analysis of Piezo1 and ghrelin in the gastric mucosa of Piezo1fl/fl and Ghrl-Piezo1-/- mice under NCD in Fig. 2k,l.

a, Quantitative analysis of Piezo1-positive X/A-like cells in the stomach of male mice under NCD. 342 Piezo1-positive cells and 153 ghrelin-positive cells from 6 Piezo1fl/fl mice, 305 Piezo1-positive cells and 271 Ghrelin-positive cells from 6 Ghrl-Piezo1-/- mice were quantified for double-labelling immunofluorescence (n = 6 mice per group). 325 Piezo1-positive cells and 145 Ghrelin-positive cells from six control mice, 297 Piezo1-positive cells and 245 Ghrelin-positive cells from six Ghrl-Piezo1-/- mice were quantified for in situ hybridization. b, Quantitative analysis of ghrelin intensity in the stomach of mice of indicated genotypes fed NCD. Three view from each mice (six Piezo1fl/fl and six Ghrl-Piezo1-/- mice) were chose for quantitative analysis of ghrelin intensity (n = 6 mice per group). Data are shown as mean values ± SEM, and are representative of six biological replicates, P values were calculated by two-sided t-tests, *p < 0.05, **p < 0.01, ***p < 0.001,****p < 0.0001.

Source data

Extended Data Fig. 5 Female Ghrl-Piezo1-/- mice presented hyperghrelinmia and body weight gain.

a, Female Piezo1fl/fl and Ghrl-Piezo1-/- mice were fed an NCD and then placed into metabolic cages. Food intake was monitored in 24 h (n = 5 mice per group). b, Food consumption in light/dark cycle relative to body weight (g/g BW) (n = 5 mice per group). c, Body weight curves of female Piezo1fl/fl and Ghrl-Piezo1-/- mice (n = 5 mice per group). d, Respiratory exchange rate (n = 5 mice per group). e, Energy expenditure were monitored (n = 5 mice per group). f, Intraperitoneal Glucose Tolerance Test (IPGTT) and associated area under the curve (AUC) values of female Piezo1fl/fl and Ghrl-Piezo1-/- mice (n = 6 mice per group). g, Insulin tolerance tests (ITT) and AUC (n = 6 mice per group). h, Piezo1, Piezo2 and Ghrl mRNA levels in gastric corpus mucosa (n = 6 mice per group). i, Plasma des-acyl Ghrelin and acylated Ghrelin of female Piezo1fl/fl and Ghrl-Piezo1-/- mice (n = 6 mice per group). j, Representative Western blots for PIEZO1, CaMKKII, pCaMKIV, CaMKIV, pmTOR, mTOR, pS6K, S6K, pS6, S6, Pro-GHRELIN and β-ACTIN (n = 6 mice per group). Data are shown as mean values ± SEM, and are representative of five or six biological replicates, P values were calculated by two-sided t-tests. *p < 0.05, **p < 0.01, ***p < 0.001,****p < 0.0001.

Source data

Extended Data Fig. 6 Quantification for double-labelling immunofluorescence in male Piezo1fl/fl and Ghrl-Piezo1-/-mice under HFD in Fig. 3i.

a, Quantitative analysis of Piezo1-positive ghrelin cells in the stomach of male Piezo1fl/fl and Ghrl-Piezo1-/-mice fed HFD (n = 6/group). 358 Piezo1-positive cells and 190 Ghrelin-positive cells from six control mice, 280 Piezo1-positive cells and 229 Ghrelin-positive cells from six Ghrl-Piezo1-/- mice under HFD were quantified (n = 6 mice per group). b, Quantitative analysis of Ghrelin intensity of male mice of indicated genotypes fed HFD (n = 6 mice per group). Three typical images from each mice were chosen for quantitative analysis of ghrelin intensity. c, Quantitative analysis of pCaMKIV-positive X/A-like cells in the stomach of male mice. 356 pCaMKIV-positive cells and 176 Ghrelin-positive cells from six control mice, 181 pCaMKIV-positive cells and 189 Ghrelin-positive cells from six Ghrl-Piezo1-/- mice under HFD were quantified for double-labelling immunofluorescence (n = 6 mice per group). d, Quantitative analysis of Ghrelin intensity in the stomach male mice of indicated genotypes fed HFD. Three typical images from each mice (n = 6 mice per group) were chosen for quantitative analysis of ghrelin intensity. Data are shown as mean values ± SEM, and are representative of six biological replicates, P values were calculated by two-sided t-tests.*p < 0.05, **p < 0.01, ***p < 0.001,****p < 0.0001.

Source data

Extended Data Fig. 7 Double immunofluorescence staining of chromogranin A (ChrA) and Ghrelin in the gastric mucosa of mice treated with yoda1 and/or GsMTx4.

a, Co-localization of chromogranin A (red) and Ghrelin (green) in the mouse gastric mucosa. b, Quantitative analysis of Ghrelin intensity. Three typical images from each mice were chosen for quantitative analysis of ghrelin intensity (n = 6 mice per group). Data are shown as mean values ± SEM, and are representative of six biological replicates, P values were calculated by two-sided t-tests.*p < 0.05, **p < 0.01, ***p < 0.001,****p < 0.0001.

Source data

Extended Data Fig. 8 Evaluation of mouse comfort.

a, Assessment of abdominal mechanical sensitivity. Mechanical sensitivity of the abdomen was assessed with calibrated (0.07, 0.16, and 1 g) von Frey flaments (VFFs) in sham and bead implanted mice (n = 4 mice per group). b and c, Bars show the time spent in the centre and the total distance moved in sham and bead implanted mice (n = 4 mice per group). Data are shown as mean values ± SEM, and are representative of four biological replicates, P values were calculated by two-sided t-tests.

Source data

Extended Data Fig. 9 Quantitative analysis of Ghrelin intensity of male mice receiving sham or bead operation.

a, Quantitative analysis of Ghrelin intensity of male mice receiving sham or bead operation under NCD (n = 5 mice per group).Three images from each mice (five sham and five bead implanted mice) were chose for quantitative analysis of ghrelin intensity. b, Quantitative analysis of ghrelin intensity o of male mice receiving sham or bead operation under HFD (n = 6 mice per group). Three images from each mice (six sham and six bead implanted mice) were chose for quantitative analysis of ghrelin intensity. Data are shown as mean values ± SEM, and are representative of five or six biological replicates, P values were calculated by two-sided t-tests. *p < 0.05, **p < 0.01, ***p < 0.001,****p < 0.0001.

Source data

Extended Data Fig. 10 Gastric bead implantation in Ghrl-Piezo1-/- mice.

a, Food intake(n = 5 mice per group). b, Body weight(n = 5 mice per group). c, Western blot analysis of gastric corpus mucosal extracts with the indicated antibodies. d, Ghrl mRNA levels(n = 5 mice per group). e, Plasma des-acyl ghrelin. f, plasma acylated ghrelin levels of male Ghrl-Piezo1-/- mice receiving sham or intra-gastric bead implantation(n = 5 mice per group). Data are shown as mean values ± SEM, and are representative of five or six biological replicates, P values were calculated by two-sided t-tests.

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Zhao, Y., Liu, Y., Tao, T. et al. Gastric mechanosensitive channel Piezo1 regulates ghrelin production and food intake. Nat Metab 6, 458–472 (2024). https://doi.org/10.1038/s42255-024-00995-z

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