Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Jun 24:9:686173.
doi: 10.3389/fcell.2021.686173. eCollection 2021.

Involvement of TRP Channels in Adipocyte Thermogenesis: An Update

Affiliations
Review

Involvement of TRP Channels in Adipocyte Thermogenesis: An Update

Wuping Sun et al. Front Cell Dev Biol. .

Abstract

Obesity prevalence became a severe global health problem and it is caused by an imbalance between energy intake and expenditure. Brown adipose tissue (BAT) is a major site of mammalian non-shivering thermogenesis or energy dissipation. Thus, modulation of BAT thermogenesis might be a promising application for body weight control and obesity prevention. TRP channels are non-selective calcium-permeable cation channels mainly located on the plasma membrane. As a research focus, TRP channels have been reported to be involved in the thermogenesis of adipose tissue, energy metabolism and body weight regulation. In this review, we will summarize and update the recent progress of the pathological/physiological involvement of TRP channels in adipocyte thermogenesis. Moreover, we will discuss the potential of TRP channels as future therapeutic targets for preventing and combating human obesity and related-metabolic disorders.

Keywords: TRP channels; beige adipocytes; brown adipocytes; calcium; energy metabolism; obesity; thermogenesis.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
TRP channel-mediated adipocyte thermogenesis. A schematic figure of how TRPV1, TRPV2, TRPV4, TRPM8, and TRPC1-mediated calcium influx regulates thermogenic gene expression in adipocytes, which causes enhanced thermogenesis. Moreover, the increase in sympathetic nerve activity causes norepinephrine release from the sympathetic nerves and activation of β3-adrenergic receptor (β3ADR) in brown adipocytes, TRPV2 synergistically collaborated with β3ADR to involve in the regulation of peroxisome proliferator-activated receptor gamma coactivator-1 a (PGC1a) and uncoupling protein 1 (UCP1), subsequently enhances thermogenesis. On the other hand, TRPV4-mediated calcium influx negatively regulates thermogenic gene expression in adipocytes and subsequently inhibits thermogenesis.

Similar articles

Cited by

References

    1. Ahuja K. D., Robertson I. K., Geraghty D. P., Ball M. J. (2006). Effects of chili consumption on postprandial glucose, insulin, and energy metabolism. Am. J. Clin. Nutr. 84 63–69. - PubMed
    1. Baboota R. K., Singh D. P., Sarma S. M., Kaur J., Sandhir R., Boparai R. K., et al. (2014). Capsaicin induces ”brite” phenotype in differentiating 3T3-L1 preadipocytes. PLoS One 9:e103093. 10.1371/journal.pone.0103093 - DOI - PMC - PubMed
    1. Bautista D. M., Jordt S. E., Nikai T., Tsuruda P. R., Read A. J., Poblete J., et al. (2006). TRPA1 mediates the inflammatory actions of environmental irritants and proalgesic agents. Cell 124 1269–1282. 10.1016/j.cell.2006.02.023 - DOI - PubMed
    1. Bertholet A. M., Kazak L., Chouchani E. T., Bogaczynska M. G., Paranjpe I., Wainwright G. L., et al. (2017). Mitochondrial Patch Clamp of Beige Adipocytes Reveals UCP1-Positive and UCP1-Negative Cells Both Exhibiting Futile Creatine Cycling. Cell Metab. 25 811–822e814. 10.1016/j.cmet.2017.03.002 - DOI - PMC - PubMed
    1. Bishnoi M., Khare P., Brown L., Panchal S. K. (2018). Transient receptor potential (TRP) channels: a metabolic TR(i)P to obesity prevention and therapy. Obes. Rev. 19 1269–1292. 10.1111/obr.12703 - DOI - PubMed