Dietary Curcumin Intervention Targets Mouse White Adipose Tissue Inflammation and Brown Adipose Tissue UCP1 Expression

Zhuolun Song, Xavier Revelo, Weijuan Shao, Lili Tian, Kejing Zeng, Helena Lei, Hong Shuo Sun, Minna Woo, Daniel Winer, Tianru Jin

Research output: Contribution to journalArticlepeer-review

55 Scopus citations


Objective: This study aimed to determine whether dietary curcumin intervention targets both white adipose tissue (WAT) inflammation and brown adipose tissue (BAT)-mediated energy expenditure. Methods: C57BL/6J mice were fed with a low-fat diet, high-fat diet (HFD), or HFD plus curcumin. In addition to assessing the effect of curcumin intervention on metabolic profiles, this study assessed WAT macrophage infiltration and composition and inflammatory cytokine production. Metabolic cages were applied for determining energy expenditure. Raw264.7 (ATCC, Manassas, Virginia) and other cell models were utilized to test the in vitro effect of curcumin treatment. Results: Curcumin intervention reduced WAT macrophage infiltration and altered macrophage functional polarity, as the ratio of M2-like versus M1-like macrophages increased after curcumin intervention. Curcumin treatment reduced M1-like macrophage markers or proinflammation cytokine expression in both macrophages and adipocytes. Curcumin intervention also increased energy expenditure and body temperature in response to a cold challenge. Finally, the in vivo and in vitro investigations suggested that curcumin increased expression of uncoupling protein 1 (UCP1), possibly involving PPAR-dependent and -independent mechanisms. Conclusions: Curcumin intervention targets both WAT inflammation and BAT UCP1 expression. These observations advanced our knowledge on the metabolic beneficial effects of the curry compound curcumin, bringing us a novel perspective on dietary polyphenol research.

Original languageEnglish (US)
Pages (from-to)547-558
Number of pages12
Issue number3
StatePublished - Mar 2018

Bibliographical note

Funding Information:
Funding agencies: This work was supported by an operating grant by the Canadian Institutes of Health Research (MOP 97790) to TJ. ZS is supported by a Banting and Best Diabetes Centre (BBDC) graduate studentship, and LT is supported by a BBDC postdoctoral fellowship. KZ is the recipient of the Scholarship for International Program for PhD candidates, Sun Yat-Sen University. Disclosure: The authors declared no conflict of interest. Author contributions: ZS, XR, WS, LT, KZ, HL, DW, and TJ: experimental data and study design. HS: assistance on rectal temperature recording. MW: assistance on mouse metabolic cage analyses. ZS and TJ: writing of the manuscript. XR, MW, and DW: editing of the manuscript. TJ is the guarantor of this work and, as such, had full access to all the data in this study and takes responsibility for the integrity of data and the accuracy of the data analyses. *Current address: Sun Yat-Sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China. Additional Supporting Information may be found in the online version of this article. Received: 4 August 2017; Accepted: 6 December 2017; Published online 6 February 2018. doi:10.1002/oby.22110

Publisher Copyright:
© 2018 The Obesity Society


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