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T2DM is an obesity-induced inflammation syndrome characterized by chronic activation of the innate immune system in conjunction with the progression of insulin resistance and pancreatic β-cell dysfunction. Macrophages and adipose tissue contribute to the development of obesity-induced T2DM by secreting pro-inflammatory cytokines.^[@bib21]^ IL-6 is an important mediator of the progression of obesity-induced T2DM, and IL-6 levels in the plasma increase with the progression of T2DM.^[@bib22]^ The results of our study demonstrate that ART administration attenuates the development of obesity-induced inflammation by inhibiting macrophage activation and cytokine secretion, thus delaying the progression of diabetes. We also observed significant decreases in IL-6 levels in both ART- and pioglitazone-treated mice. These results are consistent with the results of clinical studies that have shown that the plasma levels of IL-6 are reduced by pioglitazone.^[@bib23]^ Our results suggest that the anti-inflammatory effects of ART are similar to those of pioglitazone and that ART may be a good therapeutic agent for the treatment of T2DM.

In conclusion, we demonstrated that ART can effectively improve hyperglycemia and dyslipidemia in *db/db* mice. We also found that ART ameliorates the hyperglycemia in *db/db* mice by suppressing inflammatory signals via inhibition of macrophage activation and cytokine secretion and subsequent enhancement of insulin sensitivity.

This work was supported by grants from the Korea Health technology R&D Project, Ministry for Health and Welfare, Republic of Korea (A102255 to S.L and H.S.). We thank Drs Jae-Goo Park and Mi-Hee Kang for conducting the animal experiments and Hye Jin Kim for assistance with the experimental work.

The authors declare no conflict of interest.

{#fig1}

![ART treatment attenuates the development of hyperglycemia in *db/db* mice. Body weight was monitored for 7 weeks (**a**), and blood glucose was measured at 3, 5, 7, 10, 13 and 15 weeks of age (**b**
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