Authors
Yanting Hou, Yinghua Ma, Qin Liu, Dingling Ma, Yuxin Tong, Lili Xu, Xiaolong Chu, Jingzhou Wang, Maodi Liang, Mengyuan Zhao, Huizi Zhang, Yurui Su, Jianxin Xie, Cuizhe Wang, Jun Zhang
Published in
Advanced science (Weinheim, Baden-Wurttemberg, Germany). Pages e09534. Feb 25, 2026. Epub Feb 25, 2026.
Abstract
Circulating odd-chain fatty acids (OCFAs), such as pentadecanoic acid (C15:0) and heptadecanoic acid (C17:0), inversely associate with metabolic syndrome-related type 2 diabetes mellitus (T2DM), cardiovascular disease, and all-cause mortality. However, the physiological function of nonadecanoic acid (C19:0) remains unclear. In this study, we identify an inverse association between plasma C19:0 levels and T2DM in the Kazakh population in Xinjiang, China. Investigations using diet-induced obese (DIO) and db/db mouse models revealed that C19:0 has the potential to improve glucose tolerance and enhance insulin sensitivity. Mechanistically, our data demonstrate that C19:0 acts as an endogenous ligand for GPR120, mediating metabolic benefits both in vitro and in vivo. Further analyses indicate that 2-hydroxyacyl-CoA lyase (HACL1) directly participates in the biosynthesis of C19:0, with its expression regulated by peroxisome proliferator-activated receptor α (PPARα). Elevated palmitic acid (PA) levels in obesity suppress PPARα via miR548ab release, thereby impairing the PPARα-HACL1-C19:0 signaling pathway. Collectively, these findings establish a novel association between C19:0 and T2DM and elucidate a distinct mechanism accounting for reduced circulating C19:0 levels in obesity.
PMID:
41738141
Bibliographic data and abstract were imported from PubMed on 25 Feb 2026.
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