The potential regulatory relationship between hsa_circ_0000973 and MBOAT2 in hypertriglyceridemia with abnormal glucose metabolism.

Authors

Fengdan Wang, Yixue Yang, Xiaotong Li, Yang Xu, Shoumeng Yan, Bo Li, Di Zhao

Published in

Human molecular genetics. Volume 35. Issue 16. Jul 28, 2026.

Abstract

Hypertriglyceridemia (HTG) frequently occurs in population with abnormal glucose metabolism (AGM), exacerbating risk. In our preliminary researches, we have screened hsa_circ_0000973 and MBOAT2 as the possible regulatory elements of HTG in AGM patients. This study enrolled 142 AGM subjects (71 with HTG, 71 with normal triglycerides) to investigate the role and mechanism of the hsa_circ_0000973 and MBOAT2 in AGM-associated HTG. Expression levels of hsa_circ_0000973 and MBOAT2 were measured by RT-qPCR. Diagnostic performance was evaluated via ROC analysis. Functional validation was performed in an insulin-resistant (IR) HepG2 cell model following knockdown of hsa_circ_0000973 or MBOAT2 using siRNA. Cellular triglyceride (TG) content, glucose uptake, proliferation, apoptosis, and expression of lipid metabolism transcription factors (SREBP-1c, PPARα, PPARγ) were assessed. In the AGM population, expression of both hsa_circ_0000973 and MBOAT2 was significantly downregulated in the HTG group and negatively correlated with serum TG levels (P <0 .01). hsa_circ_0000973 exhibited high diagnostic accuracy for HTG in the AGM population (AUC = 0.95). In HepG2-IR cells, knockdown of hsa_circ_0000973 decreased MBOAT2 expression, increased cellular TG accumulation and residual glucose, inhibited proliferation, and promoted apoptosis. Similar phenotypes were observed upon MBOAT2 knockdown. Both knockdowns upregulated SREBP-1c and downregulated PPARα and PPARγ. This study identified that hsa_circ_0000973 may serve as a candidate biomarker for identifying HTG specifically within the AGM population. Our in vitro experiments further suggested that, in the setting of AGM, hsa_circ_0000973 may jointly regulated TG metabolism alongside MBOAT2.

PMID:
42561135
Bibliographic data and abstract were imported from PubMed on 07 Aug 2026.

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