# Associations of circulating omentin-1 levels and long noncoding RNA MALAT1 expression with coronary heart disease in patients with type 2 diabetes mellitus

## TL;DR

This study finds that lower omentin-1 and higher MALAT1 levels in type 2 diabetes patients are linked to coronary heart disease and may help detect it early.

## Contribution

The study identifies omentin-1 and MALAT1 as potential non-invasive biomarkers for early detection of CHD in T2DM patients.

## Key findings

- Omentin-1 levels were significantly lower in T2DM patients with CHD compared to those without.
- MALAT1 expression was significantly higher in T2DM patients with CHD.
- Combining omentin-1 and MALAT1 improved diagnostic accuracy for CHD in T2DM patients.

## Abstract

Coronary heart disease (CHD) is a severe diabetic vascular complication and the main cause of mortality among diabetes patients. Early diagnosis of CHD could prevent its development. Both omentin-1 (Oment-1) and the long noncoding RNA MALAT1 (lncRNA MALAT1) can be detected in peripheral blood and exhibit protective or detrimental effects on CHD. However, whether these two factors could be predictive of CHD in T2DM patients remains unclear. Therefore, this study aimed to investigate the associations of circulating Oment-1 levels and the expression of MALAT1 with CHD in T2DM patients and to assess their predictive efficacy. A total of 137 T2DM patients were enrolled, including 68 patients without CHD (T2DM group) and 69 patients with CHD (T2DM + CHD group). Clinical parameters were collected, and plasma Oment-1 was measured by enzyme-linked immunosorbent assay (ELISA). RNA was isolated from peripheral monocytes, and the expression of MALAT1 was determined by quantitative PCR. Cardiac function was measured by echocardiography. Compared with that in T2DM patients, the plasma Oment-1 level was significantly lower, while the expression of MALAT1 was significantly greater in T2DM + CHD patients (all P values < 0.01). Bivariate correlation analysis indicated that Oment-1 was positively correlated with the left ventricular ejection fraction (LVEF) (P < 0.01). MALAT1 expression was negatively correlated with LVEF but positively correlated with age and DM duration (P < 0.05). Binary logistic regression suggested that Oment-1 and MALAT1 were significantly associated with the presence of CHD. Receiver operating characteristic (ROC) curve analysis demonstrated that both Oment-1 (AUC = 0.663, sensitivity = 75%, specificity = 49%) and MALAT1 (AUC = 0.749, sensitivity = 73%, specificity = 66%) had significant diagnostic value for CHD among T2DM patients. Notably, the combination of Oment-1 and MALAT1 exhibited better diagnostic efficiency (AUC = 0.771, sensitivity = 66.7%, specificity = 75.3%). In conclusion, decreased circulating Oment-1 levels and increased MALAT1 expression are closely associated with CHD in T2DM patients, and their combination offers superior diagnostic efficiency, suggesting Oment-1 and MALAT1 may serve as a non-invasive tool for the early CHD detection and risk stratification in high-risk T2DM patients. Further studies are warranted to explore the pathophysiological mechanisms of Omentin-1 and MALAT1 in the pathogenesis of CHD in T2DM and to validate their clinical utility as potential biomarkers in large cohort studies.