Omentin-1, as a novel adipocytokine, ameliorates obesity-associated disorders and suppresses the development of atherosclerotic lesions. The present research investigated the correlation between serum omentin-1 and post-infarction myocardial function. A total of 52 patients with first anterior ST-segment elevation myocardial infarction (STEMI) were recruited into this study. Participants were divided into two subgroups according to median admission omentin-1 concentration. δ1 was defined as (admission omentin-1 level) - (serum omentin-1 at 24 hours after admission) and δ2 was defined as (admission omentin-1 level) - (serum omentin-1 at 72 hours after admission). The change in left ventricular ejection fraction (LVEF) was regarded as (LVEF at 3 months post-STEMI)-(LVEF at 2 days post-STEMI). Admission omentin-1 level was the highest, while omentin-1 decreased over the following 3 days. The high admission omentin-1 group had lower peak muscle brain fraction of creatine kinase (CK-MB). Additionally, the change in LVEF and the global LVEF at 3 months post-STEMI all ameliorated significantly in the high admission omentin-1 group. For the time-dependent change in omentin-1, there were negative associations among δ1, δ2, and peak CK-MB. δ1 and δ2 also correlated positively with LVEF at 3 months post-STEMI. Most importantly, δ1 (r =0.346, p=0.012) and δ2 (r =0.439, p=0.001) also correlated positively with the change in LVEF. After multivariate linear regression analysis, δ1 (Beta=0.026, 95% CI 0.011 to 0.041, p=0.001) and δ2 (Beta=0.024, 95% CI 0.009 to 0.038, p=0.003) also remained associated with the change in LVEF. The admission omentin-1 and time-dependent change in omentin-1 level all have a significant correlation with the early improvement of post-infarction myocardial function. While only the time-dependent change in omentin-1 (δ1 and δ2) remained associated with the early improvement of post-infarction myocardial function after multivariate linear regression analysis. The present research indicated that omentin-1 represents a promising adipocytokine to retard negative cardiac remodeling after STEMI.