The relationship between insulin resistance, serum alkaline phosphatase, and left ventricular dysfunction following myocardial infarction.

The occurrence of heart failure following acute myocardial infarction (AMI) significantly increases the risk of post-infarction mortality. Alkaline phosphatase (AP) is considered to be an independent predictor of cardiovascular disease (CVD) and adverse outcomes. Furthermore, in recent years, alkaline phosphatase has been associated with insulin resistance (IR). Our aim was to investigate the correlation between IR substitutes (triglyceride-glucose (TyG) index, triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio), AP, and LV dysfunction in patients admitted after AMI. The retrospective study included 810 patients who underwent coronary angiography for myocardial infarction at the First Hospital of Hebei Medical University from August 2018 to December 2021. Patients were categorized into three groups based on their serum AP levels. Clinical characteristics at admission, cardiac echocardiography findings, coronary angiography results, and biochemical markers such as serum AP levels and triglycerides (TG) were recorded during hospitalization. Left ventricular ejection fraction (LVEF) was assessed using cardiac echocardiography conducted from the time of admission until the coronary angiography procedure. A total of 774 patients with AMI were included in this study. The TyG index is significantly correlated with the TG/HDL-C ratio. (R = 0.739, P < 0.001). Binary logistic regression analysis revealed that elevated serum AP (OR 2.598, 95% CI 1.331-5.071, P = 0.005), presence of the left anterior descending (LAD) artery as the infarct-related artery (IRA) (OR 2.452, 95% CI 1.352-4.449, P = 0.003), and triglyceride (TG) levels (OR 0.652, 95% CI 0.429-0.992, P = 0.046) were protective risk factor for an admission LVEF < 40% following AMI. The serum alkaline phosphatase and LAD as IRA are independent risk factors for severe reduction in LVEF during hospitalization for AMI. Conversely, triglyceride are independent protective factor for severe reduction in LVEF during AMI hospitalization.

Hydrogen sulfide from adipose tissue is a novel insulin resistance regulator.

Recent data suggested that endogenous hydrogen sulfide (H(2)S) contributes to the pathogenesis of diabetes. Here, we identified that cystathionine gamma lyase (CSE) was expressed in adipose tissue in rats and endogenously generated H(2)S. The CSE/H(2)S system exists in both rat adipocytes and pre-adipocytes. This system was up-regulated with aging, although a high level of glucose down-regulated the system in a concentration- and time-dependent manner. H(2)S inhibited the basal and insulin-stimulated glucose uptake of mature adipocytes, whereas administration of CSE inhibitors enhanced the glucose uptake of adipocytes. The PI3K but not K(ATP) channel pathway is involved in the inhibitory effect of H(2)S on glucose uptake. Finally, in fructose-induced diabetes in rats, we confirmed the up-regulated CSE/H(2)S system in adipose tissue, which was negatively correlated with glucose uptake in this tissue. Our findings suggest that H(2)S might be a novel insulin resistance regulator.