Adropin is a secreted protein that regulates endothelial function. However, adropin levels in obese adolescent patients are currently uncertain. Therefore, we evaluated the association between plasma adropin levels and vascular endothelial function and investigated the effect of aerobic exercise in obese adolescents. A total of 45 obese adolescents and 20 controls (age 16–19 years) were included in our study. The obese adolescents received 12 weeks of aerobic exercise training. Serum adropin was detected using enzyme-linked immunosorbent assay. Vascular reactive hyperemia indexes (RHIs) were obtained using Endo-PAT2000. Adropin levels and RHI were significantly lower in obese adolescents than in normal-weight adolescents. Adropin levels and RHI increased significantly independently of changes in body weight after an exercise intervention (P < 0.01). Pearson correlation analysis revealed that adropin levels positively correlated with HDL-C levels (r = 0.389, P < 0.01) and RHI (r = 0.32, P < 0.01). Multiple linear stepwise regression analysis showed that the insulin resistance index (t = −3.301, P < 0.01) and HDL-C level (t = 2.620, P = 0.011) were independent risk factors of adropin levels. In addition, Δadropin (t = 3.261, P < 0.01) was an independent influencing factor of ΔRHI. Our findings suggest that adropin plays an important role in vascular endothelial function in obese adolescents.

Alleviating cardiac dysfunction improves the prognosis of heart failure patients. Lycorine is an alkaloid with several beneficial biological properties. Here, we used mice to evaluate the effect of lycorine on cardiac dysfunction elicited by isoproterenol. Mice were divided into four groups: control, lycorine, isoproterenol, and isoproterenol + lycorine. Mice in the combined group were treated daily with 10 mg/kg isoproterenol intraperitoneally for 2 weeks and 5 mg/kg lycorine was given simultaneously intraperitoneally for 4 weeks. Cardiac structure and function were assessed by echocardiography, hematoxylin and eosin staining, and Masson’s trichrome staining. Isoproterenol-induced cardiac dysfunction and histopathological injury that was significantly improved by treatment with lycorine. Western blotting and the quantitative real-time polymerase chain reaction were used to explore the molecular mechanisms of these effects. Levels of the inflammatory cytokines, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α, were increased by treatment with isoproterenol; these increases were significantly reduced by lycorine, with involvement of the NF-κB signaling pathway. The fibrotic factors, collagen I and collagen III, were increased by isoproterenol and decreased by treatment with lycorine through inhibiting activation of the Smad signaling pathway. In addition, lycorine alleviated oxidative stress as evidenced by a reduction in total reactive oxygen species in the isoproterenol + lycorine group compared to the isoproterenol group. Lycorine exerted an anti-apoptotic effect as evidenced by upregulating Bcl-2 and downregulating Bax. Overall, our findings demonstrate that lycorine protects against cardiac dysfunction induced by isoproterenol by inhibiting inflammation, fibrosis, oxidative stress, and apoptosis.

Background: We aim to evaluate the four surrogate markers of insulin resistance (IR), including triglyceride-glucose index (TyG), lipid accumulation product index (LAP), visceral adiposity index (VAI), triglycerides to high-density lipoprotein cholesterol ratio (TG/HDL), on prevalence of chronic kidney disease (CKD) and to examine any possible effect modifiers in Chinese hypertensive patients.Methods: A total of 13,055 hypertensive participants were included in this cross-sectional study. In addition, average age of the study population was 63.81 ± 9.46 years, and 47.66% of them are men. The primary outcome was CKD, defined as eGFR <60 ml/min/1.73 m². Multivariate logistic regression analysis and the generalized additive model and a fitted smoothing curve (penalized spline method) were used to examine the association between the surrogate markers of IR and CKD.Results: Four surrogate markers of IR were independently and positively associated with CKD in a dose-response fashion. The association between four surrogate markers of IR and the prevalence of CKD was examined as a continuous variable per one unit increment and also as a categorical variable using tertiles with the tertiles (T1) as the reference group. In the fully adjusted model, multivariate logistic analyses showed that the per one unit increments of the TyG, LAP, VAI, and TG/HDL ratios were all significantly associated with 42, 31, 67, and 78% higher risk for CKD, respectively. Consistently, the adjusted ORs (95% CI) for CKD were 1.48 (1.21, 1.81), 1.34 (1.06, 1.69), 1.26 (1.03, 1.53), 1.35 (1.12, 1.63) when comparing the highest tertile to the lowest tertile of the TyG, LAP, VAI, and TG/HDL ratios, respectively. The stratification analysis showed that a significant positive correlation between TyG, VAI, and TG/HDL and CKD in patients over 65 years old.Conclusion: Four surrogate markers of IR were independently and positively correlated with CKD, and LAP was better than the other surrogate markers of IR for predicting CKD. Only among participants aged over 65 years were higher levels of TyG, VAI and TG/HDL found to be closely related to the increased prevalence of CKD.

Heart failure is a disease predominantly caused by an energy metabolic disorder in cardiomyocytes. The present study investigated the inhibitory effects of fenofibrate (FF) on isoproterenol (ISO)‑induced hear failure in rats, and examined the underlying mechanisms. The rats were divided into CON, ISO (HF model), FF and FF+ISO (HF animals pretreated with FF) groups. The cardiac structure and function of the rats were assessed, and contents of free fatty acids and glucose metabolic products were determined. In addition, myocardial cells were isolated from neonatal rats and used in vitro to investigate the mechanisms by which FF relieves heart failure. Western blot analysis was performed to quantify the expression levels of peroxisome proliferator‑activated receptor (PPAR)α and uncoupling protein 2 (UCP2). FF effectively alleviated the ISO‑induced cardiac structural damage, functional decline, and fatty acid and carbohydrate metabolic abnormalities. Compared with the ISO group, the serum levels of brain natriuretic peptide (BNP), free fatty acids, lactic acid and pyruvic acid were decreased in the FF animals. In the cultured myocardial cells, lactic acid and pyruvic acid contents were lower in the supernatants obtained from the FF animals, with lower levels of mitochondrial ROS production and cell necrosis, compared with the ISO group, whereas PPARα upregulation and UCP2 downregulation occurred in the FF+ISO group. The results demonstrated that FF efficiently alleviated heart failure in the ISO‑induced rat model, possibly via promoting fatty acid oxidation.