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In this study, we explored the relationship between inflammatory adipokine levels and coronary artery disease (CAD). We collected subcutaneous adipose tissues(SAT), pericardial adipose tissues(PAT), and epicardial adipose tissues (EAT) and serum samples from 26 inpatients with CAD undergone coronary artery bypass grafting and 20 control inpatients without CAD. Serum inflammatory adipokines were measured by ELISA. Quantitative real-time PCR and western blot were used to measure gene and protein expression. Adipocyte morphology was assessed by H&E staining. Immunohistochemistry and immunofluorescence were used to measure endothelial and inflammatory markers. Serum pro- and anti-inflammatory adipokine levels were higher and lower, respectively, in the CAD group than those in the control group (P < 0.05). In CAD, the pro-inflammatory adipokine levels via ELISA in EAT and PAT were elevated. Pro-inflammatory adipokine mRNA expression was increased, while anti-inflammatory adipokine mRNA expression decreased, in CAD relative to NCAD in EAT and PAT rather than SAT. In EAT, adipocyte area and macrophage-specific staining were lower, while lymphatic vessel marker expression was higher in CAD. Additionally, the endothelial marker expression in EAT was higher than PAT in CAD. The three tissue types had different blood vessel amounts in CAD. The regulation and imbalance expression of the novel biomarkers, including inflammatory adipokine, macrophage infiltration, angiogenesis, and lymphangiogenesis in EAT and PAT, may be related to the pathogenesis of CAD. The serum levels of inflammatory adipokines may correlate to CAD, which requires large sample size studies to get further validation before clinic practice. [ABSTRACT FROM AUTHOR]

In this study, we aimed to determine whether liraglutide could effectively reduce insulin resistance (IR) by regulating Sestrin2 (SESN2) expression in L6 rat skeletal muscle cells by examining its interactions with SESN2, autophagy, and IR. L6 cells were incubated with liraglutide (10–1000 nM) in the presence of palmitate (PA; 0.6 mM), and cell viability was detected using the cell counting kit-8 (CCK-8) assay. IR-related and autophagy-related proteins were detected using western blotting, and IR and autophagy-related genes were analyzed using quantitative real-time polymerase chain reaction. Silencing SESN2 was used to inhibit the activities of SESN2. A reduction in insulin-stimulated glucose uptake was observed in PA-treated L6 cells, confirming IR. Meanwhile, PA decreased the levels of GLUT4 and phosphorylation of Akt and affected SESN2 expression. Further investigation revealed that autophagic activity decreased following PA treatment, but that liraglutide reversed this PA-induced reduction in autophagic activity. Additionally, silencing SESN2 inhibited the ability of liraglutide to up-regulate the expression of IR-related proteins and activate autophagy signals. In summary, the data showed that liraglutide improved PA-induced IR in L6 myotubes by increasing autophagy mediated by SESN2. [ABSTRACT FROM AUTHOR]

Purpose: Asprosin is a newly discovered adipose factor secreted by white fat, which is involved in glucose metabolism and inflammation. Neuregulin-4 (Nrg-4) is a new adipose factor released from brown adipose tissue and is considered to play an important role in metabolism. This study aims to explore the association between serum Asprosin, Nrg-4 level and coronary heart disease(CHD) in patients with type 2 diabetes mellitus(T2DM) and the diagnostic value. Patients and methods: 157 patients with T2DM were enrolled from Affiliated Hospital of Chengde Medical University between December 2020 to July 2021. These patients were divided into T2DM without CHD group (T2DM-0, n = 80) and T2DM with CHD (T2DM-CHD, n = 77). Serum Asprosin and Nrg-4 expression was detected by enzyme-linked immunosorbent assay, and the correlations between Asprosin or Nrg-4 and clinical and biochemical indicators were analyzed. A receiver operating characteristics curve analysis and area under the curve (AUC) were used to evaluate diagnostic accuracy. Results: Serum Asprosin level of the T2DM-CHD group were significantly higher and Nrg-4 level significantly lower than those of the T2DM-0 group.Spearman correlation analysis showed that serum Asprosin levels were significantly positively correlated with diabetes course,history of hypertension, fasting plasma glucose(FPG), glycosylated hemoglobin A1c(HbA1C), triglycerides(TG),triglyceride glucose index(TyG index) and urea, and negatively correlated with ALT (all p < 0.05). Nrg-4 was negatively correlated with history of hypertension, body mass index(BMI), FPG, HbA1C, TG, and TyG indexes (all p < 0.05), and positively correlated with high-density lipoprotein cholesterol(HDL-C)(p < 0.05).Logistic regression analysis showed that after adjusting potential confounders, Asprosin was a risk factor for diabetes mellitus, Nrg-4 was a protective factor.The AUC of Asprosin for diagnosing T2DM-CHD was 0.671 (95% confidence interval [CI] 0.584–0.759), and the AUC of the Nrg4 index for diagnosing T2DM-CHD was 0.772 (95% CI 0.700-0.844). The AUC of Asprosin and Nrg-4 for the combined diagnosis of T2DM-CHD was 0.796 (95% CI 0.726–0.864). Conclusion: Asprosin and Nrg-4 may be novel diagnostic biomarkers for T2DM with CHD, as they effectively improved the diagnostic accuracy for T2DM-CHD. [ABSTRACT FROM AUTHOR]

• Novel adipocytokines may form part of an important pathogenic mechanism of CAD. • Inflammatory cell infiltration could serve as promising medicating targets of CAD. • Increased number of blood vessels could lead to the onset and development of CAD. • EAT inflammation may be part of the pathological mechanism of CAD. This study investigates the expression of novel adipocytokines and inflammatory cells infiltration in epicardial adipose tissue (EAT) and subcutaneous adipose tissue (SAT) between 27 coronary artery disease (CAD) and 21 non-CAD (NCAD) patients enrolled from September 2020 to September 2021. Serum, gene, and protein expression levels of the novel adipocytokines were determined using ELISA, RT-qPCR, and western blot analyses. The number of blood vessels and adipocytes morphology were measured via hematoxylin-eosin staining, and inflammatory cells infiltration was examined via immunohistochemistry. Serum ANGPTL8, CTRP5, and Wnt5a levels were higher in the CAD than in the NCAD group, while serum CTRP3, Sfrp5, and ZAG levels were lower in the CAD than in the NCAD group. Compared to the EAT of NCAD and SAT of CAD patients, the EAT of CAD patients had higher mRNA levels of ANGPTL8, CTRP5, and Wnt5a while lower levels of CTRP3, Sfrp5, and ZAG; higher protein expression levels of ANGPTL8 and CTRP5 but lower levels of CTRP3; more blood vessels; and higher infiltration rates of macrophages (CD68 +), pro-inflammatory M1 macrophages (CD11c +), mast cells (Tryptase +), T lymphocytes (CD3 +), and B lymphocytes (CD20 +) but lower infiltration rates of anti-inflammatory M2 macrophages (CD206 +). Novel adipocytokines and inflammatory cells infiltration are dysregulated in human EAT, and could be important pathophysiological mechanisms and novelly promising medicating targets of CAD. [ABSTRACT FROM AUTHOR]