With the increasing incidence of metabolic diseases year by year and their impact on the incidence of cardiovascular diseases, metabolic diseases have attracted great attention as a major health care problem, but there is still no effective treatment. Oxidative stress and inflammation are the main mechanisms leading to metabolic diseases. T cells are involved in the inflammatory response, which can also regulate the development of metabolic diseases, CD4+ T cells and CD8+ T cells are mainly responsible for the role. Th1 and Th17 differentiated from CD4+ T promote inflammation, while Th2 and Treg inhibit inflammation. CD8+ T cells also contribute to inflammation. The severity and duration of inflammatory reactions can also lead to different degrees of progression of metabolic diseases. Moreover, mTOR, PI3K-Akt, and AMPK signaling pathways play unique roles in the regulation of T cells, which provide a new direction for the treatment of metabolic diseases in the future. In this review, we will elaborate on the role of T cells in regulating inflammation in various metabolic diseases, the signaling pathways that regulate T cells in metabolic diseases, and the latest research progress.

Therapeutic hypothermia (TH) may attenuate myocardial ischaemia–reperfusion injury, thereby improving outcomes in acute myocardial infarction. However, the specific mechanism by which TH alleviates MIRI has not been elucidated so far. In this study, 120 healthy male Sprague‐Dawley rats were randomly divided into five groups. Haemodynamic parameters, myocardial infarction area, histological changes and the levels of cardiac enzymes, caspase‐1 and inflammatory cytokines were determined. In addition, the extent of myocardial fibrosis, the degree of cardiomyocyte apoptosis and the expression levels of SIRT3, GSDMD‐N, fibrosis‐related proteins and inflammation‐related proteins were estimated.TH reduced myocardial infarct area and cardiac enzyme levels, improved cardiomyopathic damage and haemodynamic indexes, and attenuated myocardial fibrosis, the protein expression levels of collagen I and III, myocardial apoptosis, the levels of inflammatory cytokines and inflammation‐related proteins. Notably, the immunofluorescence and protein expression levels of SIRT3 were upregulated in the 34H+DMSO group compared to the I/R group, but this protective effect was abolished by the SIRT3 inhibitor 3‐TYP. After administration of Mcc950, the reversal effects of 3‐TYP were significantly abolished, and TH could protect against MIRI in a rat isolated heart model by inhibiting inflammation and fibrosis. The SIRT3/NLRP3 signalling pathway is one of the most important signalling pathways in this regard.

Non-alcoholic fatty liver disease (NAFLD) is a metabolic disease spectrum associated with insulin resistance (IR), from non-alcoholic fatty liver (NAFL) to non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC). O-GlcNAcylation is a posttranslational modification, regulated by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA). Abnormal O-GlcNAcylation plays a key role in IR, fat deposition, inflammatory injury, fibrosis, and tumorigenesis. However, the specific mechanisms and clinical treatments of O-GlcNAcylation and NAFLD are yet to be elucidated. The modification contributes to understanding the pathogenesis and development of NAFLD, thus clarifying the protective effect of O-GlcNAcylation inhibition on liver injury. In this review, the crucial role of O-GlcNAcylation in NAFLD (from NAFL to HCC) is discussed, and the effect of therapeutics on O-GlcNAcylation and its potential mechanisms on NAFLD have been highlighted. These inferences present novel insights into the pathogenesis and treatments of NAFLD.

Background: Inflammation parameters, such as white blood cell (WBC) counts, are closely related to the severity and mortality of Coronavirus disease 2019 (COVID-19). Nevertheless, the association between inflammation fluctuation and clinical outcomes in patients with COVID‐19 is not clear.Methods: We performed a secondary analysis of the ORCHID trial. Inflammation fluctuation was assessed by WBC variability indices (SD [standard deviation], and CV [coefficient of variation]). Cox regression was used to compute the hazard ratio for WBC variability and associated hospitalization and death over 28 days.Results: During the 28 days post-randomization, 46 (10.8%) patients died, and 345 (81.4%) patients were discharged. In multivariable analysis, a worse clinical outcome, including decreased risk of hospital discharge (SD: HR: 2.32; P65), hydroxychloroquine treatment group, and WBC variability indices were not significant (P>0.05).Conclusion: In conclusion, our results showed that COVID-19 patients with higher WBC variability had lower discharge rates and higher mortality. Our study contributes to our understanding of the relationship between inflammation and COVID-19-related adverse outcomes.Clinical trial registration: URL: https://clinicaltrials.gov. Unique identifier: NCT04332991.