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Highlights (a) Why did we undertake this study? Stress hyperglycemia is classic but a long-overlooked pathophysiological process and a recently validated parameter, stress hyperglycemia ratio (SHR), facilitates its estimation. (b) What is the specific question(s) we wanted to answer? Is SHR associated with the in-hospital prognosis in non-surgical patients with type 2 diabetes and heart failure? (iii) What did we find? Compared to the nadir range of SHR at 0.79 to 1.08, both high and low SHR at admission elicit elevated risks of cardiac, kidney, and infectious adverse events during hospitalization in non-surgical patients with type 2 diabetes and heart failure. (iv) What are the implications of our findings? Clinicians should understand the inconsistency between the blood glucose at admission and HbA1c indicates poor prognosis during hospitalization and warrants additional monitoring.

Introduction: We aimed to explore the prognostic value of the aspartate aminotransferase to alanine aminotransferase (AST/ALT) ratio in non-surgical patients with type 2 diabetes hospitalized for heart failure. Material and methods: Using a large electronic medical record-based cohort of diabetes in China (WECODe), we gathered data on non-surgical hospitalized patients with type 2 diabetes and heart failure from 2011 to 2019. Baseline AST/ALT ratio was calculated. The primary outcomes were all-cause death within 30 days after discharge, composite cardiac events, major acute kidney injury, and major systemic infection. A multivariable Cox proportional regression model was utilized to evaluate the association between the AST/ ALT ratio and outcomes. Results: This retrospective cohort included 8,073 patients (39.4% women) with type 2 diabetes hospitalized for heart failure. The median age was 71 years. Higher AST/ALT ratio was associated with higher risks of poor endpoints (with per standard deviation increment in AST/ALT ratio, for death within 30 days after discharge: adjusted hazard ratio [HR] = 1.35, 95% confidence interval [CI], 1.21 to 1.50; for composite cardiac events: HR = 1.18, 95% CI: 1.06 to 1.31). Compared to patients in the lowest quartile for the AST/ALT ratio, those in the highest quartile have elevated risk of death within 30 days after discharge and major systemic infection (HRs [95% CIs] 1.61 [1.18 to 2.19] and 1.28 [1.06 to 1.56], respectively). Subgroup analyses and sensitivity analyses confirmed the robustness of the findings. Conclusions: Type 2 diabetes patients hospitalized for heart failure with the AST/ALT ratio in the highest quartile face a poor short-term prognosis. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of Neferine (Nef) on diabetic nephropathy (DN) and to explore the mechanism of Nef in DN based on miRNA regulation theory., Methods: A DN mouse model was constructed and treated with Nef. Serum creatinine (Crea), blood urea (UREA) and urinary albumin were measured in mice by kits, and renal histopathological changes and fibrosis were observed by hematoxylin-eosin staining and Masson staining. Renal tissue superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) activities were measured by enzyme-linked immunosorbent assay (ELISA). Western blotting was used to detect the expression of nuclear factor E2-related factor 2 (Nrf2)/ heme oxygenase 1 (HO-1) signaling pathway-related proteins in kidney tissues. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-17-5p in kidney tissues. Subsequently, a DN in vitro model was constructed by high glucose culture of human mesangial cells (HMCs), cells were transfected with miR-17-5p mimic and/or treated with Nef, and we used qRT-PCR to detect cellular miR-17 expression, flow cytometry to detect apoptosis, ELISAs to detect cellular SOD, MDA, and GSH-Px activities, Western blots to detect Nrf2/HO-1 signaling pathway-related protein expression, and dual luciferase reporter gene assays to verify the targeting relationship between Nrf2 and miR-17-5p., Results: Administration of Nef significantly reduced the levels of blood glucose, Crea, and UREA and the expression of miR-17-5p, improved renal histopathology and fibrosis, significantly reduced MDA levels, elevated SOD and GSH-Px activities, and activated Nrf2 expression in kidney tissues from mice with DN. Nrf2 is a post-transcriptional target of miR-17-5p. In HMCs transfected with miR-17-5p mimics, the mRNA and protein levels of Nrf2 were significantly suppressed. Furthermore, miR-17-5p overexpression and Nef intervention resulted in a significant increase in high glucose-induced apoptosis and MDA levels in HMCs and a significant decrease in the protein expression of HO-1 and Nrf2., Conclusion: Collectively, these results indicate that Nef has an ameliorative effect on DN, and the mechanism may be through the miR-17-5p/Nrf2 pathway.