Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association最新文献

The article Morin Attenuates Ferroptosis via Activation of the SIRT1/p53/SLC7A11 Signaling Pathway to Alleviate Diabetic Cardiomyopathy In Vivo, by Qingmei Wang, Xuanguo Zhang and Li Xi, published online on March 12, 2025 has been retracted by the Editor-in-Chief and the Publisher. Following an internal investigation by the Publisher, irregularities with respect to the submission and peer review were found. Consequently, the Editor-in-Chief therefore no longer has confidence in the results and conclusions presented in the article. The authors do not agree with this retraction.

Diabetic foot ulcer (DFU) represents a severe complication of diabetes, mainly caused by peripheral vascular occlusion and infection, presenting significant clinical challenges in treatment and potentially resulting in gangrene, amputation, or even fatality. This study aimed to investigate the involvement and underlying mechanisms of Meteorin-like (Metrnl) in the pathogenic process of DFU. Mice underwent diabetes induction by streptozotocin, while human umbilical vein endothelial cells (HUVECs) were exposed to 5.5, 10, 20 or 40 mM glucose. HUVECs were transfected with negative or Metrnl or si-nc or si-Metrnl plasmids via Lipofectamine 2000. The expression of Metrnl was down-regulated in both patients and the murine model of DFU. Elevated glucose levels diminished Metrnl through enhanced Metrnl ubiquitination. The suppression of Metrnl exacerbated foot ulcer in the mouse model of DFU. Metrnl alleviated oxidative stress and ferroptosis in the DFU model by inhibiting mitochondrial damage. Metrnl induced liver kinase B1 (LKB1)/AMP-activated protein kinase (AMPK) signaling in the DFU model. LKB1 attenuated the effects of Metrnl on oxidative stress and ferroptosis in the DFU model.  The data cumulatively demonstrate that Metrnl ameliorates ferroptosis in the DFU model by inhibiting mitochondrial damage via LKB1/AMPK signaling, suggesting that targeting Metrnl may emerge as a potential preventive approach against ferroptosis of DFU or other diabetes.

Introduction: Maintaining and optimizing quality of life (QoL) is a central issue and one of the most important goals in therapy for patients with chronic diseases, such as diabetes mellitus (DM). Despite its importance, there is little data on the QoL of patients with DM in Austria. The objective of this study was to extend an established population-based cohort, the Diabetes-Landeck cohort, by including patient-reported outcomes.

Methods: We performed a survey on quality of life (QoL) and treatment satisfaction in patients from the Diabetes-Landeck cohort using the EQ-5D-5L, the problem areas in diabetes survey (PAID), and the diabetes treatment satisfaction questionnaire (DTSQ). Mean sum scores were calculated and compared between patient characteristic subgroups.

Results: In total 58 patients were recruited, with a mean age of 63 years and a mean hemoglobin A1c (HbA1c) of 7.1%. The mean sum score of EQ-5D-5L was 92 (SD=10.6), and that of DTSQ and PAID were 32.2 (SD=6.6) and 10.8 (SD=11.6), respectively. Patients with obesity (body mass index ≥ 30 kg/m²) showed a statistically significant decreased mean sum score of EQ-5D-5L and a statistically significant increased mean sum score of DTSQ. Patients with HbA1c ≥7.5% showed a statistically significant decreased mean sum score of DTSQ.

Conclusion: We observed patient-reported outcomes significantly associated with obesity and HbA1c, which could be used for targeted patient monitoring. Limited by small sample size and questions in generalizability, we strongly suggest the rollout of a larger study.

Recent studies have suggested that improved glycemic control in patients with diabetes may cause acute Charcot foot. To conduct a narrative review of studies investigating whether improved glycemic control in patients with diabetes causes acute Charcot foot.Publications found by searching PubMed, EMBASE, and Cochrane Library as well as reference lists of identified publications were reviewed.Very few publications were found, primarily consisting of case reports and case studies without control groups, documenting instances where cases of acute Charcot foot had been preceded by improved glycemic control. Recent large multicenter randomized placebo-controlled clinical trials of anti-hyperglycemic agents in patients with diabetes, where significant improvement of glycemic control occurred, have not reported incidences of acute Charcot foot.There is so far no solid evidence to suggest that improvement of glycemic control in patients with diabetes causes acute Charcot foot.