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

Little is known about temporal trends in the incidence of male hypogonadism and its correlation with socioeconomic status, which we examined in the present study.Data were extracted from the Maccabi Health Services computerized database between 2001-2017. The study population included 4,261 men aged 21 to 80 years with biochemically proven hypogonadism defined and classified according to the European Male Aging Study criteria. Patients on testosterone or testosterone-modifying drugs were excluded. The socioeconomic status was assessed based on verified financial data pertinent to the area of residence.The incidence of male hypogonadism increased with age in all the socioeconomic strata. Among the hypogonadal men, 75% had hypogonadotropic hypogonadism. The overall incidence of hypogonadism increased 1.4-fold between the 2001-2009 and 2010-2017 periods [from 41.7 (39.7-43.8) to 58.5 (56.4-60.8) per 100,000 person-years) (95% CI)], mainly due to an increase in hypogonadotropic hypogonadism. The temporal increase in hypogonadotropic hypogonadism occurred in all age groups and all socioeconomic strata but was notably more prominent in >51-year age groups of the more affluent socioeconomic strata. The mean body mass index remained unchanged throughout the study period.A temporal increase was observed in male hypogonadism, mainly hypogonadotropic hypogonadism, corresponding with previously observed temporal decreases in testosterone levels in men. This trend could be possibly partly attributed to an underappreciated increase in mental distress due to decreasing global happiness indices, increasing stress, and occupational burnout in specific occupations associated with more affluent populations (i.e., high-tech, finance, medical). This preliminary proposition deserves further investigation.

The aim of this narrative review was to discuss data on contraception in diabetes mellitus (DM). Women with DM rarely discuss contraception with their physicians, and healthcare providers offer advice to a very limited number of them. Overall, 1 in 8 women with DM using contraception methods was found to use an ineffective one. A further issue relates to drug-drug interactions between anti-diabetic medications and oral contraceptives. Generally, anti-diabetic agents do not alter the pharmacologic profile of hormonal contraception. However, preliminary results indicate that some novel anti-diabetic agents may even render oral contraceptive methods ineffective. Several implants can be also generally used by women with both DM types. The relationship between oral contraceptives and diabetic complications has not been clarified yet. In general, implants, intra-uterine devices or progestin-only contraceptives are considered safe options for women with DM. However, short-term use of combined hormonal contraception is also feasible for women without severe complications or risk factors.

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.