Evaluating the role of biological age in osteoporosis risk among middle-aged and older adults: A nationwide perspective.

OBJECTIVES: This study aimed to investigate the association between biological age acceleration and osteoporosis (OP) risk in middle-aged and older adults using data from the National Health and Nutrition Examination Survey (NHANES). The research focused on analyzing the relationship between two biological aging metrics, Klemera-Doubal Method Age (KDMAge) and Phenotypic Age (PhenoAge), and OP risk. METHODS: The study analyzed data from NHANES, which included 6550 participants aged 50 and above from survey cycles 2005-2010 and 2017-2018. Linear and logistic regression were used to investigate the relationship between biological age acceleration (KDMAgeAccel and PhenoAgeAccel) and OP. Subgroup analysis was performed by age, gender and other factors. Multivariable Cox regression analysis yielded Hazard Ratios (HRs) relating biological age acceleration to mortality were evaluated. The study also considered the mediating roles of body mass index (BMI). RESULTS: KDMAgeAccel (odds ratio [OR] = 2.34, 95 % CI, 1.72-3.18) and PhenoAgeAccel (OR = 2.03, 95 % CI, 1.48-2.78) were significantly associated with increased OP risk and reduced bone mineral density (BMD). Specifically, higher KDMAgeAccel and PhenoAgeAccel were linked to higher OP prevalence and lower BMD at multiple sites. Subgroup analyses indicated that the association between accelerated biological age acceleration and OP risk was consistent across different demographics. Mediation analysis revealed that BMI partially mediated the relationship between accelerated biological age and OP, although other mechanisms are likely involved. Statistical analysis indicated that individuals with higher biological age metrics had increased mortality risk related to OP. CONCLUSION: The findings suggest that accelerated biological age is a robust predictor of OP risk and related mortality. KDMAgeAccel and PhenoAgeAccel could serve as valuable biomarkers for identifying individuals at high risk for OP, guiding preventive strategies.

Roles of Mitochondrial Dysfunction in Diabetic Kidney Disease: New Perspectives from Mechanism to Therapy.

Diabetic kidney disease (DKD) is a common microvascular complication of diabetes and the main cause of end-stage renal disease around the world. Mitochondria are the main organelles responsible for producing energy in cells and are closely involved in maintaining normal organ function. Studies have found that a high-sugar environment can damage glomeruli and tubules and trigger mitochondrial dysfunction. Meanwhile, animal experiments have shown that DKD symptoms are alleviated when mitochondrial damage is targeted, suggesting that mitochondrial dysfunction is inextricably linked to the development of DKD. This article describes the mechanisms of mitochondrial dysfunction and the progression and onset of DKD. The relationship between DKD and mitochondrial dysfunction is discussed. At the same time, the progress of DKD treatment targeting mitochondrial dysfunction is summarized. We hope to provide new insights into the progress and treatment of DKD.

Diabetes-induced male infertility: potential mechanisms and treatment options.

Male infertility is a physiological phenomenon in which a man is unable to impregnate a fertile woman during a 12-month period of continuous, unprotected sexual intercourse. A growing body of clinical and epidemiological evidence indicates that the increasing incidence of male reproductive problems, especially infertility, shows a very similar trend to the incidence of diabetes within the same age range. In addition, a large number of previous in vivo and in vitro experiments have also suggested that the complex pathophysiological changes caused by diabetes may induce male infertility in multiple aspects, including hypothalamic-pituitary-gonadal axis dysfunction, spermatogenesis and maturation disorders, testicular interstitial cell damage erectile dysfunction. Based on the above related mechanisms, a large number of studies have focused on the potential therapeutic association between diabetes progression and infertility in patients with diabetes and infertility, providing important clues for the treatment of this population. In this paper, we summarized the research results of the effects of diabetes on male reproductive function in recent 5 years, elaborated the potential pathophysiological mechanisms of male infertility induced by diabetes, and reviewed and prospected the therapeutic measures.