Risk Factors for Sarcopenia in the Elderly with Type 2 Diabetes Mellitus and the Effect of Metformin: Aims. Sarcopenia is a common condition in older individuals, especially in the elderly with type 2 diabetes mellitus (T2DM). The aim of the present study was to examine the risk factors for sarcopenia in elderly individuals with T2DM and the effects of metformin. Methods. A total of 1732 elderly with T2DM were recruited to this cross-sectional observational study, and we analyzed the data using logistic regression analyses. Skeletal muscle mass, grip strength, and usual gait speed were measured to diagnose sarcopenia according to the criteria of the Asian Working Group for Sarcopenia, combined with expert consensus on sarcopenia in China. Results. The overall prevalence of sarcopenia was 10.37% of the participants. In the multivariate analysis, sex, age, educational level, and BMI were risk factors for sarcopenia, with women more likely to develop sarcopenia relative to men ( , 95% –4.371; ). We observed that sarcopenia increased with age and decreased with increasing BMI and educational level ( ). Participants who took metformin alone or combined with other drugs exhibited a lower risk for sarcopenia than those who took no medication ( , 95% –0.904 and , 95% –0.702, respectively; ). Conclusions. We showed that being female and at an older age, lower educational level, and lower BMI were risk factors for sarcopenia in elderly T2DM and that metformin acted as a protective agent against sarcopenia in these patients.

The Nucleotide binding and oligomerization domain-like receptorfamily pyrin domain-containing 3 (NLRP3)-inflammasome plays an important role in various diseases, including a variety of kidney diseases. Naringin exhibits anti-inflammatory and anti-oxidation effects among others, but its specific mechanisms are not clear. We investigated the expression of the NLRP3-inflammasome under high-glucose conditions, assessed the effects of naringin on that process, and further elucidated the role of naringin in the pathogenesis of diabetic kidney disease(DKD). To assess the therapeutic potential of naringin and the mechanisms involved, we cultured rat glomerular mesangial cells and grouped them according to different glucose concentrations, different action times, different concentrations of MCC950, and different concentrations of naringin.The cell proliferation was measured by MTT assay. The expression of Interleukin-1β(IL-1β) and Interleukin18 (IL-18) in the cell supernatant were detected by ELISA. The expression and activity of NLPR3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) and Caspase-1 were detected by Western Blot. The expressions of NLRP3, ASC, caspase-1, IL-1β, and IL-18 in rat glomerular mesangial cells were significantly higher in the high glucose (HG) group than in the control normal glucose (NG) group and exhibited time-dependence activity. The expression levels of NLRP3, caspase-1, IL-1β, and IL-18 in different treatment groups were significantly lower compared with the HG group after 48 h of MCC950 pre-treatment (p < 0.05). Pre-treatment with naringin produced the same results. Naringin also inhibited the proliferation of cells. The NLRP3-inflammasome potentially plays a role in the process of activation and inflammation of glomerular mesangial cells as induced by high-glucose conditions. Naringin inhibited the proliferation of cells that were induced by high glucose. Further, it reduced the expression of inflammatory factors that are mediated by NLRP3 through the NLRP3-caspase-1-IL-1β/IL-18 signaling pathway, which makes naringin a potentially novel treatment for DKD disease.

Human life expectancy increases as society becomes more developed. This increased life expectancy poses challenges associated with the rapid aging of the population. Sarcopenia, an age-related disease, has become a worldwide health issue. Patients with sarcopenia experience decreases in muscle mass and function, becoming frail and eventually bedridden. Type 2 diabetes mellitus (T2DM) is also a major health issue; the incidence of T2DM increases with aging. T2DM is associated with reduced muscle strength and poor muscle quality and may contribute to acceleration of the aging process, augmenting age-related sarcopenia. Recent studies indicate that elderly patients with diabetes are at an increased risk for sarcopenia. Therefore, these older diabetic patients with sarcopenia need specific anti-diabetic therapies targeting not only glycemic control but also sarcopenia, with the goal of preventing sarcopenia in pre-sarcopenic patients. Presently, various types of hypoglycemic drugs are available, but which hypoglycemic drugs are better suited for geriatric T2DM patients with sarcopenia remains undetermined. In this review, we discuss the association between diabetes and sarcopenia in geriatric patients, and how anti-diabetic drugs may influence sarcopenia outcomes. This review will guide clinical workers in the selection of drugs best suited for this patient population.

Objective. The inability to intervene in Alzheimer’s disease (AD) forces the search for promising gene‐targeted therapies. This study was aimed at exploring molecular signatures and mechanistic pathways to improve the diagnosis and treatment of AD. Methods. Microarray datasets were collected to filter differentially expressed genes (DEGs) between AD and nondementia controls. Weight gene correlation network analysis (WGCNA) was employed to analyze the correlation of coexpression modules with AD phenotype. A global regulatory network was established and then visualized using Cytoscape software to determine hub genes and their mechanistic pathways. Receiver operating characteristic (ROC) analysis was conducted to estimate the diagnostic performance of hub genes in AD prediction. Results. A total of 2,163 DEGs from 13,049 background genes were screened in AD relative to nondementia controls. Among the six coexpression modules constructed by WGCNA, DEGs of the key modules with the strongest correlation with AD were extracted to build a global regulatory network. According to the Maximal Clique Centrality (MCC) method, five hub genes associated with mitochondrial complexes were chosen. Further pathway enrichment analysis of hub genes, such as oxidative phosphorylation and retrograde endocannabinoid signaling, was identified. According to the area under the curve (AUC) of about 70%, each hub gene exhibited a good diagnostic performance in predicting AD. Conclusions. Our findings highlight the perturbation of mitochondrial complexes underlying AD onset, which is mediated by molecular signatures involved in oxidative phosphorylation (COX5A, NDUFAB1, SDHB, UQCRC2, and UQCRFS1) and retrograde endocannabinoid signaling (NDUFAB1) pathways.