Background Sarcopenia was a frequent chronic complication in patients with type 2 diabetes mellitus (T2DM), and previous evidence showed conflicting results regarding the prevalence and risk factors of sarcopenia in T2DM. In the current study, we aimed at systematically exploring the prevalence and risk factors of sarcopenia in patients with T2DM. Methods PubMed, Embase, and Cochrane Central Register of Controlled Trials were systematically searched to identify observational studies which investigated the prevalence and risk factors of sarcopenia in patients with T2DM. The quality of individual included studies was evaluated using The Newcastle–Ottawa scale. Pooled effects regarding prevalence and associated factors were calculated using random-effects models. The potential publication bias was assessed via funnel plot and Egger test. Results Twenty-eight studies involving 16,800 patients were included in our meta-analysis. The pooled prevalence of sarcopenia in patients with T2DM was 18% (95% CI 0.15–0.22; I2 = 97.4%). The pooled results showed that elder age (OR 4.73; 95% CI 4.30–5.19; I2 = 85.6%), male gender, chronic hyperglycemia (higher HbA1c) (OR 1.16; 95% CI 1.05–2.47; I2 = 99.2%) and osteoporosis (OR 1.16; 95% CI 1.05–2.47; I2 = 99.2%) was predictors for sarcopenia, whereas patients with lower BMI (OR 1.16; 95% CI 1.05–2.47; I2 = 99.2%) and metformin administrations (OR 1.16; 95% CI 1.05–2.47; I2 = 99.2%) were not prone to get sarcopenia. The funnel plot and statistical tests showed no obvious publication bias. Conclusions Sarcopenia was frequent in T2DM patients. Elder age, male gender and chronic hyperglycemia, Osteoporosis were significant risk factors for Sarcopenia. Lower BMI and metformin administrations were associated with lower risk of sarcopenia.

Objective: To uncover the potential effect of metformin on proliferation and apoptosis of thyroid cancer TPC-1 cell line, and the underlying mechanism. Methods: Viability, apoptosis and LRP2 level in TPC-1 cells treated with different doses of metformin for different time points were determined. Besides, protein levels of p-JNK1 and c-Jun N-terminal kinases (JNK) in metformin-treated TPC-1 cells were detected by Western blot. Regulatory effects of LRP2 on the JNK pathway and cell viability in metformin-treated TPC-1 cells were assessed. Results: Viability in TPC-1 cells gradually decreased with the treatment of increased doses of metformin either for 24 h or 48 h. The apoptotic rate was concentration-dependently elevated by metformin treatment. Relative levels of LRP2 and p-JNK1 were concentrationdependently downregulated by metformin treatment. In addition, overexpression of LRP2 partially abolished the inhibitory effect of metformin on the viability of TPC-1 cells. Conclusion: Metformin treatment suppresses the proliferative ability and induces apoptosis of TPC-1 cells by downregulating LRP2 to block the JNK pathway.

Rosiglitazone (RSG) is widely used to reduce the amount of sugar in the blood of patients with diabetes mellitus. Diabetic nephropathy is the most common microvascular complication of diabetes. The role of RSG in diabetic nephropathy is not fully understood. Diabetic nephropathy model was constructed in high glucose (HG)-treated mouse mesangial cells. The effects of RSG on cell viability and cell cycle were investigated using cell counting kit-8 (CCK-8) assay and flow cytometry assay. Oxidative stress was assessed according to ROS production and SOD activity in cells. Inflammatory responses were assessed according to the releases of inflammatory cytokines. Extracellular matrix (ECM) accumulation was determined by the levels of fibronectin and collagen IV using western blot. The expression of Gm26917 and microRNA-185-5p (miR-185-5p) was detected by quantitative real-time polymerase chain reaction (qPCR). The interaction between Gm26917 and miR-185-5p was validated by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and pull-down assay. RSG significantly inhibited HG-induced proliferation, oxidative stress, inflammatory responses and ECM accumulation in mouse mesangial cells. The expression of Gm26917 was induced by HG but weakened by RSG. Gm26917 knockdown alleviated HG-induced proliferation, oxidative stress, inflammatory responses and ECM accumulation in mouse mesangial cells, and Gm26917 overexpression partly abolished the effects of RSG. Moreover, miR-185-5p was a target of Gm26917, and miR-185-5p inhibition recovered proliferation, oxidative stress, inflammatory responses and ECM accumulation in mouse mesangial cells that were alleviated by Gm26917 knockdown. RSG ameliorated HG-induced mouse mesangial cell proliferation, oxidative stress, inflammation and ECM accumulation partially by governing the Gm26917/miR-185-5p pathway.