Background: Type 2 diabetes (T2DM) is characterized by hyperglycemia and insulin deficiency. Sirtuin 1 (SIRT1), serving as a deacetylase, is critical in the regulation of glucose and lipid metabolism. Recently, a number of studies have been conducted to investigate the role of SIRT1 in the pathogenesis of T2DM. However, there are no sufficient data about the relationship between SIRT1 and T2DM. The aim of this study was to analyze the expressions of microRNAs (miRNAs) (miR‑ 34a, miR‑ 9, miR‑ 132, and miR‑ 181a) involved in SIRT1 regulation and SIRT1 protein in the serum of T2DM patients and controls. Materials and Methods: miRNA expressions were determined by real‑ time polymerase chain reaction, and enzyme‑ linked immunosorbent assay was used to measure the SIRT1 protein levels in 25 T2DM patients and 25 controls. Results: Fasting blood glucose and glycated hemoglobin levels were significantly higher in patients when compared with controls (P < 0. 001). There was no difference for miRNA expressions between the groups (P > 0. 05). SIRT1 protein level was significantly increased in patients as compared to controls (P = 0. 044). Moreover, SIRT1 was negatively correlated with miR‑ 181a (r = − 0. 558, P = 0. 005) and miR‑ 132 (r = − 0. 435, P = 0. 034) in patients. Conclusion: Obtained results indicate that serum SIRT1 may be a potentially new biomarker for T2DM and also miR‑ 181a and miR‑ 132 may be involved in the development of T2DM by targeting SIRT1. This is the first study reporting on the effects of SIRT1 and related miRNAs in Turkish T2DM patients.

Objective(s): To explore the regulation mechanism of Sirtuin 3 (SIRT3) on the mitochondrial function and apoptosis of acute kidney injury (AKI) in septic mice. Materials and Methods: The sepsis-induced AKI model was constructed in the wild-type and SIRT3 knockout (KO) mice, and the levels of serum creatinine (Scr) and plasma kidney injury molecule 1 (pKIM-1) in mice were detected by ELISA. The mitochondrial damage of kidney tubular epithelial cells (KTEC) was observed by electron microscopy, the apoptosis of KTEC was detected by TUNEL assay, and the mRNA levels of SIRT3, Bax, Caspase-3, and Bcl-2 were detected by RT-qPCR. Results: SIRT3 KO caused increased expression of Scr, pKIM-1, and inducible nitric oxide synthase protein in the kidneys of septic mice, and decreased the levels of superoxide dismutase, catalase, and mitochondrial complex enzymes I/II/III/IV. SIRT3 deficiency exacerbated histopathological and mitochondrial damage to the proximal tubules of the kidney. In addition, SIRT3 KO resulted in a significantly increased apoptosis of KTEC, increased the mRNA levels of Bax and Caspase-3, and decreased the mRNA levels of Bcl-2. Conclusion: Our study suggests that SIRT3 deficiency promotes sepsis-induced AKI via increasing oxidative stress, mitochondrial dysfunction, and inducing apoptosis.

Objective(s): AMP-activated protein kinase/Sirtuin 1 (AMPK/SIRT1) signaling pathway has been proved to be involved in the regulation of autophagy in various models. The aim of this study was to evaluate the effect of AMPK/SIRT1 pathway on autophagy after spinal cord injury (SCI).Materials and Methods: The SCI model was established in rats in vivo and the primary spinal cord neurons were subjected to mechanical injury (MI) in vitro. The apoptosis in spinal cord tissue and neurons was assessed by TUNEL staining and Hoechst 33342 staining, respectively. The autophagy-related proteins levels were detected by Western blot. The activation of AMPK/SIRT1 pathway was determined by Western blot and immunohistochemical staining.Results: We found that the apoptosis of spinal cord tissue and cell damage of spinal cord neurons was obvious after the trauma. The ratio of LC3II/LC3I and level of p62 were first increased significantly and then decreased after the trauma in vivo and in vitro, indicating the defect in autophagy. The levels of p-AMPK and SIRT1 were increased obviously after the trauma in vivo and in vitro. Further activation of the AMPK/SIRT1 pathway by pretreatment with resveratrol, a confirmed activator of the AMPK/SIRT1 pathway, alleviated the cell damage and promoted the autophagy flux via downregulation of p62 in spinal cord neurons at 24 hr after MI.Conclusion: Our results demonstrate that regulation of autophagy by AMPK/SIRT1 pathway can restrain spinal cord neurons damage, which may be a potential intervention of SCI.