Dysfunction of PTEN-Associated MicroRNA Regulation: Exploring Potential Pathological Links in Type 1 Diabetes Mellitus.

Type 1 Diabetes Mellitus (T1DM) is an autoimmune disease with T cell-mediated pathogenesis of pancreatic β-cell destruction, leading to insulin deficiency. MicroRNAs such as miR-223 and miR-106b, along with PTEN, have been reported to participate in the pathophysiology of diabetes and its complications. The current study has explored the expression of miR-223, miR-106b, and PTEN and their association with various clinical and biochemical parameters in subjects diagnosed with T1DM.

Protective effect of Apelin-13 on D-glutamic acid-induced excitotoxicity in SH-SY5Y cell line: An in-vitro study.

Excitotoxicity, resulting from excessive accumulation of glutamate in the extracellular space, leads to neuronal cell death. This study investigates the protective effects of Apelin-13 on D-Glutamic acid-induced excitotoxicity in SH-SY5Y human neuroblastoma cells, an in-vitro model for neurodegenerative diseases. Unlike the commonly studied L-glutamic acid, this research focuses on D-Glutamic acid to understand its specific impacts.

The Associations between Asprosine, Clusterin, Zinc Alpha-2-Glycoprotein, Nuclear Factor Kappa B, and Peroxisome Proliferator-Activated Receptor Gamma in the Development of Complications in Type 2 Diabetes Mellitus.

: The aim of this study was to investigate the circulating levels of asprosin, clusterin, zinc-alpha-2-glycoprotein (ZAG), nuclear factor-kappa B (NF-κB), and peroxisome proliferator-activated receptor-gamma (PPAR-γ) in patients with T2DM in relation to microvascular and macrovascular complications. Measuring these biomarkers may provide insight into the pathophysiology of T2DM and indicate novel targets for the therapy of diabetes-related complications. : A total of 260 subjects consisting of four groups: healthy controls (Group-1), T2DM patients without complications (Group-2), T2DM patients with microvascular complications (Group-3), and T2DM patients with macrovascular complications (Group-4).

The Role of Glycogen Synthase Kinase-3β in the Zinc-Mediated Neuroprotective Effect of Metformin in Rats with Glutamate Neurotoxicity.

Metformin has been suggested to have protective effects on the central nervous system, but the mechanism is unknown. The similarity between the effects of metformin and the inhibition of glycogen synthase kinase (GSK)-3β suggests that metformin may inhibit GSK-3β. In addition, zinc is an important element that inhibits GSK-3β by phosphorylation.