The intricate mechanisms underlying pathophysiology and progression of diabetes involve a complex interplay of genetic, metabolic, and immune factors. Type 1 diabetes results from autoimmune destruction of pancreatic beta cells, leading to absolute insulin deficiency, whereas type 2 diabetes is primarily driven by insulin resistance and progressive beta-cell dysfunction. Chronic hyperglycemia induces oxidative stress and inflammation, accelerating vascular and neural complications. Key signaling pathways, such as those involving insulin receptor substrates and glucose transporters, play crucial roles in disease development. Recent studies highlight the impact of gut microbiota, mitochondrial dysfunction, and lipid metabolism on diabetes progression. Understanding these molecular and cellular alterations is vital for developing targeted therapies aimed at preserving beta-cell function, enhancing insulin sensitivity, and preventing long-term complications.
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