Biochemistry, Pathophysiological Perspective, and Therapeutic Advances in Diabetes, Obesity, and Pancreatic Cancer

Diabetes, obesity, and pancreatic cancer are interconnected diseases that share overlapping biochemical and molecular pathways, presenting formidable challenges for global healthcare. This review examines their complex link through a biochemical lens, emphasizing shared pathophysiological mechanisms such as insulin resistance, chronic inflammation, oxidative stress, and dysregulated metabolic signaling. The bidirectional relationship between type 2 diabetes and pancreatic cancer has been explored, and obesity has been identified as a critical mediator influencing hormone secretion, adipokine balance, and energy metabolism. Key molecular pathways, including the PI3K/Akt/mTOR and JAK/STAT axes, as well as alterations in glucose and lipid metabolism, are discussed in terms of their roles in tumorigenesis and metabolic dysfunction. The review also evaluates current and emerging therapeutic strategies, including metabolic reprogramming, targeted therapies, immunotherapies, and surgical approaches, within the context of the biochemical alterations observed in these conditions. Advances in precision medicine, biomarker discovery, and personalized treatment approaches have been highlighted and supported by innovations in systems biology, gene editing, and artificial intelligence. A deeper biochemical understanding of the interactions between diabetes, obesity, and pancreatic cancer holds promise for identifying novel therapeutic targets and improving patient outcomes in this multifactorial disease landscape.