Iron and β-Cell Function: Implications for Diabetes Pathophysiology

Abstract

Background: The intricate relationship between iron metabolism and diabetes mellitus has become a subject of increasing interest, with a growing body of evidence suggesting that iron plays a significant role in the pathophysiology of diabetes. Spe-cifically, the impact of iron on β-cell function has emerged as a critical area of study. Β cells, located in the pancreatic islets of Langerhans, are responsible for insulin synthesis and secretion. Purpose: Understanding how iron influences these vital cells is crucial for unraveling the complexities of diabetes development and progression. Methods: This review synthesizes current literature on the interaction between iron and β-cell function, exploring the molecular and cellular mechanisms underlying this relationship. We conducted a systematic search of databases, including PubMed and Scopus, to identify relevant studies published up to the present date. Articles were selected based on their focus on iron homeostasis, β-cell function, and their implica-tions for diabetes pathophysiology. Results: Iron is an essential micronutrient that participates in various cellular pro-cesses, including energy metabolism and reactive oxygen species (ROS) regulation. In β cells, iron is intricately involved in insulin synthesis, folding, and maturation. However, an imbalance in iron homeostasis can lead to oxidative stress, mitochon-drial dysfunction, and impaired insulin secretion. The reviewed literature provides compelling evidence that alterations in iron levels can adversely affect β-cell func-tion, contributing to the development and progression of diabetes. Excess iron has been associated with increased oxidative stress within β cells, leading to damage and dysfunction. Furthermore, iron-induced ROS may activate inflammatory pathways, promoting β-cell apoptosis and insulin resistance in peripheral tissues. Conversely, iron deficiency may also impact β-cell health. Insufficient iron availability can com-promise the efficiency of insulin synthesis and secretion, potentially contributing to glucose dysregulation. Iron-deficient conditions may lead to alterations in cellular energy metabolism, further exacerbating the vulnerability of β cells to stressors. Conclusions: Understanding the nuanced interplay between iron and β-cell function has implications for diabetes management. Therapeutic strategies aimed at modulating iron levels, such as iron chelation or dietary interventions, hold promise for preserving β-cell health and improving glycemic control. This review underscores the intricate relationship between iron and β-cell function, providing valuable insights into the pathophysiology of diabetes. Whether through excess or deficiency, iron significantly influences the health and function of β cells, shaping the landscape of diabetes development. Further research is warranted to delineate the precise mecha-nisms involved and to explore targeted interventions that may harness the therapeutic potential of modulating iron levels in diabetes management.