Insulin Resistance Mechanisms: From Epigenetics to Receptor-Mediated Signaling Pathways

Dear Colleagues,

Insulin resistance is a systemic disorder characterized by the inability of cells to respond appropriately to physiological concentrations of circulating insulin. Under these conditions, insulin-mediated actions in hepatic, muscular, and adipose tissues, including glucose uptake and glycogen, lipid, and protein synthesis, are impaired. Despite extensive investigations from both molecular and clinical perspectives, insulin resistance remains a major research challenge. At the molecular level, insulin resistance results from disruptions in insulin signaling caused by epigenetic modifications in genes encoding proteins of the insulin signaling cascade, mutations, or post-translational modifications of the insulin receptor and its downstream effectors, including insulin receptor substrate, PI3K, and Akt. A critical priority is to elucidate how environmental factors, such as Western-style diets, air pollution, physical inactivity, and psychosocial stress associated with urban living, contribute to these molecular alterations. These factors may promote epigenetic changes in genes encoding insulin signaling proteins or induce post-translational modifications that interfere with receptor function and downstream signaling.

We invite contributions to this Special Issue addressing these topics. Original research articles and reviews are welcome on the following topics: the impact of Western-style diets, environmental pollutants, and stress on insulin receptor signaling; protective and reversal effects of physical activity on insulin resistance at the molecular level; molecular and cellular mechanisms underlying insulin resistance; and the role of insulin resistance in the development of inflammatory, cardiovascular, neurological, cognitive, and cancer-related disorders.

Prof. Dr. Angélica Rueda
Prof. Dr. Jesús Alberto Olivares-Reyes
Guest Editors

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