Nutrient overload, lipid peroxidation and pancreatic beta cell function

Publication date: Available online 4 September 2016
Source:Free Radical Biology and Medicine
Author(s): Shlomo Sasson
Since the landmark discovery of α,β-unsaturated 4-hydroxyalkenals by Esterbauer and colleagues most studies have addressed the consequences of the tendency of these lipid peroxidation products to form covalent adducts with macromolecules and modify cellular functions. Many studies describe detrimental and cytotoxic effects of 4-hydroxy-2E-nonenal (4-HNE) in myriad tissues and organs and numerous pathologies. Other studies similarly assigned unfavorable effects to 4-hydroxy-2E-hexenal (4-HHE) and 4-hydroxy-2E,6Z-dodecadienal (4-HDDE). Nutrient overload (e.g., hyperglycemia, hyperlipidemia) modifies lipid metabolism in cells and promotes lipid peroxidation and the generation of α,β-unsaturated 4-hydroxyalkenals. Advances glycation- and lipoxidation end products (AGEs and ALEs) have been associated with the development of insulin resistance and pancreatic beta cell dysfunction and the etiology of type 2 diabetes and its peripheral complications. Less acknowledged are genuine signaling properties of 4-hydroxyalkenals in hormetic processes that provide defense against the consequences of nutrient overload. This review addresses recent findings on such lipohormetic mechanisms that are associated with lipid peroxidation in pancreatic beta cells.



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