While long-term exposure to high glucose induces oxidative stress in beta cells, conflicting results have been published regarding the impact of amino acid exposure and their role in oxidative stress and insulin secretion. Although beta cells are considered to be particularly vulnerable to oxidative damage, as they express relatively low levels of some peroxide-metabolizing enzymes such as catalase and glutathione peroxidase, other less known glutathione-based antioxidant systems are expressed in beta cells at higher levels. Specific interactions between RNS and ROS may be the cause of the vulnerability of pancreatic beta-cells to oxidative damage. While this presentation will provide background information as to the  importance of metabolic integration of nutritional and endocrine signals in the beta cell for insulin secretion, the emerging role of amino acid and small peptide availability for glutathione synthesis and for the maintenance of beta cell function and viability during periods of metabolic disturbance will be described.