Signaling by Reactive Oxygen Species (ROS) in β‐cells and Fat Cells

Insulin is the main hormone mediator that communicates fuel excess or fuel need is to facilitate both storage and release of glucose and fatty acids (FA). Chronic excess nutrient supply is associated with basal hyperinsulinemia, insulin resistance, inflammation, and hyperlipidemia. Insulin resistance decreases peripheral insulin‐sensitive glucose uptake while adipose tissue FA storage increases. We hypothesize that insulin resistance may be beneficial to prevent hypoglycemia caused by the need for high insulin to store FA. Excess FA also stimulate the β‐cell and implicate the fat cell as co‐conspirator in insulin resistance and hyperinsulinemia. High ROS has been identified as a cause of cell damage, however, we will focus on the complimentary signaling roles of low physiological levels of ROS in fat cells and β‐cells. In the fat cell, increased FA inhibits oxidation by generating ROS forcing FA into TG and increasing both fat mass and lipolysis, whereas ROS scavengers have the opposite effect. On the other hand, ROS stimulates and is essential for insulin secretion. ROS scavenging totally blocks secretion. The increase in ROS caused by excess fuel supply was mediated by an increased mitochondrial redox state. We hypothesize that ROS signals differently in different cell types, increasing insulin secretion in β‐cells and increasing TG formation and turnover while inhibiting respiration in adipocytes.