Programming of Fetal Insulin Resistance in Pregnancies with Maternal Obesity by ER Stress and Inflammation

Figure 1

Balance of pro-inflammatory and anti-inflammatory cytokines in the development of ER stress and insulin resistance. In this scheme we highlight the role of several pro-inflammatory cytokines (a) and anti-inflammatory cytokines (b). These models integrate information from animal and cellular different models, which can be extrapolated to other systems. Cytokines or other molecules with pro-inflammatory effects have a tendency to induce the ER stress and produce insulin resistance. Interestingly, cytokines or other molecules with anti-inflammatory effects, such as TUDCA, omega 3 fatty acids, or quercetin, prevent the release of pro-inflammatory cytokines, inhibit the development of ER stress, and induce insulin sensitizing, improving glucose metabolism (icResistin = intracellular resistin; sKlotho = soluble Klotho; icKlotho = intracellular Klotho; ipIL-6 = intraperitoneally injected IL-6; ihIL-6 = intrahypothalamically injected IL-6).