Leptin Activates NLRP3 Inflammasome-Associated with Type II Diabetes and Obesity.
Leptin also operates similarly to pro-inflammatory cytokines known as adipocytokines. The hormone has been reported to control energy expenditure and metabolism, and modulate the
innate and adaptive immune responses. The stimulation of natural killer cells, chemotaxis of neutrophils, and secretion of tumor necrosis factor (TNF)-α, IL-6 and IL-12 from macrophages
also involves leptin. These increase leptin concentrations in adipose cells and create a cycle of constant stimulation of reactants that encourage inflammation.
Furthermore, leptin promotes Th17 cell responses which are a subset of effector memory T-cells that induce tissue inflammation and destruction that are markers of immune inflammatory diseases and decrease the number of T-regulatory cells. Fat stores release leptin around various lymph nodes signaling to the rest of the immune system if the body has enough energy stored to initiate an immune response which causes continuous leptin circulation in obese or individuals with type II diabetes.
Improvements Inflammation is a player in the pathogenesis of obesity. The chronic overfeeding associated with obesity causes macrophage saturation in the adipose tissue and results in proinflammatory cytokine production. This endogenous signaling triggers the intracellular innate immune NLRP3 sensor, results in caspase-1 activation and the production of IL-1ß and IL-18.21
These cytokines are directly related to the development of insulin resistance that we observe in type II diabetes. Specifically, IL-1ß inhibits adipocyte differentiation while the absence of IL-18 induces obesity and insulin resistance. Conversely, the absence of the NLRP3 inflammasome has been shown inhibit the development of obesity-induced insulin resistance, which would suggest that the inflammasome is a contributor.
Adv Food Technol Nutr Sci Open J. 2018; 4(2): e13-e16. doi: 10.17140/AFTNSOJ-4-e016