Evidence suggests that disruption of signaling/homeostasis plays an important role in the mechanistic basis of PAF as a growth inhibitor. PAF also elicits hyperpolarization of the plasma membrane and the activation of ion channels, followed by an increase in reactive oxygen species in the cell and the induction of an apoptosis-like phenotype Cumulative evidence reveals that diabetes is a condition in which cell homeostasis is impaired. Defects in cell regulation were found in erythrocytes, cardiac muscle, platelets, skeletal muscle, kidney, aorta, adipocytes, liver, osteoblasts, arteries, lens, peripheral nerves, brain synaptosomes, retinal tissue, and pancreatic beta cells, confirming that this defect in cell metabolism is a basic pathology associated with the diabetic state. The defects identified in the mechanical activity of the hearts from type 1 diabetic animals include alteration of signaling via changes in critical processes. Function PAF is used to transmit signals between neighboring cells and acts as a hormone, cytokines, and other signaling molecules. The PAF signaling system can trigger inflammatory and thrombotic cascades, amplify these cascades when acting with other mediators, and mediate molecular and cellular interactions (cross talk) between inflammation and thrombosis. Unregulated PAF signaling can cause pathological inflammation and has been found to be a cause in sepsis, shock, and traumatic injury. PAF can be used as a local signaling molecule and travel over very short distances or it can be circulated throughout the body and act via endocrine. PAF initiates an inflammatory response in allergic reactions. This has been demonstrated in the skin of humans and in the paws and skin of lab rabbits and rodents. The inflammatory response is enhanced by the use of vasodilators, including prostaglandin E1 (PGE,) and PGE2 and inhibited by vasoconstrictors. PAF also induces apoptosis in a different way that is independent of the PAF receptor. The pathway to apoptosis can be inhibited by negative feedback from PAF acetylhydrolase (PAF-AH), an enzyme that catabolizes platelet-activating factor. It is an important mediator of bronchoconstriction. It causes platelets to aggregate and blood vessels to dilate. Thus, it is important to the process of hemostasis. At a concentration of 10−12 mol/L, PAF causes life-threatening inflammation of the airways to induce asthma like symptoms. Toxins such as fragments of destroyed bacteria induce the synthesis of PAF, which causes a drop in blood pressure and reduced volume of blood pumped by the heart, which leads to shock and possibly death. Structure Several molecular species