Endocrine Abstracts

Decreased insulin action has been proposed as the common factor that is in the background of the different components of the metabolic syndrome. Insulin resistance is also associated with a chronic activation of the innate immune system. The innate immune system constitutes the first line of body’s defence and it is constituted by different barriers (epithelia, adipose tissue), and different blood and tissue components as macrophages, and neutrophils. Once activated, the acute phase response is activated, with generation of different acute phase proteins and cytokines that are produced in order to struggle against different aggresions, as infections and traumatisms. The aim of this response is to eradicate these agents, to repair the harmed tissues, and, through increased insulin resistance, to optimize the energetic substrates, which will be drained to vital tissues and organs (i.e. brain and the immune system). Evolution pressures have led to survival of the fittest individuals, those with genetics that allows the best defence against infection and periods of famine. The initial evolutive advantages of increased inflammatory responses, hypersecretion of proinflammatory cytokines (TNF-α, interleukin 6, interleukin 18), counterbalanced by antiinflammatory molecules (adiponectin, sCD14, BPI, MBL), turn into chronic inflammation conditions, such as obesity and type 2 diabetes. Increasing evidence is reported according to which chronic inflammation precedes these conditions. The knowledge of how these metabolic pathways interact with the inflammatory cascade will facilitate new therapeutic approaches.