Endocrine Abstracts

Hypothalamic inflammation has been the focus of an increasing number of studies in recent years as it is thought to underlie the pathogenesis of obesity-associated insulin resistance and type 2 diabetes. These studies have also highlighted the role of glial cells in metabolic control, due to the fact that both microglia and astrocytes are involved in central inflammatory processes. High fat diet (HFD)-induced obesity has been the most commonly used model for the analysis of this phenomenon, with the diet itself shown to play an important role as hypothalamic inflammation can occur even before significant weight gain is observed. Indeed, fatty acids (FAs) can directly activate glial cells and trigger neuroinflammation. However, this response differs depending on the FA involved, with some FAs possibly being protective. Moreover, not all obesity is induced by HFD intake. The hypothalamic inflammatory/gliosis response in animals that are obese or overweight due to genetic causes, early nutritional manipulations or high carbohydrate diets differs from that seen in HFD-induced obesity. This talk will focus on the advances in our understanding of the metabolic signals involved in hypothalamic inflammation/gliosis and how this might influence the development of secondary complications such as insulin and leptin resistance.

Disclosure: This work was funded by grants from Fondos de Investigación Sanitaria (PI100747; PI1302195), Ministerio de Ciencia e Innovación (BFU2011–27492), Centro de Investigación Biomédica en Red Fisiopatología de Obesidad y Nutrición (CIBEROBN), Instituto Carlos III, Madrid, Spain.