The timeline of neuronal and glial alterations in experimental obesity.

Abstract

In experimental models, hypothalamic dysfunction is a key component of the pathophysiology of diet-induced obesity. Early after the introduction of a high-fat diet, neurons, microglia, astrocytes and tanycytes of the

mediobasal hypothalamus undergo structural and functional changes that impact caloric intake, energy expen- diture and systemic glucose tolerance. Inflammation has emerged as a central component of this response, and as

in other inflammatory conditions, there is a time course of events that determine the fate of distinct cells involved in the central regulation of whole-body energy homeostasis. Here, we review the work that identified key mechanisms, cellular players and temporal features of diet-induced hypothalamic abnormalities.