The timeline of neuronal and glial alterations in experimental obesity*

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 expenditure 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. This article is part of the special Issue on 'Cross Talk between Periphery and the Brain'.

Automated summary

In experimental models, hypothalamic dysfunction is a crucial component in the pathophysiology of diet-induced obesity. Structural and functional changes in neurons, microglia, astrocytes, and tanycytes of the mediobasal hypothalamus, shortly after the introduction of a high-fat diet, impact caloric intake, energy expenditure, and systemic glucose tolerance. Inflammation plays a central role in this response, and there is a temporal sequence of events determining the fate of different cells involved in the central regulation of whole-body energy homeostasis.