Glial cells are the most abundant cell type in the CNS. Although they were originally thought to only play a supportive role for neurons, it is now clear that glial cells are involved in all aspects of brain function. Understanding how glia, and in particular astrocytes, tanycytes and microglia, participate in the neuroendocrine control of metabolic homeostasis has come to the forefront in recent years. This is largely due to the observation that high fat diet-induced hypothalamic inflammation and gliosis have been implicated in the development of obesity associated secondary complications such as central insulin and leptin resistance. However, in addition to participating in pathophysiological processes, glial cells are also involved in the physiological control of metabolic homeostasis. Glia are the first line of defense against any attack on neurons, including nutritional assaults. Tanycytes and astrocytes transport circulating nutrients and metabolic factors fundamental for neuronal viability and activity into and within the hypothalamus. Astrocytes also participate in the rewiring of hypothalamic metabolic circuits. Astroglia express receptors for diverse metabolic signals, including various forms of the leptin receptor. Not only does leptin induce cytokine production by astrocytes, but it stimulates morphological changes in these glial cells and this is associated with modifications in synaptic inputs to neurons involved in metabolic control. The capacity of astrocytes to transport glucose and glutamate is modified by both leptin and ghrelin, indicating an additional mechanism by which these hormones can modify neuronal metabolism and synaptic transmission. Indeed, knock-out of the leptin receptor specifically in astrocytes modifies an individuals metabolic response to this hormone. The aim of this talk will be to present our current understanding of how astrocytes participate in both the physiological and pathophysiological control of metabolic homeostasis.
Funding: This work was funded by grants from Fondos de Investigación Sanitaria (PI1302195), Ministerio de Ciencia e Innovación (BFU201127492), Centro de Investigación Biomédica en Red Fisiopatología de Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, and Fundación de Endocrinología y Nutrición.
01 - 03 Oct 2015
European Society for Paediatric Endocrinology