Endocrine Abstracts

The underlying basis for understanding of how brain control energy homeostasis, resides in a functional and coordinate communicating pathways between peripheral endocrine organs and the brain, in which the hypothalamus plays a pivotal role in the integration and processing of peripheral metabolic cues into satiety and feeding signals. Glial cells in particular astrocytes, as being an integral cell type of the neurovascular unit forming direct physical contacts with cerebral blood vessels, occupy a privileged position within the brain parenchyma to survey the metabolic status of the organism and to, in turn, modulate the activity of local neurocircuitries to match with whole-body energy demands. Via both physical contact and by releasing an array of soluble factors, astrocytes crucially contribute to control the selective access of circulating factors into the brain. Consistent with this, our previous studies have demonstrated that insulin signaling in astrocytes regulate the glucose entry into the brain and in turn cooperate with neurons in the regulation of feeding and systemic glucose metabolism. We have recently reported that astrocytes also respond to other peripheral hormones like leptin to promote hypothalamic angiogenesis and hypertension in diet-induced obesity. Interestingly, we observed that silencing specific metabolic receptors in hypothalamic astrocytes prevent microvascular dysfunction and the rise of systemic blood pressure in response to high-calorie diets. Therefore, our findings and ongoing studies are focused on unraveling the cellular and molecular basis in the communication between astrocytes and neurovascular beds for the brain control of metabolism, as representing potential cellular targets to fight obesity and its comorbidities such as hypertension.