| Literature DB >> 35108515 |
Ioannis Papazoglou1, Ji-Hyeon Lee2, Zhenzhong Cui2, Chia Li2, Gianluca Fulgenzi3, Young Jae Bahn2, Halina M Staniszewska-Goraczniak4, Ramón A Piñol2, Ian B Hogue5, Lynn W Enquist4, Michael J Krashes2, Sushil G Rane6.
Abstract
The central nervous system has long been thought to regulate insulin secretion, an essential process in the maintenance of blood glucose levels. However, the anatomical and functional connections between the brain and insulin-producing pancreatic β cells remain undefined. Here, we describe a functional transneuronal circuit connecting the hypothalamus to β cells in mice. This circuit originates from a subpopulation of oxytocin neurons in the paraventricular hypothalamic nucleus (PVNOXT), and it reaches the islets of the endocrine pancreas via the sympathetic autonomic branch to innervate β cells. Stimulation of PVNOXT neurons rapidly suppresses insulin secretion and causes hyperglycemia. Conversely, silencing of these neurons elevates insulin levels by dysregulating neuronal signaling and secretory pathways in β cells and induces hypoglycemia. PVNOXT neuronal activity is triggered by glucoprivation. Our findings reveal that a subset of PVNOXT neurons form functional multisynaptic circuits with β cells in mice to regulate insulin secretion, and their function is necessary for the β cell response to hypoglycemia.Entities:
Keywords: central nervous system; glucoprivation; hypoglycemia; insulin secretion; oxytocin neurons; pancreatic β cells; paraventricular hypothalamic nucleus; pseudorabies tracing; sympathetic innervation; transneuronal circuit
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Year: 2022 PMID: 35108515 PMCID: PMC8935365 DOI: 10.1016/j.cmet.2021.12.020
Source DB: PubMed Journal: Cell Metab ISSN: 1550-4131 Impact factor: 27.287