Journal
CELL METABOLISM
Volume 20, Issue 6, Pages 1030-1037Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2014.11.006
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Funding
- University of Edinburgh Chancellor's Fellowship
- Wellcome Trust [WT098012]
- National Institutes of Health [R01 DK096010, R01 DK089044, R01 DK071051, R01 DK075632, R37 DK053477, R01 DK098853]
- VUMC Hormone Assay Core (NIH) [DK059637, DK020593]
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Hypoglycemia engenders an autonomically mediated counterregulatory (CR)-response that stimulates endogenous glucose production to maintain concentrations within an appropriate physiological range. Although the involvement of the brain in preserving normoglycemia has been established, the neurocircuitry underlying centrally mediated CR-responses remains unclear. Here we demonstrate that lateral parabrachial nucleus cholecystokinin (CCKLPBN) neurons are a population of glucose-sensing cells (glucose inhibited) with counterregulatory capacity. Furthermore, we reveal that steroidogenic-factor 1 (SF1)-expressing neurons of the ventromedial nucleus of the hypothalamus (SF1(VMH)) are the specific target of CCKLPBN glucoregulatory neurons. This discrete CCKLPBN -> SF1(VMH) neurocircuit is both necessary and sufficient for the induction of CR-responses. Together, these data identify CCKLPBN neurons, and specifically CCK neuropeptide, as glucoregulatory and provide significant insight into the homeostatic mechanisms controlling CR-responses to hypoglycemia.
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