Growth hormone enhances the recovery of hypoglycemia via ventromedial hypothalamic neurons

Aug 2, 2019FASEB journal : official publication of the Federation of American Societies for Experimental Biology

Growth hormone helps brain cells in the ventromedial hypothalamus recover from low blood sugar

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Abstract

Ablation of growth hormone receptors in specific brain cells led to impaired recovery from insulin-induced hypoglycemia.

Growth hormone is secreted during low blood sugar levels and influences neuronal responses in the brain.
In mice lacking growth hormone receptors in leptin receptor-expressing cells, the recovery from insulin-induced hypoglycemia was significantly impaired.
Ablation of growth hormone receptors in steroidogenic factor-1-expressing cells also weakened the body's counter-regulatory response to low glucose levels.
The reduced counter-regulatory response was linked to abnormal activity in parasympathetic neurons.
Activation of specific brain regions was altered in mice without growth hormone receptors in steroidogenic factor-1 cells.

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Growth hormone (GH) is secreted during hypoglycemia, and GH-responsive neurons are found in brain areas containing glucose-sensing neurons that regulate the counter-regulatory response (CRR). However, whether GH modulates the CRR to hypoglycemiaspecific neuronal populations is currently unknown. Mice carrying ablation of GH receptor (GHR) either in leptin receptor (LepR)- or steroidogenic factor-1 (SF1)-expressing cells were studied. We also investigated the importance of signal transducer and activator of transcription 5 (STAT5) signaling in SF1 cells for the CRR. GHR ablation in LepR cells led to impaired capacity to recover from insulin-induced hypoglycemia and to a blunted CRR caused by 2-deoxy-d-glucose (2DG) administration. GHR inactivation in SF1 cells, which include ventromedial hypothalamic neurons, also attenuated the CRR. The reduced CRR was prevented by parasympathetic blockers. Additionally, infusion of 2DG produced an abnormal hyperactivity of parasympathetic preganglionic neurons, whereas the 2DG-induced activation of anterior bed nucleus of the stria terminalis neurons was reduced in mice without GHR in SF1 cells. Mice carrying ablation ofgenes in SF1 cells showed no defects in the CRR. In summary, GHR expression in SF1 cells is required for a normal CRR, and these effects are largely independent of STAT5 pathway.-Furigo, I. C., de Souza, G. O., Teixeira, P. D. S., Guadagnini, D., Frazão, R., List, E. O., Kopchick, J. J., Prada, P. O., Donato, J., Jr. Growth hormone enhances the recovery of hypoglycemiaventromedial hypothalamic neurons. via Stat5a/b via

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Growth hormone enhances the recovery of hypoglycemia via ventromedial hypothalamic neurons

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