Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/340566
Type: Artigo
Title: Growth hormone enhances the recovery of hypoglycemia via ventromedial hypothalamic neurons
Author: Furigo, Isadora C.
de Souza, Gabriel O.
Teixeira, Pryscila D. S.
Guadagnini, Dioze
Frazao, Renata
List, Edward O.
Kopchick, John J.
Prada, Patricia O.
Donato Jr., Jose
Abstract: 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 hypoglycemia via specific 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 of Stat5 a/b genes 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
Subject: Hipotálamo
Country: Estados Unidos
Editor: Federation of American Societies for Experimental Biology
Rights: Fechado
Identifier DOI: 10.1096/fj.201901315R
Address: https://faseb.onlinelibrary.wiley.com/doi/full/10.1096/fj.201901315R
Date Issue: 2019
Appears in Collections:FCM - Artigos e Outros Documentos
FCA - Artigos e Outros Documentos

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