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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Growth hormone enhances the recovery of hypoglycemia via ventromedial hypothalamic neurons

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Author(s):
Furigo, Isadora C. [1] ; de Souza, Gabriel O. [1] ; Teixeira, Pryscila D. S. [1] ; Guadagnini, Dioze [2] ; Frazao, Renata [3] ; List, Edward O. [4, 5] ; Kopchick, John J. [4, 5] ; Prada, Patricia O. [2] ; Donato, Jr., Jose [1]
Total Authors: 9
Affiliation:
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, Av Prof Lineu Prestes 1524, BR-05508000 Sao Paulo - Brazil
[2] Univ Estadual Campinas, Sch Appl Sci, Limeira - Brazil
[3] Univ Sao Paulo, Inst Biomed Sci, Dept Anat, Sao Paulo - Brazil
[4] Ohio Univ, Edison Biotechnol Inst, Athens, OH 45701 - USA
[5] Ohio Univ, Heritage Coll Osteopath Med, Athens, OH 45701 - USA
Total Affiliations: 5
Document type: Journal article
Source: FASEB JOURNAL; v. 33, n. 11, p. 11909-11924, NOV 2019.
Web of Science Citations: 2
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. (AU)

FAPESP's process: 17/02983-2 - The role of growth hormone in the brain: relevance for neural functions and in disease
Grantee:Jose Donato Junior
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 17/18498-6 - IMPACT OF THE PERINATAL EXPOSURE TO ENVIRONMENTAL POLLUTANTS IN THE GENESIS OF OBESITY AND TYPE 2 DIABETES MELLITUS: METABOLIC AND EPIGENETIC ASPECTS
Grantee:Patrícia de Oliveira Prada
Support Opportunities: Regular Research Grants
FAPESP's process: 18/20087-7 - The specific deletion of CLK2 in GABA neurons: the impact on feeding behavior and energy metabolism in mice
Grantee:Patrícia de Oliveira Prada
Support Opportunities: Regular Research Grants
FAPESP's process: 16/09679-4 - Central effects of growth hormone on energetic metabolism and glicemic control
Grantee:Isadora Clivatti Furigo
Support Opportunities: Scholarships in Brazil - Post-Doctoral