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Endocrine Abstracts (2018) 56 OC13.5 | DOI: 10.1530/endoabs.56.OC13.5

ECE2018 Oral Communications The curious case of growth hormone (5 abstracts)

Growth hormone acts in AgRP neurons to control energy expenditure during food restriction and promotes counter-regulatory responses to hypoglycemia via the ventromedial hypothalamus

Isadora C Furigo 1 , Pryscila DS Teixeira 1 , Gabriel O Souza 1 , Eduard List 2 , John Kopchick 2 & José Donato 1


1Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil; 2Edison Biotechnology Institute, Ohio University, Athens, Ohio, USA.


Growth hormone (GH) responsive cells are extensively distributed in central nervous system, including in neurons of the arcuate (ARH) and ventromedial nucleus (VMH) of hypothalamus, areas that control food intake, energy expenditure and blood glucose. During metabolic stresses, such as food restriction and hypoglycemia, GH secretion is stimulated and may be important to maintain survival. In the present study, we first verified that an acute GH injection stimulates food intake by increasing AgRP and NPY mRNA expression in the hypothalamus of wild-type mice. Then we generated mice lacking GH receptor (GHR) specifically in AgRP neurons or in steroidogenic factor-1 (SF1) cells, which include neurons in the VMH, in order to evaluate whether these cells mediate the effects of GH during conditions of metabolic stress. AgRP GHR KO mice exhibited similar body weight, food intake, energy expenditure, glucose tolerance and leptin sensitivity, compared to control animals. However, fasting induced a lower cFOS expression in the ARH of AgRP GHR KO than control animals. Remarkably, while control mice adapted to a 60% food deprivation period by progressively saving energy, AgRP GHR KO mice exhibited a blunted metabolic adaptation to starvation, which led to higher energy expenditure and weight loss, followed by higher T4 production and UCP-1 mRNA expression in the iBAT. Blockage of sympathetic system with propranolol equalized the energy expenditure between the groups. In contrast, SF1 GHR KO mice exhibited similar responses to control group in food restriction, but a blunted counter-regulatory response evoked by 2-deoxyglucose (2DG) administration, indicating that GH may act in VMH cells to reverse the hypoglycemic state. In summary, GH signaling in AgRP neurons regulates the metabolic adaptations to starvation, while GH signaling in the VMH controls the counter-regulatory responses to hypoglycemia. These findings indicate a previously unidentified function of GH by acting in specific neuronal populations in order to ensure survival via the induction of appropriate metabolic responses.

Volume 56

20th European Congress of Endocrinology

Barcelona, Spain
19 May 2018 - 22 May 2018

European Society of Endocrinology 

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