Growth Hormone Overexpression Induces Hyperphagia and Intestinal Morphophysiological Adaptations to Improve Nutrient Uptake in Zebrafish

The excess of circulating growth hormone (GH) in most transgenic animals implies mandatory growth resulting in higher metabolic demand. Considering that the intestine is the main organ responsible for the digestion, absorption, and direction of dietary nutrients to other tissues, this study aimed to...

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Main Authors: Marcela G. Meirelles, Bruna F. Nornberg, Tony L. R. da Silveira, Mateus T. Kütter, Caroline G. Castro, Juan Rafael B. Ramirez, Virgínia Pedrosa, Luis Alberto Romano, Luis Fernando Marins
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-09-01
Series:Frontiers in Physiology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fphys.2021.723853/full
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author Marcela G. Meirelles
Bruna F. Nornberg
Tony L. R. da Silveira
Mateus T. Kütter
Caroline G. Castro
Juan Rafael B. Ramirez
Virgínia Pedrosa
Luis Alberto Romano
Luis Fernando Marins
author_facet Marcela G. Meirelles
Bruna F. Nornberg
Tony L. R. da Silveira
Mateus T. Kütter
Caroline G. Castro
Juan Rafael B. Ramirez
Virgínia Pedrosa
Luis Alberto Romano
Luis Fernando Marins
author_sort Marcela G. Meirelles
collection DOAJ
description The excess of circulating growth hormone (GH) in most transgenic animals implies mandatory growth resulting in higher metabolic demand. Considering that the intestine is the main organ responsible for the digestion, absorption, and direction of dietary nutrients to other tissues, this study aimed to investigate the mechanisms by which gh overexpression modulates the intestine to support higher growth. For this purpose, we designed an 8-weeks feeding trial to evaluate growth parameters, feed intake, and intestinal morphometric indices in the adult gh-transgenic zebrafish (Danio rerio) model. To access the sensitivity of the intestine to the excess of circulating GH, the messenger RNA (mRNA) expression of intestine GH receptors (GHRs) (ghra and ghrb) was analyzed. In addition, the expression of insulin-like growth factor 1a (igf1a) and genes encoding for di and tripeptide transporters (pept1a and pept1b) were assessed. Gh-transgenic zebrafish had better growth performance and higher feed intake compared to non-transgenic sibling controls. Chronic excess of GH upregulates the expression of its cognate receptor (ghrb) and the main growth factor related to trophic effects in the intestine (igf1a). Moreover, transgenic zebrafish showed an increased intestinal absorptive area and higher expression of crucial genes related to the absorption of products from meal protein degradation. These results reinforce the ability of GH to modulate intestinal morphology and the mechanisms of assimilation of nutrients to sustain the energy demand for the continuous growth induced by the excess of circulating GH.
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spelling doaj.art-896ece4a4dbc4b4f94bb024e89ef77e22022-12-21T18:37:32ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2021-09-011210.3389/fphys.2021.723853723853Growth Hormone Overexpression Induces Hyperphagia and Intestinal Morphophysiological Adaptations to Improve Nutrient Uptake in ZebrafishMarcela G. Meirelles0Bruna F. Nornberg1Tony L. R. da Silveira2Mateus T. Kütter3Caroline G. Castro4Juan Rafael B. Ramirez5Virgínia Pedrosa6Luis Alberto Romano7Luis Fernando Marins8Laboratório de Biologia Molecular, Instituto de Ciências Biológicas, Departamento de Ciências Fisiológicas, Universidade Federal do Rio Grande – FURG, Rio Grande, BrazilLaboratório de Biologia Molecular, Instituto de Ciências Biológicas, Departamento de Ciências Fisiológicas, Universidade Federal do Rio Grande – FURG, Rio Grande, BrazilLaboratório de Biologia Molecular, Instituto de Ciências Biológicas, Departamento de Ciências Fisiológicas, Universidade Federal do Rio Grande – FURG, Rio Grande, BrazilLaboratório de Biologia Molecular, Instituto de Ciências Biológicas, Departamento de Ciências Fisiológicas, Universidade Federal do Rio Grande – FURG, Rio Grande, BrazilLaboratório de Biologia Molecular, Instituto de Ciências Biológicas, Departamento de Ciências Fisiológicas, Universidade Federal do Rio Grande – FURG, Rio Grande, BrazilLaboratório de Bioquímica Funcional de Organismos Aquáticos, Instituto de Oceanografia, Estação Marinha de Aquicultura, Universidade Federal do Rio Grande – FURG, Rio Grande, BrazilLaboratório de Imunologia e Patologia de Organismos Aquáticos, Instituto de Oceanografia, Estação Marinha de Aquicultura, Universidade Federal do Rio Grande – FURG, Rio Grande, BrazilLaboratório de Imunologia e Patologia de Organismos Aquáticos, Instituto de Oceanografia, Estação Marinha de Aquicultura, Universidade Federal do Rio Grande – FURG, Rio Grande, BrazilLaboratório de Biologia Molecular, Instituto de Ciências Biológicas, Departamento de Ciências Fisiológicas, Universidade Federal do Rio Grande – FURG, Rio Grande, BrazilThe excess of circulating growth hormone (GH) in most transgenic animals implies mandatory growth resulting in higher metabolic demand. Considering that the intestine is the main organ responsible for the digestion, absorption, and direction of dietary nutrients to other tissues, this study aimed to investigate the mechanisms by which gh overexpression modulates the intestine to support higher growth. For this purpose, we designed an 8-weeks feeding trial to evaluate growth parameters, feed intake, and intestinal morphometric indices in the adult gh-transgenic zebrafish (Danio rerio) model. To access the sensitivity of the intestine to the excess of circulating GH, the messenger RNA (mRNA) expression of intestine GH receptors (GHRs) (ghra and ghrb) was analyzed. In addition, the expression of insulin-like growth factor 1a (igf1a) and genes encoding for di and tripeptide transporters (pept1a and pept1b) were assessed. Gh-transgenic zebrafish had better growth performance and higher feed intake compared to non-transgenic sibling controls. Chronic excess of GH upregulates the expression of its cognate receptor (ghrb) and the main growth factor related to trophic effects in the intestine (igf1a). Moreover, transgenic zebrafish showed an increased intestinal absorptive area and higher expression of crucial genes related to the absorption of products from meal protein degradation. These results reinforce the ability of GH to modulate intestinal morphology and the mechanisms of assimilation of nutrients to sustain the energy demand for the continuous growth induced by the excess of circulating GH.https://www.frontiersin.org/articles/10.3389/fphys.2021.723853/fullgh-transgenic fishDanio reriopeptide transporterfeed intakeintestinal morphology
spellingShingle Marcela G. Meirelles
Bruna F. Nornberg
Tony L. R. da Silveira
Mateus T. Kütter
Caroline G. Castro
Juan Rafael B. Ramirez
Virgínia Pedrosa
Luis Alberto Romano
Luis Fernando Marins
Growth Hormone Overexpression Induces Hyperphagia and Intestinal Morphophysiological Adaptations to Improve Nutrient Uptake in Zebrafish
Frontiers in Physiology
gh-transgenic fish
Danio rerio
peptide transporter
feed intake
intestinal morphology
title Growth Hormone Overexpression Induces Hyperphagia and Intestinal Morphophysiological Adaptations to Improve Nutrient Uptake in Zebrafish
title_full Growth Hormone Overexpression Induces Hyperphagia and Intestinal Morphophysiological Adaptations to Improve Nutrient Uptake in Zebrafish
title_fullStr Growth Hormone Overexpression Induces Hyperphagia and Intestinal Morphophysiological Adaptations to Improve Nutrient Uptake in Zebrafish
title_full_unstemmed Growth Hormone Overexpression Induces Hyperphagia and Intestinal Morphophysiological Adaptations to Improve Nutrient Uptake in Zebrafish
title_short Growth Hormone Overexpression Induces Hyperphagia and Intestinal Morphophysiological Adaptations to Improve Nutrient Uptake in Zebrafish
title_sort growth hormone overexpression induces hyperphagia and intestinal morphophysiological adaptations to improve nutrient uptake in zebrafish
topic gh-transgenic fish
Danio rerio
peptide transporter
feed intake
intestinal morphology
url https://www.frontiersin.org/articles/10.3389/fphys.2021.723853/full
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