Autor(es)

Meirelles, Marcela G. ; Fenero, Camila I. M. ; Nornberg, Bruna F. ; da Silveira, Tony L. R. ; Kutter, Mateus T. ; Camara, Niels Olsen S. ; Marins, Luis Fernando

• Tipo de documento: Artigo Científico
• Fonte: COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-MOLECULAR & INTEGRATIVE PHYSIOLOGY; v. 310, p. 9-pg., 2025-12-01.

Resumo

Intestinal permeability refers to the regulated passage of luminal contents into the internal milieu via transcellular or paracellular routes. Tight junctions (TJs), components of the apical junctional complex (AJC), are critical determinants of paracellular permeability and intestinal barrier integrity. Disruptions in growth hormone (GH) signaling have been implicated in gastrointestinal dysfunction; however, the effects of chronically elevated GH levels on intestinal barrier function remain poorly understood. In this study, we investigated whether GH overexpression affects intestinal permeability and epithelial structure using a transgenic zebrafish model. ghtransgenic zebrafish and their non-transgenic full siblings were evaluated for intestinal architecture and barrier function. Images of transmission electron microscopy revealed a greater frequency of AJC disruption in ghtransgenic fish. These ultrastructural changes were associated with increased transcription of TJ-related genes, including cldn15a, oclna, and zo1a, as assessed by qRT-PCR, and a higher intestinal permeability to macromolecule (RITC-dextran 10,000 MW). These findings demonstrate that chronic gh overexpression alters intercellular epithelial architecture and enhances intestinal paracellular permeability. This may reflect an adaptive mechanism to meet increased energy demands under anabolic conditions. Moreover, these results suggest a mechanistic link between GH signaling pathways and modulation of the intestinal barrier, with potential implications for biomedical science. (AU)

• Processo FAPESP: 15/21644-9 - Inflamação induzida pela obesidade, alterações da microbiota e seus efeitos no sistema nervoso entérico: estudo num modelo experimental de zebrafish.
• Beneficiário: Camila Idelí Morales Fénero
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 17/05264-7 - Metabolismo celular, microbiota e sistema imune: novos paradigmas na fisiopatologia das doenças renais
• Beneficiário: Niels Olsen Saraiva Câmara
• Modalidade de apoio: Auxílio à Pesquisa - Temático