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Intestinal alterations and mild glucose homeostasis impairments in the offspring born to overweight rats.
Heinecke, Florencia; Fornes, Daiana; Capobianco, Evangelina; Flores Quiroga, Jeremias Pablo; Labiano, Marina; Faletti, Alicia G; Jawerbaum, Alicia; White, Verónica.
Afiliação
  • Heinecke F; Centre for Pharmacological and Botanical Studies (CEFYBO-CONICET-UBA), School of Medicine, University of Buenos Aires, Buenos Aires, Argentina.
  • Fornes D; Centre for Pharmacological and Botanical Studies (CEFYBO-CONICET-UBA), School of Medicine, University of Buenos Aires, Buenos Aires, Argentina.
  • Capobianco E; Centre for Pharmacological and Botanical Studies (CEFYBO-CONICET-UBA), School of Medicine, University of Buenos Aires, Buenos Aires, Argentina.
  • Flores Quiroga JP; Centre for Pharmacological and Botanical Studies (CEFYBO-CONICET-UBA), School of Medicine, University of Buenos Aires, Buenos Aires, Argentina.
  • Labiano M; Centre for Pharmacological and Botanical Studies (CEFYBO-CONICET-UBA), School of Medicine, University of Buenos Aires, Buenos Aires, Argentina.
  • Faletti AG; Centre for Pharmacological and Botanical Studies (CEFYBO-CONICET-UBA), School of Medicine, University of Buenos Aires, Buenos Aires, Argentina.
  • Jawerbaum A; Centre for Pharmacological and Botanical Studies (CEFYBO-CONICET-UBA), School of Medicine, University of Buenos Aires, Buenos Aires, Argentina.
  • White V; Centre for Pharmacological and Botanical Studies (CEFYBO-CONICET-UBA), School of Medicine, University of Buenos Aires, Buenos Aires, Argentina. Electronic address: vernica73@gmail.com.
Mol Cell Endocrinol ; 587: 112201, 2024 Jun 01.
Article em En | MEDLINE | ID: mdl-38494045
ABSTRACT
The gut plays a crucial role in metabolism by regulating the passage of nutrients, water and microbial-derived substances to the portal circulation. Additionally, it produces incretins, such as glucose-insulinotropic releasing peptide (GIP) and glucagon-like derived peptide 1 (GLP1, encoded by gcg gene) in response to nutrient uptake. We aimed to investigate whether offspring from overweight rats develop anomalies in the barrier function and incretin transcription. We observed pro-inflammatory related changes along with a reduction in Claudin-3 levels resulting in increased gut-permeability in fetuses and offspring from overweight rats. Importantly, we found decreased gip mRNA levels in both fetuses and offspring from overweight rats. Differently, gcg mRNA levels were upregulated in fetuses, downregulated in female offspring and unchanged in male offspring from overweight rats. When cultured with high glucose, intestinal explants showed an increase in gip and gcg mRNA levels in control offspring. In contrast, offspring from overweight rats did not exhibit any response in gip mRNA levels. Additionally, while females showed no response, male offspring from overweight rats did exhibit an upregulation in gcg mRNA levels. Furthermore, female and male offspring from overweight rats showed sex-dependent anomalies when orally challenged with a glucose overload, returning to baseline glucose levels after 120 min. These results open new research questions about the role of the adverse maternal metabolic condition in the programming of impairments in glucose homeostasis, enteroendocrine function and gut barrier function in the offspring from overweight mothers and highlight the importance of a perinatal maternal healthy metabolism.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Polipeptídeo Inibidor Gástrico / Sobrepeso Limite: Animals Idioma: En Revista: Mol Cell Endocrinol Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Argentina País de publicação: Irlanda

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Polipeptídeo Inibidor Gástrico / Sobrepeso Limite: Animals Idioma: En Revista: Mol Cell Endocrinol Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Argentina País de publicação: Irlanda