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Long-term increase of insulin secretion in mice subjected to pregnancy and lactation

PURPOSE: Observational studies show that longer breastfeeding periods reduce maternal risk of type 2 diabetes mellitus. However, it is currently unknown if the long-term benefits of breastfeeding for maternal glucose homeostasis are linked to changes in the endocrine pancreas. METHODS: We presently...

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Detalles Bibliográficos
Autores principales: Vicente, Julia Modesto, Santos-Silva, Junia Carolina, Teixeira, Caio Jordão, de Souza, Dailson Nogueira, Vettorazzi, Jean Franciesco, Furtuoso, Fabiola Sales, Adabo, Isabel Gouveia, Sato, Fabio Takeo, Vinolo, Marco Aurélio Ramirez, Carneiro, Everardo Magalhães, Bordin, Silvana, Anhê, Gabriel Forato
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bioscientifica Ltd 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7159261/
https://www.ncbi.nlm.nih.gov/pubmed/32182583
http://dx.doi.org/10.1530/EC-20-0020
Descripción
Sumario:PURPOSE: Observational studies show that longer breastfeeding periods reduce maternal risk of type 2 diabetes mellitus. However, it is currently unknown if the long-term benefits of breastfeeding for maternal glucose homeostasis are linked to changes in the endocrine pancreas. METHODS: We presently evaluated functional, morphological and molecular aspects of the endocrine pancreas of mice subjected to two sequential cycles of pregnancy and lactation (L21). Age-matched mice not allowed to breastfeed (L0) and virgin mice were used as controls. RESULTS: L21 mice exhibited increased tolerance and increased glucose-stimulated insulin secretion (GSIS) by isolated islets. Pancreatic islets of L21 mice did not present evident morphological changes to justify the increased GSIS. On the other hand, islets of L21 mice exhibited a reduction in Cavb3 and Kir6.2 expression with concordant increased intracellular Ca(2+) levels after challenge with glucose. CONCLUSION: Altogether, the present findings show the breastfeeding exerts long-term benefits for maternal endocrine pancreas by increasing intracellular Ca(2+) levels and GSIS.