Amino acid restriction alters survival mechanisms in pancreatic beta cells: possible role of the PI3K/Akt pathway

Author(s)

Alves, Bruna Lourenconi ^[1] ; Araujo, Thiago dos Reis ^[1] ; Guimaraes, Dimitrius Santiago Passos Simoes Froes ^[1] ; Zoppi, Claudio Cesar ^[1] ; Figueiredo, Mariana Sarto ^[2] ; Carneiro, Everardo Magalhaes ^[1]

Affiliation

^[1] Univ Campinas UNICAMP, Inst Biol, Dept Struct & Funct Biol, Obes & Comorbid Res Ctr OCRC, BR-13083865 Campinas, SP - Brazil

^[2] Fed Fluminense Univ, Fac Nutr, Dept Nutr & Dietet, Niteroi, RJ - Brazil

• Document type: Journal article
• Source: EUROPEAN JOURNAL OF NUTRITION; v. 60, n. 7, p. 3947-3957, OCT 2021.
• Web of Science Citations: 0

Abstract

Background and aims Malnutrition in the early stages of life may lead to changes in the glycemic metabolism during adulthood, such as pancreatic beta cells dysfunction and failure. Therefore, this study aimed to evaluate the effects of an in vitro amino acid restriction model on the function and viability of pancreatic beta cells. Methods Insulin-producing cells (INS-1E) were maintained in control or amino acid restricted culture medium containing 1 x or 0.25 x of amino acids, respectively, for 48 h. Results Amino acid restricted group showed lower insulin secretion and insulin gene expression, reduced mitochondrial oxygen consumption rate and reactive oxygen species production. Besides, amino acid restricted group also showed higher levels of endoplasmic reticulum stress and apoptosis markers and enhanced Akt phosphorylation. However, even with higher levels of apoptosis markers, amino acid restricted group did not show higher levels of cell death unless the PI3K/Akt pathway was inhibited. Conclusion Amino acid restricted beta cell viability seems to be dependent on the PI3K/Akt pathway. (AU)

• FAPESP's process: 15/12611-0 - Molecular mechanisms involved in pancreatic beta cell disfunction and dead in diabetes mellitus: strategies for the inhibition of these processes and restoration of the insular mass
• Grantee: Antonio Carlos Boschiero
• Support Opportunities: Research Projects - Thematic Grants