Expression of Phosphatidylinositol-3-kinase Mediated by the AKT Signaling Pathway in a Hyperglycemic Model

Revista/Jornal:

Endocrinologia & Diabetes Clínica e Experimental, v. XVIII, n. 3, p. 2211-2217, 2021.

Autores:

Lovato FC, Klockner GMD, Rebouças RL, Langer LIV, Hoegen IO, Ronkoski ML, Carvalhal SRS, Collaço LM, Marques CM, Kubrusly LF.

Link/Doi:

Não Aplicável

Resumo/Abstract:

Introduction: Akt pathway when linked to growth factors like insulin activates phosphatidylinositol-3-kinase (PI3K), an enzyme that acts on growth processes, cell proliferation and protection against apoptosis. Objective: The aims of this study was to induce sustained hyperglycemia in Wistar rats and evaluate Akt expression in renal tissue and changes in cardiovascular, renal and muscular systems. Methods: 30 male Wistar rats were divided into two groups: Control (CO) and STZ. STZ group received Streptozotocin (STZ) in order to induce diabetes mellitus. After 62 days of experiment, the animals were euthanized and the kidney, heart, aorta, gastrocnemius muscle and mesenteric fat were removed for further analysis. Results: STZ group showed significantly higher glucose and triglyceride and lower fructosamine values compared to the CO group. Regarding immunohistochemical analysis, the animals in the STZ group showed a reduction in the expression of the Akt pathway in renal tissue, compared to the CO group. Regarding histological analysis, there was a predominance of glomerular hypertrophy, mesangial expansion and capillary congestion in the kidneys of animals in the STZ group, in addition to a significant increase in renal weight compared to CO. Comparing with the CO group, pathological changes were found in the myocardium, aorta and gastrocnemius of diabetic rats, as well as a significant reduction in the diameter of the mesenteric adipocytes of these animals. Conclusion: Deleterious effects on tissue integrity and function were caused by the diabetic metabolic environment, causing significant changes both in PI3K / Akt signal transduction and in cell growth.

Keywords: Hyperglycemia, Wistar Rats, Immunohistochemistry.