Abstract

Alpha-Linolenic Acid Supplementation is Associated with Changes in Inflammatory Markers and Endoplasmic Reticulum Stress in Diabetic Rats

Ferraz RC, Foss-Freitas MC, Vidal TR, Griffo TN, Gonçalves NB, Jordao Jr AA and Foss MC

Background: The aim of this study was to evaluate the effects of α-linolenic acid (ALA) supplementation on inflammation and endoplasmic reticulum stress (ERS) in streptozotocin induced diabetic rats.
Methods: We studied 40 Wistar rats divided into four groups: control, control+ALA, diabetes and diabetes+ALA. The +ALA groups received supplementation of 3 g of ALA from flaxseed, daily for a period of 8 weeks. Measurements of blood glucose levels, serum insulin, lipid profile, serum cytokines (TNF-α, IL-6 and INF-γ) and body weight were performed before and after the ALA supplementation. Protein expression of AKT, IRE1-α, XBP-1, BIP, HSP-70, HSP-90, TNF-α and CHOP were evaluated in liver tissue.
Results: The diabetes+ALA group had lower liver and greater epidydimal adipose tissue weight in relation to the diabetes group, besides no difference in total body weight. Diabetes+ALA group showed lower glucose and triglyceride levels after the ALA supplementation compared to diabetes group, but no difference in total cholesterol. Insulin levels were significantly lower in the diabetic group compared to the control, but there was no difference between the control group and diabetes+ALA group. The ALA supplementation did not determine significant changes in TNF-α and IL-6 levels. However, the diabetic+ALA group showed a decrease in the serum INF-γ levels after the supplementation period. We also observed increased expression of HSP-90 and HSP-70 in hepatic tissue of the diabetes+ALA animals compared to the diabetes group, associated to lower BIP and XBP-1 protein expression. We also observed a decrease in AKT protein expression in the diabetes+ALA group
Conclusion: In conclusion, supplementation of ALA reduced blood glucose and serum triglyceride levels associated to a reduction in systemic inflammation and it was also able to influence important pathways involved in the modulation of ERS.