Skip to main content
ARS Home » Northeast Area » Boston, Massachusetts » Research » Publications at this Location » Publication #317510
Title: Effect of blueberries and insulin on glucose induced neurotoxicity in brain cells in vitro

Author
item HININGER-FAVIER, ISABELLE - Joseph Fourier University
item Thangthaeng, Nopporn
item Shukitt-Hale, Barbara
item POULOSE, SHIBU - Jean Mayer Human Nutrition Research Center On Aging At Tufts University

Submitted to: Federation of European Nutrition Societies European Nutrition Conference
Publication Type: Abstract Only
Publication Acceptance Date: 4/27/2015
Publication Date: 10/20/2015
Citation: Hininger-Favier, I., Thangthaeng, N., Shukitt Hale, B., Poulose, S. 2015. Effect of blueberries and insulin on glucose induced neurotoxicity in brain cells in vitro. Federation of European Nutrition Societies European Nutrition Conference. Annals of Nutrition and Metabolism (2015), vol 67 (Suppl.1), p. 467-468.

Interpretive Summary:

Technical Abstract: Introduction Literature had shown that disruption in glucose metabolism seen in metabolic syndrome maybe responsible for neuronal cell-death. Oxidative stress (OS) and inflammation (INF) triggered by the impaired metabolic process are considered to be the primary factors for the toxic neuronal atmosphere. Blueberries (BB) have been shown to improve cognitive function by reducing OS and neuroinflammation. Objectives 1) To investigate the effect of glucose on OS and INF signalings in microglia and 2) To examine the effect of insulin and BB on these signaling molecules. Method / Design Rat microglial cells (HAPI) were grown in various glucose concentrations (1g/L-9g/L) and treated with either BB (2%), insulin (INS; 50mM), lipopolysaccharide (LPS; 100nM) or in combination. After 24 hours, expression of iNOS, NOX2, COX2, GLUT1, and GLUT4 were assessed using immunoblotting or immunocytochemistry; while NO2 production was measured in the media via ELISA. Results Elevation in glucose induced neurotoxicity through OS and INF; further enhanced by LPS. BB and INS significantly reduced LPS-mediated neurotoxicity under high glucose conditions by altered the expression of signaling molecules related to OS and INF. Conclusions High blood glucose levels may induce neurotoxicity via OS and INF. Under low-glucose conditions, blueberries primed the cells to withstand the deleterious effects of LPS. While, under high-glucose conditions, BB and INS attenuated the glucose-induced neuronal damage by altering insulin sensitivity and reducing the OS and INF. These results provide possible mechanisms for neuroprotective effects of BBs during metabolic syndrome.