(OR23-03-25) BDNF Homeostasis Upon Consumption of a High Fat Meal: Modulation by Anthocyanins

Objectives: Background

High circulating levels of lipopolysaccharides (LPS) are associated with obesity and consumption of high-fat diets (HFD). LPS binds to TLR4 receptors triggering inflammation. Conditions of chronic inflammation are frequently accompanied by a downregulation of Brain Derived Neurotrophic Factor (BDNF); a peptide critical for health. Circulating concentrations of BDNF are inversely associated with altered cognition, cardiovascular disease, depression, multiple sclerosis, and addiction. We previously showed that anthocyanin (AC) consumption mitigates HFD-induced intestinal permeability and endotoxemia, hippocampal inflammation, and decreased BDNF expression in mice fed a HFD.

Objective
This work investigated whether a single high fat meal (HFM) could: i) cause endotoxemia and inflammation, ii) downregulate BDNF expression in peripheral blood mononuclear cells (PBMCs), and if dietary supplementation with a cyanidin-and delphinidin-rich extract (CDRE) could counteract these alterations.

Methods: A double-blinded placebo-controlled crossover study was conducted including 25 healthy adults who consumed a HFM along with a CDRE supplement or placebo. To further investigate how inflammation impacts BDNF expression in immune cells, Jurkat cells (immortalized human T lymphocytes) were incubated with LPS for 3-24 hours to mimic HFM-induced postprandial endotoxemia.

Results: The HFM caused endotoxemia and inflammation, which were mitigated by CDRE consumption. The CDRE significantly increased serum BDNF levels (64% higher than placebo). Even though differences in PBMCs BDNF expression were not observed between groups, in the placebo group BDNF and IL-1β/TNFα mRNA levels were inversely correlated, suggesting a relationship between inflammation and low BDNF expression. In Jurkat cells, LPS caused a decrease in the mRNA levels of BDNF and an increase in those of TNFα. Similar to observations in vivo, BDNF and TNFα mRNA levels were inversely correlated.

Conclusions: In summary, HFD can affect BDNF metabolism which can be mitigated by consumption of AC-rich foods. Altered BDNF homeostasis could in part contribute to obesity-associated neurological alterations.

Funding Sources: Pharmanex Research, NSE Products Inc., Provo, UT, USA, NIFA-USDA (grants CA-D∗-XXX-7244-H and CA-D-NTR-2819-H), Jastro-Shields Research