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Bioactive compounds in pomace olive oil modulate the inflammatory response elicited by postprandial triglyceride-rich
Juan Manuel Espinosa1, Angélica Quintero-Flórez2, Natalia Carrasquilla1
1Instituto de la Grasa, Department of Food and Health, Spanish National Research Council (CSIC), Campus University Pablo de Olavide, 41013, Seville, Spain. jmcas@ig.csic.es.
Abstract:
Modulation of microglial response could be a target to reduce neuroinflammation associated with Alzheimer's disease. In this study, we propose that lipophilic bioactive molecules present in pomace olive oil (POO), transported in triglyceride-rich lipoproteins (TRLs), are able to modulate microglial high-oleic sunflower oil (HOSO, points) or pomace olive oil (POO, stripes). In order to prove this hypothesis, a randomized crossover postprandial trial was performed in 18 healthy young women. POO was assayed in opposition to high-oleic sunflower oil (HOSO), a common dietary oil which shares with POO an almost identical fatty acid composition but lacks certain biomolecules with recognized antioxidant and anti-inflammatory activities. TRLs were isolated from blood at the baseline and 2 and 4 hours postprandially and used to treat BV-2 cells to assess their ability to modulate the microglial function. We found that the intake of POO leads to the constitution of postprandial TRLs that are able to modulate the inflammatory response in microglia compared to HOSO. TRL-derived POO reduced the release of pro-inflammatory cytokines (tumor necrosis factor-α, and interleukins 1β and 6) and nitric oxide and downregulated genes codifying for these cytokines and inducible nitric oxide synthase (iNOS) in BV-2 cells. Moreover, the ingestion of POO by healthy women slightly improved glycemic control and TRL clearance throughout the postprandial phase compared to HOSO. In conclusion, we demonstrated that consuming POO results in postprandial TRLs containing lipophilic bioactive compounds capable of regulating the inflammatory response prompted by microglial activation.
Insights
Pomace olive oil (POO) contains bioactive compounds that reduce neuroinflammation by modulating microglial response. Postprandial triglyceride-rich lipoproteins (TRLs) from POO intake regulate inflammatory cytokines and improve metabolic health.
Area of Science:
- Neuroscience
- Immunology
- Nutritional Science
Background:
- Neuroinflammation, driven by microglial activation, is a key factor in Alzheimer's disease.
- Dietary bioactive molecules may offer a strategy to modulate microglial responses and reduce neuroinflammation.
- Pomace olive oil (POO) is rich in bioactive compounds with potential antioxidant and anti-inflammatory properties.
Purpose of the Study:
- To investigate if lipophilic bioactive molecules in pomace olive oil (POO), transported via triglyceride-rich lipoproteins (TRLs), can modulate microglial inflammatory responses.
- To compare the effects of POO against high-oleic sunflower oil (HOSO) on microglial function postprandially.
- To assess the impact of POO consumption on glycemic control and TRL clearance.
Main Methods:
- A randomized crossover postprandial trial involving 18 healthy young women.
- Isolation of TRLs from blood at baseline, 2, and 4 hours postprandial after consuming POO or HOSO.
- Treatment of BV-2 microglial cells with isolated TRLs to assess modulation of inflammatory markers.
Main Results:
- Postprandial TRLs derived from POO intake modulated microglial inflammatory response compared to HOSO.
- POO-derived TRLs reduced the release of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and nitric oxide.
- POO consumption improved glycemic control and TRL clearance postprandially compared to HOSO.
Conclusions:
- Consuming POO yields postprandial TRLs with lipophilic bioactive compounds that regulate microglial activation and neuroinflammation.
- POO demonstrates potential as a dietary intervention to mitigate neuroinflammation associated with Alzheimer's disease.
- POO consumption offers benefits beyond neuroinflammation, including improved glycemic control and lipid metabolism.
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