Coffee pulp simulated digestion enhances its in vitro ability to decrease emulsification and digestion of fats, and attenuates lipid accumulation in HepG2 cell model
The coffee industry produces a considerable quantity of coffee pulp (CP), a by-product with high levels of caffeine, phenolic compounds, and dietary fiber, which are reportedly involved in the lipid homeostasis regulation required to maintain human health. This work's objective was to evaluate...
| Autores: | , , , , , |
|---|---|
| Tipo de documento: | artigo |
| Estado: | Versão publicada |
| Data de publicação: | 2024 |
| País: | España |
| Recursos: | Consejo Superior de Investigaciones Científicas (CSIC) |
| Repositório: | DIGITAL.CSIC. Repositorio Institucional del CSIC |
| OAI Identifier: | oai:digital.csic.es:10261/372728 |
| Acesso em linha: | http://hdl.handle.net/10261/372728 |
| Access Level: | Acceso aberto |
| Palavra-chave: | Coffee pulp In vitro static digestion In vitro hypolipidemic properties HepG2 Intracellular lipid accumulation |
| Resumo: | The coffee industry produces a considerable quantity of coffee pulp (CP), a by-product with high levels of caffeine, phenolic compounds, and dietary fiber, which are reportedly involved in the lipid homeostasis regulation required to maintain human health. This work's objective was to evaluate the hypolipidemic activity of coffee pulp flour (CPF) and aqueous extract (CPE) after static simulated digestion by the assessment of their in vitro capacity to decrease emulsification and digestion of fats, and lipid-lowering capacity in HepG2 cells after the induction of intracellular fat accumulation. The CPF and CPE digested fractions displayed in vitro hypolipidemic properties by preserving the reduction of micellar cholesterol solubility (27–34%) and the secondary bile acid-binding capacity (22–30%), increasing their primary bile acid-binding ability (2.7-fold and 2.4-fold, respectively), and inhibiting the lipase and the HMGCR (77–79% and 36–85%, respectively) activities. Moreover, the hypolipidemic properties of non-digested fractions enhanced the CPF potential to decrease lipid absorption. Both ingredients (CPF and CPE) demonstrated lipid-lowering effects since they effectively counteract the accumulation of intracellular triglycerides and cholesterol triggered by palmitic acid in hepatic cells after the simulated digestion. This study suggests that phenolic compounds, caffeine, and dietary fiber may be responsible for the lipid-lowering properties exhibited by the CP ingredients and their composition differences affect the above-mentioned properties exhibited in the simulated digestion. These results contribute to demonstrating that the CPF and the CPE may act as modulators of pathways involved in hepatic lipid accumulation and could be a key element in its prevention. |
|---|