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In vitro effects of theaflavins on micelle formation
Author(s) -
Vermeer Mario,
Mulder Theo P.J.,
Molhuizen Henri O.F.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.723
Subject(s) - micelle , chemistry , theaflavin , vesicle , oleic acid , cholesterol , chromatography , high performance liquid chromatography , absorption (acoustics) , particle size , centrifugation , biophysics , food science , biochemistry , organic chemistry , membrane , polyphenol , biology , materials science , aqueous solution , composite material , antioxidant
Tea is one of the most widely consumed beverages in the world and may be associated with reduced heart disease rates. Theaflavins (TFs), which are formed in the production of black tea, have been suggested being responsible for the blood cholesterol lowering (BCL) effects of tea. Aim We hypothesized that the effect of TFs on BCL could be through interference in the formation of dietary mixed micelles which could result in reduced intestinal cholesterol absorption. Methods Micelles were produced by mixing oleic acid, bile acids, phosphatidylcholine, and cholesterol. TF‐treated micelles/particles were analysed using electron microscopy (cryo‐TEM), HPLC analysis and light scattering particle size measurements. Results A dose‐dependent inhibitory effect of TFs on the incorporation of 14 C‐cholesterol into micelles and a TF‐dependent increase in particle size was found. These particles consisted of insoluble large multi‐lamellar vesicles with onion‐like structures. Ultra‐centrifugation and HPLC‐analysis revealed that the pellets contained mainly theaflavin‐3‐gallate, while the remaining TFs were found to be present in the supernatant. Using pure TF‐subtypes, confirmed that only theaflavin‐3‐gallate is responsible for multi‐lamellar vesicle formation. Conclusion These results show that TFs can play a role in decreased intestinal cholesterol uptake via inhibition of micelle formation.