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Sterol

About: Sterol is a research topic. Over the lifetime, 8117 publications have been published within this topic receiving 309926 citations. The topic is also known as: sterols & sterol lipids.


Papers
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Journal ArticleDOI
TL;DR: In this paper, the formation of phytosterols oxidation products (POPs) in oil-in-water emulsions and bulk corn oil was evaluated, and the extent of lipid oxidation was monitored by measuring the lipid hydroperoxides and hexanal.

96 citations

Journal ArticleDOI
TL;DR: The results demonstrate that the activity of hepatic 3-hydroxy-3-methylglutaryl-CoA reductase can be controlled by the rate of endogenous sterol synthesis both in vitro and in vivo.

96 citations

Journal ArticleDOI
TL;DR: The results suggest that the hypocholesterolemic effect of the BL, compared with the CAS, is attributable to impaired intestinal cholesterol absorption, probably involving increased bile acid reabsorption and higher contents of dietary phytosterols, both factors that reduce the micellar solubilization of cholesterol.

96 citations

Journal ArticleDOI
TL;DR: Concentrations of unsaturated plant sterols in serum reflect their dietary intakes, saturated Plant sterols are virtually not absorbed, plant sterol-induced reduction of sterol absorption may be positively related to absorption efficiency of sterols.

96 citations

Journal ArticleDOI
TL;DR: A minimal peptide containing the GM1-binding domain but lacking the amino acid residues involved in cholesterol recognition is designed, showing that cholesterol significantly accelerates the interaction of Abeta5-16 with GM1 and supports the emerging concept that cholesterol is a universal modulator of protein-glycolipid interactions in the broader context of membrane recognition processes.
Abstract: Age-related alterations of membrane lipids in brain cell membranes together with high blood cholesterol are considered as major risk factors for Alzheimer's disease. Yet the molecular mechanisms by which these factors increase Alzheimer's risk are mostly unknown. In lipid raft domains of the plasma membrane, neurotoxic Alzheimer's beta-amyloid (Abeta) peptides interact with both cholesterol and ganglioside GM1. Recent data also suggested that cholesterol could stimulate the binding of Abeta to GM1 through conformational modulation of the ganglioside headgroup. Here we used a combination of physicochemical and molecular modeling approaches to decipher the mechanisms of cholesterol-assisted binding of Abeta to GM1. With the aim of decoupling the effect of cholesterol on GM1 from direct Abeta-cholesterol interactions, we designed a minimal peptide (Abeta5-16) containing the GM1-binding domain but lacking the amino acid residues involved in cholesterol recognition. Using the Langmuir technique, we showed that cholesterol (but not phosphatidylcholine or sphingomyelin) significantly accelerates the interaction of Abeta5-16 with GM1. Molecular dynamics simulations suggested that Abeta5-16 interacts with a cholesterol-stabilized dimer of GM1. The main structural effect of cholesterol is to establish a hydrogen-bond between its own OH group and the glycosidic-bond linking ceramide to the glycone part of GM1, thereby inducing a tilt in the glycolipid headgroup. This fine conformational tuning stabilizes the active conformation of the GM1 dimer whose headgroups, oriented in two opposite directions, form a chalice-shaped receptacle for Abeta. These data give new mechanistic insights into the stimulatory effect of cholesterol on Abeta/GM1 interactions. They also support the emerging concept that cholesterol is a universal modulator of protein-glycolipid interactions in the broader context of membrane recognition processes.

96 citations


Network Information
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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023104
2022250
2021131
2020154
2019151
2018117