Results 41 to 50 of about 25,763 (118)

Lipoprotein lipase activity and interactions studied in human plasma by isothermal titration calorimetry

open access: yesJournal of Lipid Research, 2017
LPL hydrolyzes triglycerides in plasma lipoproteins. Due to the complex regulation mechanism, it has been difficult to mimic the physiological conditions under which LPL acts in vitro.
Mart Reimund   +3 more
doaj   +1 more source

Effects of a dietary intervention with lacto-ovo-vegetarian and Mediterranean diets on apolipoproteins and inflammatory cytokines: results from the CARDIVEG study

open access: yesNutrition & Metabolism
Background Apolipoproteins have been recently proposed as novel markers of cardiovascular disease (CVD) risk. However, evidence regarding effects of diet on apolipoproteins is limited.
Giuditta Pagliai   +9 more
doaj   +1 more source

N-terminal mutation of apoA-I and interaction with ABCA1 reveal mechanisms of nascent HDL biogenesis

open access: yesJournal of Lipid Research, 2019
ApoA-I and ABCA1 play important roles in nascent HDL (nHDL) biogenesis, the first step in the pathway of reverse cholesterol transport that protects against cardiovascular disease. On the basis of the crystal structure of a C-terminally truncated form of
Minjing Liu   +3 more
doaj   +1 more source

Protective associations of HDL with blood-brain barrier injury in multiple sclerosis patients

open access: yesJournal of Lipid Research, 2015
The purpose of this work was to investigate the associations of serum cholesterol and apolipoproteins with measures of blood-brain barrier (BBB) permeability and CNS inflammation following the first clinical demyelinating event.
Kelly Fellows   +12 more
doaj   +1 more source

A thumbwheel mechanism for APOA1 activation of LCAT activity in HDL[S]

open access: yesJournal of Lipid Research, 2018
APOA1 is the most abundant protein in HDL. It modulates interactions that affect HDL';s cardioprotective functions, in part via its activation of the enzyme, LCAT.
Allison L. Cooke   +12 more
doaj   +1 more source

Impact of individual acute phase serum amyloid A isoforms on HDL metabolism in mice[S]

open access: yesJournal of Lipid Research, 2016
The acute phase (AP) reactant serum amyloid A (SAA), an HDL apolipoprotein, exhibits pro-inflammatory activities, but its physiological function(s) are poorly understood.
Myung-Hee Kim   +7 more
doaj   +1 more source

Reduction in apolipoprotein-mediated removal of cellular lipids by immortalization of human fibroblasts and its reversion by cAMP: lack of effect with Tangier disease cells

open access: yesJournal of Lipid Research, 1999
High density lipoprotein (HDL) phospholipids and apolipoproteins remove cellular lipids by two distinct mechanisms, but their relative contribution to reverse cholesterol transport is unknown.
John F. Oram   +4 more
doaj   +1 more source

The ratio of low-density lipoprotein cholesterol to apolipoprotein-B as a marker of low-density lipoprotein particle size

open access: yesАтеросклероз, 2018
The aim of this study was to determine the informative value and clinical significance of the ratio of low-density lipoprotein cholesterol to apolipoprotein-B (LDL-C/apoB) in the overall evaluation of blood lipid profile atherogenicity.
A. M. Kaneva   +2 more
doaj   +1 more source

Omega-3 fatty acids, lipids, and apoE lipidation in Alzheimer's disease: a rationale for multi-nutrient dementia prevention

open access: yesJournal of Lipid Research, 2017
In the last decade, it has become obvious that Alzheimer's disease (AD) is closely linked to changes in lipids or lipid metabolism. One of the main pathological hallmarks of AD is amyloid-β (Aβ) deposition.
Marcus O.W. Grimm   +2 more
doaj   +1 more source

Lipid and lipoprotein metabolism in microglia: Alzheimer’s disease mechanisms and interventions

open access: yesJournal of Lipid Research
Alzheimer's disease (AD) presents a significant challenge owing to its widespread prevalence and complex neuropathogenesis, affecting millions worldwide. Current therapeutic strategies that predominantly target amyloid-beta accumulation are insufficient,
Kayla G. Sprenger   +3 more
doaj   +1 more source

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