<<snip>>
Lipid replacement therapy (LRT) administered as a nutritional
supplement with antioxidants can prevent excess oxidative membrane
damage, restore mitochondrial and other cellular membrane functions and
reduce fatigue
<<snip>>
Metabolic syndrome and mitochondrial function: Molecular replacement
and antioxidant supplements to prevent membrane peroxidation and
restore mitochondrial function.
Nicolson GL
J Cell Biochem. 2007 Jan 22;
Metabolic syndrome consists of a cluster of metabolic conditions, such
as hypertriglyeridemia, hyper-low-density lipoproteins,
hypo-high-density lipoproteins, insulin resistance, abnormal glucose
tolerance and hypertension, that-in combination with genetic
susceptibility and abdominal obesity-are risk factors for type 2
diabetes, vascular inflammation, atherosclerosis, and renal, liver and
heart disease. One of the defects in metabolic syndrome and its
associated diseases is excess cellular oxidative stress (mediated by
reactive oxygen and nitrogen species, ROS/RNS) and oxidative damage to
mitochondrial components, resulting in reduced efficiency of the
electron transport chain. Recent evidence indicates that reduced
mitochondrial function caused by ROS/RNS membrane oxidation is related
to fatigue, a common complaint of MS patients. Lipid replacement
therapy (LRT) administered as a nutritional supplement with
antioxidants can prevent excess oxidative membrane damage, restore
mitochondrial and other cellular membrane functions and reduce fatigue.
Recent clinical trials have shown the benefit of LRT plus antioxidants
in restoring mitochondrial electron transport function and reducing
moderate to severe chronic fatigue. Thus LRT plus antioxidant
supplements should be considered for metabolic syndrome patients who
suffer to various degrees from fatigue. J. Cell. Biochem. (c) 2007
Wiley-Liss, Inc.
Abstract · PubMed FullText · SFX · GS Clip Export InterDB ·
Terms Related · Graph Tag · Scopus · Cites
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ironjustice@aol.com - 27 Jan 2007 07:07 GMT
> <<snip>>
> Lipid replacement therapy (LRT) administered as a nutritional
[quoted text clipped - 46 lines]
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Influence of lecithin on mitochondrial DNA and age-related hearing loss
Auteur(s) / Author(s)
SEIDMAN Michael D. ; KHAN Mumtaz J. ; WEN XUE TANG ; QUIRK Wayne S. ;
Résumé / Abstract
OBJECTIVES: Lecithin is a polyunsaturated phosphatidylcholine (PPC),
which are high energy functional and structural elements of all
biologic membranes. PPC play a rate-limiting role in the activation of
numerous membrane-located enzymes, including superoxide dismutase and
glutathione, which are important antioxidants protecting cell membranes
from damage by reactive oxygen species (ROS). ROS-induced damage to
mitochondrial DNA may lead to reduced mitochondrial function in the
cochlea and resultant hearing loss. STUDY DESIGN AND SETTING: The
effects of lecithin on aging and age-associated hearing loss were
studied in rats by measuring hearing sensitivities using auditory
brainstem responses (ABR). In addition, mitochondrial function as a
measure of aging was assessed by determining mitochondrial membrane
potentials using flow cytometry and by amplifying mitochondrial DNA
deletions associated with aging. Harlan-Fischer rats aged 18 to 20
months (n = 14) were divided into 2 groups. The experimental group was
supplemented orally for 6 months with lecithin, a purified extract of
soybean phospholipid (Nutritional Therapeutics, Allendale, NJ).
RESULTS: The data obtained were compared with the control group. ABRs
were recorded at 2-month intervals and showed significant preservation
of hearing sensitivities in the treated subjects. Flow cytometry
revealed significantly higher mitochondrial membrane potentials in the
treated subjects, suggesting preserved mitochondrial function. Finally,
the common aging mitochondrial DNA deletion (mtDNA[4][8][3][4]) were
amplified from brain and cochlear tissue including stria vascularis and
auditory nerve. This specific deletion was found significantly less
frequent in all tissues in the treated group compared with the
controls. CONCLUSION: These experiments support our hypothesis and
provide evidence that lecithin may preserve cochlear mitochondrial
function and protect hearing loss associated with aging.
Revue / Journal Title
Otolaryngology and head and neck surgery (Otolaryngol. head neck
surg.) ISSN 0194-5998 CODEN OHNSDL
Source / Source
2002, vol. 127, no3, pp. 138-144 [7 page(s) (article)]
Langue / Language
Anglais
Editeur / Publisher
Elsevier, Saint Louis, MO, ETATS-UNIS (1979) (Revue)
Localisation / Location
INIST-CNRS, Cote INIST : 20388, 35400010932995.0020
Copyright 2006 INIST-CNRS. All rights reserved
Toute reproduction ou diffusion même partielle, par quelque procédé
ou sur tout support que ce soit, ne pourra être faite sans l'accord
préalable écrit de l'INIST-CNRS.
No part of these records may be reproduced of distributed, in any form
or by any means, without the prior written permission of INIST-CNRS.
Nº notice refdoc (ud4) : 13939065
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Man Is A Herbivore!
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DEAD PEOPLE WALKING
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