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Physical activity and high -density lipoprotein cholesterol in sedentary male smokersShaw, BS, Shaw, I 16 December 2007 (has links)
High-density lipoprotein (HDL) with its cardio-
protective effects has provided remarkable
optimism to the ever-increasing incidences of
coronary artery disease. Therefore, the aim of this
randomized, comparative, research trial was to
determine whether endurance exercise training,
weight training and/or a combination of aerobic and
weight training can be utilized in the management
of high-density lipoprotein cholesterol (HDL-C).
Subsequent to the 16-week intervention period,
dependant t-Tests revealed that the non-exercising
and weight training groups demonstrated non-
significant mean 1.3% (p = 0.754) and 11.1% (p =
0.069) increases in fasting serum HDL-C,
respectively. Conversely, there was a significant
increase in HDL-C following the 16 weeks of
endurance training (p = 0.003) and combination
training (p = 0.005) (22.4% and 37.9%,
respectively). Further, Spearman’s rho indicated no
correlations between HDL-C and BMI (r = -0.131),
percentage body fat (r = - 0.141), cholesterol intake
(r = - 0.026) and total fat intake (r = - 0.239). The
absence of changes in these inter-correlations
indicated that changes in these parameters had no
effect on the HDL-C. On the contrary, moderate
correlations were established between HDL-C and
number of cigarettes smoked daily (r = - 0.344) and
intake of saturated fat (r = - 0.317) indicating that
exercise effect on these variables could have
indirectly contributed significantly in altering HDL-
C in the endurance and combination training
groups. As such, endurance and combination
training can be utilized as an effective method in the
management of HDL-C in sedentary male smokers.
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The Role of Macrophage Scavenger Receptor Class B, Type 1 (SR-BI) in the development of Atheroscelerosis in Apolipoprotein E Deficient MiceRisvi, Ali Amjad 11 1900 (has links)
The high density lipoprotein (HDL) receptor Scavenger Receptor, Class B, Type I (SRBI)
is a 509 amino acid integral membrane protein which has been shown to have an
important role in HDL-mediated reverse cholesterol transport. SR-BI has been shown to
mediate selective uptake of cholesterol, and also mediates efflux of cholesterol to HDL as
seen in in vitro cell culture studies. SR-BI is abundant in the liver and steroidogenic
tissues, and is also present in macrophages, which play an important role in the initial
stages of atherosclerotic development. SR-BI has been shown to be protective against
atherosclerosis by way of overexpression and knockout (KO) studies in murine
atherosclerosis models, including low density lipoprotein receptor (LDLR) knockout
mice, apolipoprotein E (ApoE) knockout mice, and human apolipoprotein B (ApoB)
transgenic mice. SR-BI/LDLR double knockout (dKO) mice show a 6-fold increase in
diet-induced atherosclerosis compared to LDLR single KO controls, and SR-BI/ApoE
dKO mice show severe coronary occlusion, myocardial infarction, and premature death
on a normal chow diet. In both, plasma total cholesterol levels are significantly elevated,
and associated with abnormally large HDL particles. The majority ofSR-BI's
atheroprotective effect has been shown to result from plasma cholesterol clearance by
way of selective uptake in the liver. Recently, Covey et al showed that elimination of SRBI
expression in macrophages of LDLR KO mice resulted in increased diet-induced
atherosclerosis. To see if SR-BI in macrophages contributes to the overall
atheroprotective effect of SR-BI in ApoE KO mice, presumably by mediating cellular
cholesterol efflux to HDL, selective deletion ofSR-BI was induced in bone marrow
derived cells of ApoE KO mice using bone marrow transplantation. Female ApoE -/recipient
mice were transplanted with either SR-BI +/+ ApoE -/-or SR-BI -/- ApoE -/bone
marrow from male donor mice, and fed a high fat diet for 12 weeks. This resulted in
significantly increased atherosclerosis in mice transplanted with SR-BI -/- ApoE -/-bone
marrow, with a concomitant decrease in cholesterol associated with HDL-sized
lipoproteins. No significant differences were seen in plasma total cholesterol levels or
levels of cholesterol associated with non-HDL lipoproteins. These data suggest that SRBI
in macrophages contributes to SR-BI's overall protective effect against
atherosclerosis, and also plays a role in the regulation ofHDL cholesterol, in ApoE
deficient mice. / Thesis / Master of Science (MSc)
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Η HDL ως καινοτόμος φαρμακολογικός στόχος : διδάγματα από μελέτες έκθεσης πειραματόζωων σε χαμηλή θερμοκρασίαΞεπαπαδάκη, Ευστρατία 05 February 2015 (has links)
Πρόσφατα δεδομένα σε πειραματικά μοντέλα ζώων αλλά και σε ασθενείς καταδεικνύουν την σημαντικότητα της «ποιότητας» της λιποπρωτεΐνης υψηλής πυκνότητας (HDL), σε σχέση με την ποσότητά της, στην προστασία από τη στεφανιαία νόσο. Τα κύρια χαρακτηριστικά της HDL τα οποία καθορίζουν την «ποιότητά» της, είναι η ανάστροφη μεταφορά χοληστερόλης, οι αντιοξειδωτικές και αντιφλεγμονώδεις ιδιότητές της καθώς επίσης και η ικανότητά της να προάγει την παραγωγή ΝΟ στο αρτηριακό επιθήλιο και να ρυθμίζει την ομοιόσταση της γλυκόζης αίματος.
Στην συγκεκριμένη ερευνητική εργασία μελετάμε την επίδραση που έχει η ενεργοποίηση του φαιού λιπώδους ιστού, μέσω της έκθεσης φυσιολογικών πειραματικών μοντέλων μυών, σε περιβάλλον χαμηλής θερμοκρασίας, στο λιπιδαιμικό προφίλ, καθώς και στην λειτουργικότητα της HDL.
Είναι γνωστό είναι ότι η ενεργοποίηση του φαιού λιπώδους ιστού, λόγω έκθεσης πειραματόζωων σε περιβάλλον χαμηλής θερμοκρασίας, οδηγεί σε θερμογένεση, κάθαρση των τριγλυκεριδίων από το αίμα παχύσαρκων ποντικών, μείωση του βάρους τους, έλεγχο του καταβολισμού των λιποπρωτεϊνών και ομαλοποίηση της ανοχής τους στην γλυκόζη. Έτσι θελήσαμε να επεκτείνουμε την μελέτη μας, στον ενδεχόμενο ρόλο του εγκλιματισμού των πειραματόζωων μετά από μακρόχρονη έκθεσή τους στο ψύχος στους παραπάνω παράγοντες.
Για την επίτευξη των πειραματικών μας στόχων δημιουργήθηκαν τρεις ομάδες C57BL/6 μυών εκ των οποίων η μια εκτέθηκε σε περιβάλλον χαμηλής θερμοκρασίας για 2 εβδομάδες (βραχύχρονη έκθεση στο ψύχος), η άλλη ομάδα για 12 εβδομάδες (μακρόχρονη έκθεση στο ψύχος), ενώ η τρίτη αποτέλεσε την ομάδα ελέγχου.
Στις δύο ομάδες μυών έγιναν κινητικές μελέτες έκκρισης και κάθαρσης τριγλυκεριδίων. Επίσης απομονώθηκαν από το πλάσμα του αίματος, τα λιποπρωτεϊνικά κλάσματα στα οποία έγιναν αναλύσεις για τον έλεγχο της ποσότητας και της ποιότητας της HDL.
Τα αποτελέσματά μας καταδεικνύουν την επαγωγή θερμογένεσης από τον φαιό λιπώδη ιστό και στις δύο πειραματικές ομάδες, με αυτή να είναι πιο έντονη κατά την βραχύχρονη έκθεση στο ψύχος. Παρόλο που η κατανάλωση τροφής στις ομάδες που εκτέθηκαν στο ψύχος αυξήθηκε, το σωματικό τους βάρος παρέμεινε το ίδιο, μιας και η περίσσεια διατροφικών λιπιδίων χρησιμοποιούνταν από τον φαιό λιπώδη ιστό για την παραγωγή θερμότητας παρά για αποθήκευσή τους στον λευκό λιπώδη ιστό. Η εντερική απορρόφηση τριγλυκεριδίων αυξήθηκε σε σχέση με την ομάδα ελέγχου καθώς πιθανά ο οργανισμός χρειαζόταν τα λιπίδια για θερμογένεση, ενώ η ηπατική έκκριση τριγλυκεριδίων μειώθηκε. Η ολική χοληστερόλη των λιποπρωτεϊνικών κλασμάτων, στις πειραματικές ομάδες, έτεινε να βρίσκεται συγκεντρωμένη στα πιο ώριμα κλάσματα, ιδιαίτερα έπειτα από μακρόχρονη έκθεση στο πειραματικό περιβάλλον. Επιπλέον η HDL την 12η εβδομάδα, παρουσίασε καλύτερη αντιοξειδωτική δράση καθώς και διατήρησε αμιγή την ικανότητα να επιτελεί εκροή χοληστερόλης από τα κύτταρα.
Τα ευρήματά μας οδηγούν σε δύο ενδιαφέρουσες ανακαλύψεις: 1) Η βραχεία έκθεση στο ψύχος έχει μεγαλύτερη επίδραση στη θερμογένεση και την παραγωγή ATP, απ’ ότι η μακρά έκθεση. 2) Η μακρά έκθεση στο ψύχος οδηγεί σε πιο λειτουργική HDL σε σχέση με την ομάδα βραχείας έκθεσης.
Κατά συνέπεια τα αποτελέσματα μας αυτά, καταδεικνύουν εγκλιματισμό των πειραματόζωων στο ψύχος, ο οποίος συνοδεύεται από ποιοτικότερη και πιο λειτουργική HDL. / Recent data indicate the significance of “HDL quality” in atherosclerosis, rather than HDL cholesterol levels in plasma, suggesting that composition as well as functionality of HDL particle, imparts the atheroprotective property of HDL. The main atheroprotective property of HDL is cholesterol efflux in addition to anti-inflammatory and antioxidant properties. HDL has also the ability to promote NO production in the arterial lining and to regulate blood glucose levels.
In this study we intend to examine whether brown adipose tissue activation, through low environmental temperature, affects lipid profile and functionality of HDL in C57BL/6 mice.
Previous studies have shown that BAT is activated in animals which have been exposed to low temperature environment, resulting in thermogenesis, blood triglycerides clearance, weight reduction, control of lipoproteins catabolism and normalization of glucose tolerance.
Thus we intended to study the possible role of acclimatization after long-term exposure to cold temperature regarding the above factors. Therefore we formed three groups of C57BL/6 mice, one of which was exposed to 4oC environment for 2 weeks (short-term exposure), the other one for 12 weeks (long-term exposure) and the last one at 28oC environment (control group).
Kinetic studies of triglyceride secretion and clearance where performed, to all groups of animals. Analyses regarding HDL quantity and quality, where performed in lipoprotein fractions isolated from plasma.
Our data demonstrate the induction of thermogenesis in BAT in both experimental groups, which appeared to be more intense during the short-term exposure. Although food consumption, in groups exposed to cold, was increased, body weight did not change, as BAT used the excess dietary lipids in order to produce heat rather than storing them in white adipose tissue. Intestinal absorption of triglycerides was increased compared to the control group, possibly because lipids are needed due thermogenesis. Total cholesterol in HDL fractions, tended to be concentrated in more mature fragments, especially after long-term exposure. In addition HDL, during long-term exposure, showed to have more effective antioxidant potential and cholesterol efflux, compared to the group exposed to cold temperature for 2 weeks.
Our observations lead to two interesting findings: 1) Short-term exposure to cold has greater effect on thermogenesis and ATP production rather than long-term exposure. 2) After long-term exposure to cold, HDL appears to be more functional compared to the short-term exposure group.
Therefore our results indicate acclimation of the animals to low temperature environment, followed by a qualitative HDL.
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Role of polymorphisms of the cholesteryl ester transfer protein gene in atherogenesisKakko, S. (Sakari) 28 March 2000 (has links)
Abstract
The cholesteryl ester transfer protein (CETP) is a plasma
protein that transfers cholesteryl esters and triglycerides between
plasma lipoproteins. Humans with a genetic CETP deficiency have
high plasma high density lipopoprotein cholesterol (HDL-C) levels,
whereas the CETP transgene lowers plasma HDL-C levels in mice. The
role of CETP in the development of atherosclerosis is unclear due
to the controversial results of many human and animal studies. The
present research was designed to investigate the CETP gene as a
candidate gene in the regulation of plasma HDL-C levels and the development
of atherosclerosis in humans. The CETP gene was screened for mutations
and polymorphisms associated with these traits in a well-characterized,
homogenous population sample of 515 men and women and in a sample
of 115 men with low HDL-C levels and coronary heart disease (CHD).
Using polymerase chain reaction and single-strand conformation
polymorphism analysis (PCR-SSCP), three polymorphic sites were found
(A373P, I405V, R451Q) in the exons of the CETP gene, one in intron
9 and one in the 3'untranslated region of the CETP gene.
In addition, the genotypes of a functional promoter polymorphism
were determined.
The V405 allele was associated with lower plasma CETP activity
in the whole population sample, and the Q451 allele and the P373
allele were associated with higher plasma CETP activity in men, whereas
the genotypes of the promoter polymorphism were not significantly
associated with plasma CETP activity. The genotypes of the CETP
gene explained about 20 % of the variation of plasma CETP
activity in men. The CETP gene polymorphisms were found to be a
minor regulator of plasma HDL-C levels, and these associations interacted
with alcohol consumption, sex and triglyceride levels. The strongest
association was detected between the promoter polymorphism and HDL-C levels
in women. The variation at the CETP gene locus explained about 8 % of
the variation in plasma HDL-C levels in women, but less than 1 % in
men. CETP gene polymorphisms (A373P, I405V and R451Q) were associated
with carotid intima-media thickness, explaining about 6 % of
the variation in men and 4 % in women. However, none of
the polymorphisms were associated significantly with the CHD risk.
In conclusion, the CETP gene was found to be polymorphic and
a minor regulator of plasma HDL-C levels and the development of
atherosclerosis.
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The impact of Niacin on PCSK9 levels in vervet monkeys (Chlorocebus aethiops)Ngqaneka, Thobile January 2020 (has links)
Magister Pharmaceuticae - MPharm / Cardiovascular diseases (CVDs) such as ischaemic heart diseases, heart failure and stroke
remain a major cause of death globally. Various deep-rooted factors influence CVD
development; these include but are not limited to elevated blood lipids, high blood pressure,
obesity and diabetes. A considerable number of proteins are involved directly and indirectly in
the transport, maintenance and elimination of plasma lipids, including high and low-density
lipoprotein cholesterol (HDL-C and LDL-C). There are several mechanisms involved in the
removal of LDL particles from systemic circulation. One such mechanism is associated with
the gene that encodes proprotein convertase subtilisin/kexin type 9 (PCSK9), which has
become an exciting therapeutic target for the reduction of residual risk of CVDs. Currently,
statins are the mainstay treatment to reduce LDL-C, and a need exists to further develop more
effective LDL-C-lowering drugs that might supplement statins. This study was aimed at
contributing to the generation of knowledge regarding the effect of niacin in reducing LDL
levels through PCSK9 interaction.
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The Molecular Interaction of Apolipoprotein A-I and Lecithin: Cholesterol Acyl TransferaseCooke, Allison L., B.A. January 2018 (has links)
No description available.
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Effect of Danazol on Plasma Lipid and Lipoprotein Levels in Normal WomenLuciano, Anthony A., Wallace, Robert B., Sherman, Barry M. 01 January 1982 (has links)
Prior studies of lipid and lipoprotein levels alterations associated with the administration of danazol, a testosterone derivative, in patients treated for endometriosis have been conflicting. We administered danazol to 7 normal menstruating women and measured plasma lipid and lipoprotein cholesterol levels prior to and 2 months after treatment. Small, non-significant decreases in total plasma cholesterol and triglyceride levels were seen, largely due to a dramatic decline in one woman with type IV hyperlipoproteinemia. No significant change in low density or very low density lipoprotein cholesterol levels was seen. However, a marked (40%) reduction of high density lipoprotein cholesterol level in the mean was found. These findings have implications for the atherogenic potential of danazol, the treatment of hyperlipidemia, and the relationship between gonadal hormones and lipoprotein levels.
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INVESTIGATING THE MOLECULAR MECHANISMS OF ATHEROSCLEROSIS DEVELOPMENT IN THE MOUSE: EMPHASIS ON THE MACROPHAGE SPHINGOSINE-1-PHOSPHATE RECEPTOR 1 / MOLECULAR MECHANISMS OF ATHEROSCLEROSIS IN THE MOUSEGonzalez Jara, Leticia A January 2016 (has links)
Atherosclerosis is a chronic inflammatory disease affecting large- and medium-sized
arteries and is considered the major cause behind cardiovascular diseases (CVD).
Elevated low-density lipoprotein (LDL)-cholesterol and low high-density lipoprotein
(HDL)-cholesterol are considered major risk factors for the CVD. HDL mediates a
variety of atheroprotective actions, many of them involving the interaction with the
scavenger receptor class B, type 1 (SR-B1).
Despite the efforts placed in raising HDL-cholesterol, no improvement has been
achieved in reducing CVD risk, suggesting that other components of the HDL particles
may be responsible for HDL-mediated atheroprotection. One of these may be
sphingosine-1-phospate (S1P).
In this thesis, the role of S1P receptors (S1PRs) in atherosclerosis is explored,
with emphasis in macrophage apoptosis. In particular, the importance of the macrophage
S1PR1 and its role in apoptosis and atherosclerosis was evaluated. We demonstrated that
diabetes exacerbates atherosclerosis development and myocardial infarction in SR-B1
KO/apoE-hypomorphic mice and that treatment with FTY720, a S1PR agonist, protects
against diabetes pro-atherogenic effects. We also show that S1PR1 agonists protected
macrophages against apoptosis through phosphoinositide 3-kinase (PI3K)/AKT, and that
HDL failed to protect S1PR1 deficient macrophages against apoptosis. In vivo,
macrophage S1PR1 deficiency translated into increased atherosclerosis, necrotic core
formation and numbers of apoptotic cells in the atherosclerotic plaque.
BIM deficiency in BM cells was protective against atherosclerosis development
and HDL treatment reduced BIM protein levels in cells exposed to ER stressors,
suggesting that the pro-apoptotic protein may be an important target for HDL in
macrophages.
We conclude that signaling through the S1PRs, in particular S1PR1 is important
in controlling macrophage apoptosis and atherosclerosis development. Our data suggests
that S1PR1 signaling axis and the pro-apoptotic protein BIM play an important role in
mediating HDL anti-apoptotic signaling, however further studies are required to clarify
the interaction between all of these factors. / Thesis / Doctor of Philosophy (PhD)
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Role of Myeloperoxidase Mediated Oxidative Modification and Apolipoprotein Composition in High Density Lipoprotein FunctionUndurti, Arundhati January 2010 (has links)
No description available.
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The Role of Sphingolipids in Cholesterol Efflux Mediated by ATP-Binding Cassette Transporter AI (ABCAI)Witting, Scott R. 05 October 2004 (has links)
No description available.
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