(Circulation. 1998;98:2088-2093.)
© 1998 American Heart Association, Inc.
Cardiovascular Drugs |
Mechanism of Action of Fibrates on Lipid and Lipoprotein Metabolism
From Unité 325 INSERM (B.S., J.D., J.A., K.S., J.-C.F.), Département d'Athérosclérose, Institut Pasteur de Lille, 59019 Lille, France, and Center for Research, Prevention and Treatment of Atherosclerosis (E.L.), Division of Medicine, Hadassah University Hospital, 91120 Jerusalem, Israel.
Correspondence to Jean-Charles Fruchart, Département d'Athérosclérose et INSERM U325, Institut Pasteur de Lille, 1, rue du Prof. Calmette, 59019 Lille Cédex, France. E-mail Jean-Charles.Fruchart{at}pasteur-lille.fr
Abstract
Abstract—Treatment with
fibrates, a widely used class of lipid-modifying agents, results in a
substantial decrease in plasma triglycerides and is usually
associated with a moderate decrease in LDL cholesterol and
an increase in HDL cholesterol concentrations.
Recent investigations indicate that the effects of fibrates are
mediated, at least in part, through alterations in transcription of
genes encoding for proteins that control lipoprotein
metabolism. Fibrates activate specific
transcription factors belonging to the nuclear hormone receptor
superfamily, termed peroxisome proliferator-activated receptors
(PPARs). The PPAR-
form mediates fibrate action on HDL
cholesterol levels via transcriptional induction of
synthesis of the major HDL apolipoproteins, apoA-I and apoA-II.
Fibrates lower hepatic apoC-III production and increase
lipoprotein lipase—mediated lipolysis via PPAR. Fibrates stimulate
cellular fatty acid uptake, conversion to acyl-CoA derivatives, and
catabolism by the ß-oxidation pathways, which, combined with a
reduction in fatty acid and triglyceride synthesis, results
in a decrease in VLDL production. In summary, both enhanced
catabolism of triglyceride-rich particles and reduced
secretion of VLDL underlie the hypotriglyceridemic
effect of fibrates, whereas their effect on HDL metabolism
is associated with changes in HDL apolipoprotein expression.
Key Words: apolipoproteins • arteriosclerosis • fibrates • hypercholesterolemia • hyperlipoproteinemia • lipids • PPAR
A vast number of studies confirmed the intimate and
causative relationships between dyslipidemias and
coronary heart disease. Although
hypercholesterolemia is an important underlying
cause for coronary heart disease, other
dyslipidemias, such as hypoalphalipoproteinemia (low plasma
HDL) and hypertriglyceridemia, may be
causative in a substantial number of cases. Fibrates are useful for the
treatment of hypoalphalipoproteinemia with or without
hypertriglyceridemia.1 2
The recommendation for the use of fibrates in certain types of
dyslipidemia has gained additional support from a subgroup
analysis of the Helsinki Heart Study,3
which showed that the best preventive efficacy has been achieved in a
subset of 
10% of the study population who had a baseline LDL:HDL
cholesterol ratio of >5 and a triglyceride
level of 2.3 mmol/L.4 5 Results from
angiographic trials revealed that fibrates retard the progression of
coronary atherosclerosis and decrease the
number of coronary events.6 7
Pharmacological Action of Fibrates
Fibrates are generally effective in lowering elevated plasma triglycerides and cholesterol. The magnitude of lipid changes depends, however, on the patient's pretreatment lipoprotein status8 as well as the relative potency of the fibrate used.9 The most pronounced effects of fibrates are a decrease in plasma triglyceride-rich lipoproteins (TRLs). Levels of LDL cholesterol (LDL-C) generally decrease in individuals with elevated baseline plasma concentrations, and HDL cholesterol (HDL-C) levels are usually increased when baseline plasma concentrations are low.8 However, paradoxical increases in LDL-C have been reported in some patients with dyslipidemia.10 Fibrate treatment results in a reduction of the LDL fraction of atherogenic small, dense particles with an equivalent increase in the intermediate subfraction.11 12 13 Within the triglyceride-rich apolipoprotein (apo) B-containing lipoproteins, fibrates efficiently reduce the apoC-III–containing particles,14 15 which are markers for increased risk for atherogenesis.16 The increased HDL concentrations after fibrates are generally reflected by increased plasma levels of apoA-I and apoA-II,14 15 a change that is associated with an increase in lipoprotein (Lp) A-I:A-II, and a decrease in LpA-I concentrations in patients treated with fenofibrate.14 15
Mechanisms of Action of Fibrates
Evidence from studies in rodents and in humans is available to
implicate 5 major mechanisms underlying the above-mentioned modulation
of lipoprotein phenotypes by fibrates:
1. Induction of lipoprotein lipolysis. Increased TRL lipolysis could be a reflection of changes in intrinsic lipoprotein lipase (LPL) activity17 or increased accessibility of TRLs for lipolysis by LPL owing to a reduction of TRL apoC-III content.18
2. Induction of hepatic fatty acid (FA) uptake and reduction of hepatic triglyceride production. In rodents, fibrates increase FA uptake and conversion to acyl-CoA by the liver owing to the induction of FA transporter protein (FATP)19 and acyl-CoA synthetase (ACS) activity.20 Induction of the ß-oxidation pathway with a concomitant decrease in FA synthesis by fibrates results in a lower availability of FAs for triglyceride synthesis, a process that is amplified by the inhibition of hormone-sensitive lipase in adipose tissue by fibrates.21
3. Increased removal of LDL particles. Fibrate treatment results in the formation of LDL with a higher affinity for the LDL receptor, which are thus catabolized more rapidly.11
4. Reduction in neutral lipid (cholesteryl ester and triglyceride) exchange between VLDL and HDL may result from decreased plasma levels of TRL.22
5. Increase in HDL production and stimulation of reverse cholesterol transport. Fibrates increase the production of apoA-I and apoA-II in liver,23 24 which may contribute to the increase of plasma HDL concentrations and a more efficient reverse cholesterol transport.
Role of Transcription Factors in Mediating Fibrate Action
It has been known for several years that fibrates induce peroxisome proliferation in rodents.25 26 This process is linked to the induction of transcription of genes involved in peroxisomal ß-oxidation and is mediated by specific transcription factors, therefore termed peroxisome proliferator-activated receptors (PPARs).
The PPAR Family of Transcription Factors
PPARs are members of the superfamily of nuclear hormone receptors,
which are transcription factors transmitting signals that originate
from lipid-soluble factors (eg, hormones, vitamins, and FAs) to the
genome.25 26 Nuclear receptors recognize and bind
to DNA at specific sites, called response elements (REs), which consist
of derivatives of the AGGTCA sequence. During evolution, mutation,
duplication, and addition of flanking sequences have generated REs
distinctive for the various receptors. Once bound to its RE, the
receptor complex can activate or repress the expression of a
target gene.
PPARs heterodimerize with the retinoid X receptor (RXR) and bind to REs
arranged as direct repeats spaced by 1 nucleotide (DR1),
termed peroxisome proliferator response elements (PPREs)
(Figure
). To date, 3 different PPAR genes
(, 
[also termed ß, NUC I, or FAAR],
and 
) have been identified.25 PPARs display
distinct expression patterns, which suggests important functional
differences. PPAR- is predominantly expressed in tissues that
metabolize high amounts of FAs, such as liver, kidney, heart, and
muscle.27 The expression of PPAR- is high in
adipose tissue, where it triggers adipocyte differentiation and induces
the expression of genes critical for
adipogenesis.26
|
FAs and derivatives, such as prostaglandin J2 for
PPAR-28 29 or
8(S)hydroxyeicosatetraenoic
acid,30 31
8(S)hydroxyeicosapentaenoic
acid,31 and leukotriene
B432 for PPAR-, have been implicated as
natural PPAR ligands. Fibrates are synthetic ligands for
PPAR-.30 31 32
In rodents, fibrates induce the expression of genes involved in
intracellular FA metabolism, such as peroxisomal and
mitochondrial ß-oxidation, 
-hydroxylation, and
ketogenesis.33 By contrast, very few data are
available on the regulation of their human counterparts, and it awaits
further study to determine whether fibrates and/or PPARs also regulate
the expression of any of these genes in humans. However, in contrast to
rodents, there is no evidence that fibrates would induce peroxisome
proliferation in humans and primates.34
The Role of PPARs in Mediating Fibrate Action on Lipoprotein
Metabolism in Humans
TRL Metabolism
The hypotriglyceridemic action of fibrates
involves combined effects on LPL17 and apoC-III
expression,34 resulting in increased lipolysis.
The induction of LPL expression occurs at the transcriptional level and
is mediated by PPAR. The latter binds to a PPRE that is present
both in the human and the mouse LPL gene
promoters.35
In contrast to LPL, transcription of the apoC-III gene is
inhibited by fibrates, resulting in decreased production of
apoC-III in the liver.34 The repression of
apoC-III gene expression by fibrates is mediated via
PPAR-.36 Consistent with the
repression of apoC-III expression, turnover studies in humans indicate
that fibrates reduce apoC-III synthesis,18
leading to enhanced LPL-mediated catabolism of VLDL particles.
Moreover, fibrates also decrease apoB and VLDL
production.37 As a consequence, a reduced
secretion of VLDL particles, together with the enhanced catabolism of
triglyceride-rich particles, most likely accounts for the
hypolipidemic effect of fibrates.
Animal studies suggest that fibrates also increase the hepatic uptake of free FAs (FFAs) by specific FATPs19 and generation of acyl-CoA esters by ACS.20 Owing to an increased ß-oxidation activity and a reduction in acetyl-CoA carboxylase and FA synthase activities,38 FFA metabolism is shifted from triglyceride synthesis to catabolism. Although fibrates do not induce peroxisomal ß-oxidation in humans, it is conceivable that they also affect FA uptake, conversion, and catabolism through the mitochondrial ß-oxidation pathway in humans.
HDL Metabolism
In humans, fibrates increase plasma levels of HDL and its major
constituents, apoA-I and apoA-II, to a variable
extent39 40 and stimulate apoA-I
production in human apoA-I transgenic mice and human
hepatocytes.24 In vitro studies have
demonstrated that the induction of human apoA-I gene expression after
fibrates may be mediated by the interaction of PPAR with a functional
PPRE, localized in the A site of the apoA-I
promoter.41 Human apoA-II plasma concentrations
increase after fibrate treatment.14 15 This is a
consequence of the induction of hepatic apoA-II synthesis by fibrates
and is mediated through PPAR/RXR heterodimers.23
Indications and Clinical Use of Fibrates in Specific Lipoprotein Disorders
Primary Hypertriglyceridemia
Fibrates are first-line drugs for the treatment of primary
hypertriglyceridemia. In these patients,
fibrates most noticeably decrease plasma TRLs42;
they also decrease, albeit to a lesser extent, total
cholesterol, whereas HDL-C levels
increase.42 The reduction in
cholesterol and triglycerides is mainly due to
a fall in VLDL, which is accompanied by changes in VLDL
composition.42 Fibrates predominantly reduce the
concentrations of large VLDL subfractions.43 44
In addition, fibrates attenuate the postprandial lipid response in
hypertriglyceridemic
subjects.44
LDL lipid composition is normalized in hypertriglyceridemic patients, who generally have low levels of LDL with an abnormal lipid composition.45 The cholesteryl ester content of LDL increases in all LDL subclasses, resulting in large, less-dense LDL particles.13 43 These changes lead to increased interactions of LDL particles with the LDL receptor, thereby improving LDL clearance.46
HDL-C levels, which are low in patients with hypertriglyceridemia, increase after treatment with fibrates.42 The lowering of the pool of TRLs on treatment with fibrates results in the reduction of net cholesteryl ester transfer from HDL to TRLs,22 which, in association with unchanged lecithin:cholesterol acyl transferase (LCAT) activity, will ultimately lead to an increase in cholesteryl ester and a decrease in triglyceride content of HDL. Improvement of LPL-mediated lipolysis of TRLs43 and increased apoA-I and apoA-II synthesis may also contribute to the rise in HDL levels on treatment with fibrates by promoting the formation of HDL precursors.
Type III Dysbetalipoproteinemia
Type III dysbetalipoproteinemia is a rare lipid disorder resulting
from homozygosity for the rare apoE2 isoform in predisposed subjects.
The characteristic disturbance of this metabolic
disorder is the accumulation of cholesterol-enriched VLDL,
which migrates in ß-position on agarose gel electrophoresis. Fibrates
have a spectacular lipid-lowering potential in patients with type III
dysbetalipoproteinemia.15 47 48 The levels of
circulating triglycerides and cholesterol are
greatly diminished. The reduction in cholesterol is
accounted for by the major reduction of VLDL cholesterol
(VLDL-C) and IDL cholesterol, the most atherogenic
lipoproteins in patients with type III dysbetalipoproteinemia.
Simultaneously, LDL-C and HDL-C, which are usually low,
increase significantly. As a consequence of the reduction in
ß-VLDL,15 regression of xanthoma and
improvement of manifestations of atherosclerosis are
observed 49
Combined Hyperlipidemia
Fibrates efficiently lower plasma cholesterol, VLDL-C,
and triglycerides and increase HDL-C in combined
hyperlipidemia.50 The reduction
in total cholesterol is accounted for by the fall in both
VLDL-C and LDL-C,51 whereas the reduction of
triglyceride levels is associated with normalization of the
typical atherogenic LDL subspecies profile in this lipid disorder.
Fibrate treatment reduces the levels of dense LDL and of
LDL-triglyceride content. Mean LDL peak particle size may
increase to normal or remain small,52 but the
mean LDL flotation rate augments because of an increase in buoyant LDL
concentration.52
Primary Hypercholesterolemia
Although fibrates are not considered to be first-line drugs in
primary
hypercholesterolemia,1 2
the new generation of fibrates efficiently reduce plasma
cholesterol and LDL-C and increase HDL-C concentrations
when used in monotherapy in patients with primary
hypercholesterolemia.51 53
However, it should be emphasized that the response of
hypercholesterolemic patients to fibrate treatment is
heterogenous, and nonresponse or even a paradoxical
increase in LDL has been observed.54 55 The
reduction in total cholesterol is accounted for by a fall
in both VLDL-C and LDL-C.53 Fibrates reduce the
dense LDL but not the light LDL fraction,56 57
which is less susceptible to oxidation.13 The
affinity of LDL for cellular receptors is not affected by treatment in
patients with primary
hypercholesterolemia.57
The increase in HDL-C is related to a lower cholesteryl ester transfer
protein activity, whereas LCAT activity is not
affected.57 In patients with primary
hypercholesterolemia, LPL activity also
increases on treatment with fibrates, resulting in a reduction of
postprandial lipemia.58
Non–Insulin-Dependent Diabetes Mellitus
In non–insulin-dependent diabetes mellitus (NIDDM) with
hyperlipemia, fibrates lower plasma cholesterol,
triglycerides, VLDL, and
IDL.54 59 60 61 The levels of apoC-III decrease,
resulting in improvement of TRL lipolysis and
clearance.59 62 The effect on LDL-C and apoB is
dependent on the concentration of plasma
TG.54 60 61 The mean LDL particle diameter
increases, whereas the concentration of dense LDL decreases in
proportion to the changes in
triglycerides.63 Fibrates increase
total HDL-C mainly owing to an elevation of the
HDL3 fraction.62 As in
patients with primary hyperlipemia, fibrates reduce postprandial
lipemia in patients with NIDDM.64
Tolerability and Safety
In general, fibrates are considered to be well tolerated, with an excellent safety profile. A low incidence of fibrate-associated toxicity has been reported in almost every organ system.65 In accordance with this notion, a summary of 10 years' experience with fenofibrate with an exposure of 6 million patient-years including 7145 patients involved in clinical trials revealed a low frequency of side effects.66
Members of the 2 most popular classes of lipid-lowering drugs, HMG CoA reductase inhibitors and fibrates, cause cancer in rodents.67 Although the mechanism may be related to peroxisome proliferation, a definite link has not yet been established. In humans, long-term administration of various fibrates does not cause peroxisome proliferation or any other morphological changes in the liver.68 69 Extrapolation of this evidence of carcinogenesis from rodents to humans is uncertain.
Clinically relevant interactions of fibrates with other antihyperlipidemic drugs include rhabdomyolysis (reported in combination with HMG CoA reductase inhibitors) and decreased bioavailability when combined with some bile acid sequestrants. Finally, potentiation of the anticoagulant effect of coumarin derivatives may cause bleeding.70
Future Perspectives
The better understanding of the basic mechanisms of action of
fibrates in both rodents and humans should now allow the development of
novel compounds on a more rational basis. Because the currently
available fibrates (Table) are
rather nonspecific activators of various PPARs, it is
expected that more potent and subtype-specific PPAR ligands and/or
activators might constitute a novel class of
"superfibrates." These compounds might enhance specificity, reduce
side effects, and widen the clinical indications of this class of
lipid-lowering drugs. Ongoing large clinical studies should confirm
their effectiveness in reducing coronary events and demonstrate
a possible benefit on coronary and total mortality.
|
Acknowledgments
Dr Schoonjans was supported by fellowships from ARC and IFN; Drs Auwerx and Staels are members of the CNRS. This work was supported by INSERM U325, Institut Pasteur De Lille, Région Nord, Pas-de-Calais.
References
1. Prevention of coronary heart disease: scientific background and new clinical guidelines: recommendations of the European Atherosclerosis Society prepared by International Task Force for Prevention of Coronary Heart Disease. Nutr Metab Cardiovasc Dis. 1992;2:113–156.
2.
Summary of the second report of the National
Cholesterol Education Program (NCEP) Expert Panel on
Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults (Adult Treatment Panel II).
JAMA. 1993;269:3015–3023.
3. Frick MH, Elo O, Haapa K, Heinonen OP, Heinsalmi P, Helo P, Huttunen JK, Kaitaniemi P, Koskinen P, Manninen V, Mäenpää H, Malkönen M, Mänttäri M, Norola S, Pasternack A, Pikkarainen J, Romo M, Sjoblom T, Nikkilä EA. Helsinki Heart Study: primary prevention trial with gemfibrozil in middle-aged men with dyslipidemia: safety of treatment, changes in risk factors, and incidence of coronary heart disease. N Engl J Med. 1987;317:1237–1245.[Abstract]
4. Huttunen J, Manninen V, Manttari M, Koskinen P, Romo M, Tenkanen L, Heinonen O, Frick M. The Helsinki Heart Study: central findings and clinical implications. Ann Med. 1991;23:155–159.[Medline] [Order article via Infotrieve]
5. Huttunen J, Heinonen O, Manninen V, Koskinen P, Hakulinen T, Teppo L, Manttari M, Frick M. The Helsinki heart study: an 8.5-year safety and mortality follow-up. J Intern Med. 1994;235:31–39.[Medline] [Order article via Infotrieve]
6. Ericsson C-G, Hamsten A, Nilsson J, Grip L, Svane B, de Faire U. Angiographic assessment of effects of bezafibrate on progression of coronary artery disease in young male postinfarction patients. Lancet. 1996;347:849–853.[Medline] [Order article via Infotrieve]
7.
Frick MH, Syvanne M, Nieminen MS, Kauma H, Majahalme
S, Virtanen V, Kesaniemi YA, Pasternak A, Taskinen MR. Prevention of
the angiographic progression of coronary and vein-graft
atherosclerosis by gemfibrozil after coronary
bypass surgery in men with low levels of HDL cholesterol.
Circulation. 1997;96:2137–2143.
8. Tikkanen M. Fibric acid derivatives. Curr Opin Lipidol. 1992;3:29–33.
9. Zimetbaum P, Frishman W, Kahn S. Effects of gemfibrozil and other fibric acid derivatives on blood lipids and lipoproteins. J Clin Pharmacol. 1991;31:25–37.[Abstract]
10. Davignon J. Fibrates: a review of important issues and recent findings. Can J Cardiol. 1994;10:61B.
11.
Caslake M, Packard C, Gaw E, Murray E, Griffin B,
Vallance B, Shepherd J. Fenofibrate and LDL metabolic
heterogeneity in
hypercholesterolemia. Arterioscler
Thromb. 1993;13:702–711.
12. Bruckert E, Dejager S, Chapman M. Ciprofibrate therapy normalises the atherogenic low-density lipoprotein subspecies profile in combined hyperlipidemia (published erratum appears in Atherosclerosis. 1993 102:129). Atherosclerosis. 1993;100:91–102.[Medline] [Order article via Infotrieve]
13.
de Graaf J, Hendriks J, Demacker P, Stalenhoef A.
Identification of multiple dense LDL subfractions with enhanced
susceptibility to in vitro oxidation among
hypertriglyceridemic subjects:
normalization after clofibrate treatment. Arterioscler
Thromb. 1993;13:712–719.
14. Bard J-M, Parra HJ, Camare R, Luc G, Ziegler O, Dachet C, Bruckert E, Douste-Blazy P, Drouin P, Jacotot B, De Gennes JL, Keller U, Fruchart J-C. A multicenter comparison of the effects of simvastatin and fenofibrate therapy in severe primary hypercholesterolemia, with particular emphasis on lipoproteins defined by their apolipoprotein composition. Metabolism. 1992;41:498–503.[Medline] [Order article via Infotrieve]
15. Lussier-Cacan S, Bard J-M, Boulet L, Nestruck A, Grothé A-M, Fruchart J-C, Davignon J. Lipoprotein composition changes induced by fenofibrate in dysbetalipoproteinemia type III. Atherosclerosis. 1989;78:167–182.[Medline] [Order article via Infotrieve]
16. Luc G, Fievet C, Arveiler D, Evans A, Bard J, Cambien F, Fruchart J, Ducimetiere P. Apolipoproteins C-III and E in apo-B and non apo B-containing lipoproteins in two populations at contrasting risk for myocardial infarction: the ECTIM study. J Lipid Res. 1996;37:508–517.[Abstract]
17. Heller F, Harvengt C. Effects of clofibrate, bezafibrate, fenofibrate, and probucol on plasma lipolytic enzymes in normolipidaemic subjects. Eur J Clin Pharmacol. 1983;23:57–63.
18. Malmendier C, Lontie J-F, Delcroix C, Dubois D, Magot T, De Roy L. Apolipoproteins C-II and C-III metabolism in hypertriglyceridemic patients: effect of a drastic triglyceride reduction by combined diet restriction and fenofibrate administration. Atherosclerosis. 1989;77:139–149.[Medline] [Order article via Infotrieve]
19.
Martin G, Schoonjans K, Lefebvre A, Staels B, Auwerx J.
Coordinate regulation of the expression of the fatty acid transporter
protein (FATP) and acyl CoA synthetase (ACS) genes by PPAR and
PPAR activators. J Biol Chem. 1997;272:28210–28217.
20.
Schoonjans K, Watanabe M, Suzuki H, Mahfoudi A, Krey G,
Wahli W, Grimaldi P, Staels B, Yamamoto T, Auwerx J. Induction of
the acyl-coenzyme A synthetase gene by fibrates and fatty acids is
mediated by a peroxisome proliferator response element in the C
promoter. J Biol Chem. 1995;270:19269–19276.
21. D'Costa MA, Angel A. Inhibition of hormone-stimulated lipolysis by clofibrate: a possible mechanism for its hypolipidemic action. J Clin Invest. 1975;55:138–148.
22. Mann C, Yen F, Grant A, Bihain B. Mechanism of plasma cholesteryl ester transfer in hypertriglyceridemia. J Clin Invest. 1991;88:2059–2066.
23. Vu-Dac N, Schoonjans K, Kosykh V, Dallongeville J, Fruchart J, Staels B, Auwerx J. Fibrates increase human apolipoprotein A-II expression through activation of the peroxisome proliferator-activated receptor. J Clin Invest. 1995;96:741–750.
24. Berthou L, Duverger N, Emmanuel F, Langouët S, Auwerx J, Guillouzo A, Fruchart J-C, Rubin E, Denèfle P, Staels B, Branellec D. Opposite regulation of human versus mouse apolipoprotein A-I by fibrates in human apo A-I transgenic mice. J Clin Invest. 1996;97:2408–2416.[Medline] [Order article via Infotrieve]
25. Schoonjans K, Staels B, Auwerx J. Role of the peroxisome proliferator activated receptor (PPAR) in mediating effects of fibrates and fatty acids on gene expression. J Lipid Res. 1996;37:907–925.[Abstract]
26. Schoonjans K, Staels B, Auwerx J. The peroxisome proliferator activated receptors (PPARs) and their effects on lipid metabolism and adipocyte differentiation. Biochim Biophys Acta. 1996;1302:93–109.[Medline] [Order article via Infotrieve]
27.
Auboeuf D, Rieusset J, Fajas L, Vallier P, Frering V,
Riou JP, Laville M, Staels B, Auwerx J, Vidal H. Tissue distribution
and quantification of the expression of the peroxisome proliferator
activated receptors and of LXR mRNAs in human: effect
of obesity and NIDDM in adipose tissue. Diabetes. 1997;46:1319–1327.[Abstract]
28.
Forman B, Tontonoz P, Chen J, Brun R, Spiegelman B,
Evans R. 15-Deoxy-
12,14 prostaglandin J2 is a
ligand for the adipocyte determination factor PPAR. Cell. 1995;83:803–812.[Medline]
[Order article via Infotrieve]
29.
Kliewer S, Lenhard J, Willson T, Patel I, Morris D,
Lehman J. A prostaglandin J2 metabolite binds peroxisome
proliferator-activated receptor and promotes adipocyte
differentiation. Cell. 1995;83:813–819.[Medline]
[Order article via Infotrieve]
30.
Kliewer S, Sundseth S, Jones S, Brown P, Wisely G,
Koble C, Devchand P, Wahli W, Willson T, Lenhard J, Lehmann J. Fatty
acids and eicosanoids regulate gene expression through direct
interactions with peroxisome proliferator-activated receptors
alpha and gamma. Proc Natl Acad Sci U S A. 1997;94:4318–4323.
31.
Forman B, Chen J, Evans R. Hypolipidemic drugs,
polyunsaturated fatty acids, and eicosanoids are ligands for peroxisome
proliferator-activated receptors and . Proc
Natl Acad Sci U S A. 1997;94:4312–4317.
32.
Devchand P, Keller H, Peters J, Vazquez M, Gonzalez F,
Wahli W. The PPAR-leukotriene B4 pathway to
inflammation control. Nature. 1996;384:39–43.[Medline]
[Order article via Infotrieve]
33.
Gulick T, Cresci S, Caira T, Moore D, Kelly D. The
peroxisome proliferator-activated receptor regulates
mitochondrial fatty acid oxidative enzyme gene expression. Proc
Natl Acad Sci U S A. 1994;91:11012–11016.
34. Staels B, Vu-Dac N, Kosykh V, Saladin R, Fruchart JC, Dallongeville J, Auwerx J. Fibrates down-regulate apolipoprotein C-III expression independent of induction of peroxisomal acyl co-enzyme A oxidase. J Clin Invest. 1995;95:705–712.
35.
Schoonjans K, Peinado-Onsurbe J, Lefebvre A-M, Heyman
RA, Briggs M, Deeb S, Staels B, Auwerx J. PPAR and PPAR
activators direct a distinct tissue-specific
transcriptional response via a PPRE in the lipoprotein lipase gene.
EMBO J. 1996;15:5336–5348.[Medline]
[Order article via Infotrieve]
36.
Peters JM, Hennuyer N, Staels B, Fruchart J-C, Fievet
C, Gonzalez FJ, Auwerx J. Alterations in lipoprotein
metabolism in PPAR-deficient mice. J
Biol Chem. 1997;272:27307–27312.
37. Lamb R, Koch J, Bush S. An enzymatic explanation of the differential effects of oleate and gemfibrozil on cultured hepatocyte triacylglycerol and phosphatidylcholine biosynthesis and secretion. Biochim Biophys Acta. 1993;1165:299–305.[Medline] [Order article via Infotrieve]
38.
Maragandakis M, Hankin H. On the mode of action of
lipid lowering agents, V: kinetics of the inhibition in vitro of rat
acetyl-CoA carboxylase. J Biol Chem. 1971;246:348–354.
39. Malmendier C, Delcroix C. Effects of fenofibrate on high and low density lipoprotein metabolism in heterozygous familial hypercholesterolemia. Atherosclerosis. 1985;55:161–169.[Medline] [Order article via Infotrieve]
40. Mellies M, Stein E, Khoury P, Lamkin G, Glueck C. Effects of fenofibrate on lipids, lipoproteins and apolipoproteins in 33 subjects with primary hypercholesterolaemia. Atherosclerosis. 1987;63:57–64.[Medline] [Order article via Infotrieve]
41.
Vu-Dac N, Schoonjans K, Laine B, Fruchart J, Auwerx J,
Staels B. Negative regulation of the human apolipoprotein A-I promoter
by fibrates can be attenuated by the interaction of the peroxisome
proliferator-activated receptor with its response element.
J Biol Chem. 1994;269:31012–31018.
42. Bradford R, Goldberg A, Schonfeld G, Knopp R. Double-blind comparison of bezafibrate versus placebo in male volunteers with hyperlipoproteinemia. Atherosclerosis. 1992;92:31–40.[Medline] [Order article via Infotrieve]
43. Dachet C, Cavalerro E, Martin C, Girardot G, Jacotot B. Effect of gemfibrozil on the concentration and composition of very low density and low density lipoprotein subfractions in hypertriglyceridemic patients. Atherosclerosis. 1995;113:1–9.[Medline] [Order article via Infotrieve]
44. Simo I, Yakichuk J, Ooi T. Effect of gemfibrozil and lovastatin on postprandial lipoprotein clearance in the hypoalphalipoproteinemia and hypertriglyceridemia syndrome. Atherosclerosis. 1993;100:55–64.[Medline] [Order article via Infotrieve]
45. Bhatnagar D, Durrington P, Mackness M, Arrol S, Winocour P, Prais H. Effects of treatment of hypertriglyceridaemia with gemfibrozil on serum lipoproteins and the transfer of cholesteryl ester from high density lipoproteins to low density lipoproteins. Atherosclerosis. 1992;92:49–57.[Medline] [Order article via Infotrieve]
46. Nigon F, Lesnik P, Rouis M, Chapman M. Discrete subspecies of human low density lipoproteins are heterogeneous in their interaction with the cellular LDL receptor. J Lipid Res. 1991;32:1741–1753.[Abstract]
47. Larsen M, Illingworth D, O'Malley J. Comparative effects of gemfibrozil and clofibrate in type III hyperlipoproteinemia. Atherosclerosis. 1994;106:235–240.[Medline] [Order article via Infotrieve]
48. Zhao S, Smelt A, Leuven J, Vroom T, van der Laarse A, van't Hooft F. Changes of lipoprotein profile in familial dysbetalipoproteinemia with gemfibrozil. Am J Med. 1994;96:49–56.[Medline] [Order article via Infotrieve]
49.
Zelis R, Amsterdam A, Spann JJ, Mason D. Type IV
hyperlipoproteinemia: clofibrate without
dietary therapy. JAMA. 1972;222:326–328.
50. Wolf H. Efficacy and tolerability of etofibrate and gemfibrozil in combined hyperlipidaemia. Drug Exp Clin Res. 1994;20:109–113.
51. Cattin L, Da Col PG, Feruglio FS, Finazzo L, Rimondi S, Descovich G, Manzato E, Zambon S, Crepaldi G, Siepi D, Mannarino E, Ventura A. Efficacy of ciprofibrate in primary type II and IV hyperlipidemia: the Italian multicenter study. Clin Ther. 1990;12:482–488.[Medline] [Order article via Infotrieve]
52.
Hokanson J, Austin M, Zambon A, Brunzell J. Plasma
triglyceride and LDL heterogeneity in
familial combined hyperlipidemia. Arterioscler
Thromb. 1993;13:427–434.
53. Lupien P, Brun D, Gagne C, Moorjani S, Bielman P, Julien P. Gemfibrozil therapy in primary type II hyperlipoproteinemia: effects on lipids, lipoproteins and apolipoproteins. Can J Cardiol. 1991;7:27–33.[Medline] [Order article via Infotrieve]
54. Goldberg R, La-Belle P, Zupkis R, Ronca P. Comparison of the effects of lovastatin and gemfibrozil on lipids and glucose control in non-insulin-dependent diabetes mellitus. Am J Cardiol. 1990;66:16B–21B.[Medline] [Order article via Infotrieve]
55.
Pasternak R, Brown L, Stone P, Silverman D, Gibson C,
Sacks F. Effect of combination therapy with lipid-reducing drugs in
patients with coronary heart disease and "normal"
cholesterol levels: a randomized, placebo-controlled trial:
Harvard Atherosclerosis Reversibility Project
(HARP) Study Group. Ann Intern Med. 1996;125:529–540.
56. Tilly-Kiesi M, Tikkanen M. Low density lipoprotein density and composition in hypercholesterolaemic men treated with HMG CoA reductase inhibitors and gemfibrozil. J Intern Med. 1991;229:427–434.[Medline] [Order article via Infotrieve]
57. Franceschini G, Lovati M, Manzoni C, Michelagnoli S, Pazzucconi F, Gianfranceschi G, Vecchio G, Sirtori C. Effect of gemfibrozil treatment in hypercholesterolemia on low density lipoprotein (LDL) subclass distribution and LDL-cell interaction. Atherosclerosis. 1995;114:61–71.[Medline] [Order article via Infotrieve]
58. Simpson H, Williamson C, Olivecrona T, Pringle S, Maclean J, Lorimer A, Bonnefous F, Bogaievsky Y, Packard C, Shepherd J. Postprandial lipemia, fenofibrate and coronary artery disease. Atherosclerosis. 1990;85:193–202.[Medline] [Order article via Infotrieve]
59. Niort G, Cassader M, Gambiano R, Pagano G. Comparison of the effects of bezafibrate and acipimox on the lipid pattern and plasma fibrinogen in hyperlipidaemic type 2 (non-insulin-dependent) diabetic patients. Diabetes Metab. 1992;18:221–228.
60. Sweany A, Shapiro D, Tate A, Goldberg R, Stein E. Effects of simvastatin versus gemfibrozil on lipids and glucose control in patients with non-insulin-dependent diabetes mellitus: NIDDM Study Group. Clin Ther. 1995;17:186–203.[Medline] [Order article via Infotrieve]
61. Vuorinen-Markkola H, Yki-Jarvinen H, Taskinen M. Lowering of triglycerides by gemfibrozil affects neither the glucoregulatory nor antilipolytic effect of insulin in type 2 (non-insulin-dependent) diabetic patients. Diabetologia. 1993;36:161–169.[Medline] [Order article via Infotrieve]
62. Ohrvall M, Lithell H, Johansson J, Vessby B. A comparison between the effects of gemfibrozil and simvastatin on insulin sensitivity in patients with non-insulin-dependent diabetes mellitus and hyperlipoproteinemia. Metabolism. 1995;44:212–217.[Medline] [Order article via Infotrieve]
63. Lahdenpera S, Tilly-Kiesi M, Vuorinen-Markkola H, Kuusi T, Taskinen M. Effects of gemfibrozil on low-density lipoprotein particle size, density distribution, and composition in patients with type II diabetes. Diabetes Care. 1993;16:584–592.[Abstract]
64. Cavallero E, Piolot A, Jacotot B. Postprandial lipoprotein clearance in type 2 diabetes: fenofibrate effects. Diabetes Metab. 1995;21:118–120.
65. Sgro C, Escousse A. Side effects of fibrates (except liver and muscle). Therapie. 1991;46:351–354.[Medline] [Order article via Infotrieve]
66. Roberts W. Safety of fenofibrate: US and worldwide experience. Cardiology. 1989;76:169–179.[Medline] [Order article via Infotrieve]
67.
Newman T, Hulley S. Carcinogenicity of lipid-lowering
drugs. JAMA. 1996;275:55–60.
68. Gariot P, Barrat E, Mejean L, Pointel J, Drouin P, Debry G. Fenofibrate and human liver: lack of proliferation of peroxisomes. Arch Toxicol. 1983;53:151–163.[Medline] [Order article via Infotrieve]
69. Angelin B, Einarsson K, Leijd B. Effect of ciprofibrate treatment on biliary lipids in patients with hyperlipoproteinemia. Eur J Clin Invest. 1984;14:73–78.[Medline] [Order article via Infotrieve]
70. Blum A, Seligmann H, Livneh A, Ezra D. Severe gastrointestinal bleeding induced by a probable hydroxycoumarin-bezafibrate interaction. Isr J Med Sci. 1992;28:47–49.[Medline] [Order article via Infotrieve]
71.
Committee of Principal Investigators. A co-operative
trial in the primary prevention of ischaemic heart disease using
clofibrate. Br Heart J. 1978;40:1069–1118.
72. Oliver MF, Heady JA, Morris JN, Cooper J. WHO cooperative trial on the primary prevention of ischemic heart disease with clofibrate to lower serum cholesterol: final mortality follow-up. Lancet. 1984;2:600–604.[Medline] [Order article via Infotrieve]
73. Research Committee of the Scottish Society of Physicians. Ischaemic heart disease: a secondary prevention trial using clofibrate. Br Med J. 1971;4:775–784.
74. Trial of clofibrate in the treatment of ischaemic heart disease: five year study by a group of physicians of the Newcastle upon Tyne region. Br Med J. 1971;4:767–775.
75.
Tenkanen L, Manttari M, Manninen V. Some
coronary risk factors related to the insulin resistance
syndrome and treatment with gemfibrozil: experience of the Helsinki
Heart Study. Circulation. 1995;92:1779–1785.
76. Bloomfield Rubins H, Robins SJ, Iwane MK, Boden WE, Elam MB, Fye CL, Gordon DJ, Schaefer EJ, Schectman G, Wittes JT. Rationale and design of the department of veterans affairs high-density lipoprotein cholesterol intervention trial (HIT) for secondary prevention of coronary artery disease in men with low high-density lipoprotein cholesterol and desirable low-density lipoprotein cholesterol. Am J Cardiol. 1993;71:45–52.[Medline] [Order article via Infotrieve]
77. Goldbourt U, Behar S, Reicher-Reiss H, Agmon J, Kaplinsky E, Graff E, Kishon Y, Caspi A, Weisbort J, Mandelzweig L, Abinader E, Aharon L, Braun S, David D, Flich M, Friedman Y, Kristal N, Leil N, Markiewicz W, Marmor A, Palant A, Pelled B, Rabinowitz B, Reisin L, Roguin N, Rosenfeld T, Schlesinger Z, Sclarovsky S, Sherf L, Tzivoni D, Zahavi I, Zion M, Brunner D. Rationale and design of a secondary prevention trial of increasing serum high-density lipoprotein cholesterol and reducing triglycerides in patients with clinically manifest atherosclerotic heart disease (the Bezafibrate Infarction Prevention Trial). Am J Cardiol. 1993;71:909–915.[Medline] [Order article via Infotrieve]
78. Steiner G. The Diabetes Atherosclerosis Intervention Study (DAIS): a study conducted in cooperation with the World Health Organization: the DAIS Project Group. Diabetologia. 1996;39:1655–1661.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  S. M. Rahman, I. Qadri, R. C. Janssen, and J. E. Friedman Fenofibrate and PBA prevent fatty acid-induced loss of adiponectin receptor and pAMPK in human hepatoma cells and in hepatitis C virus-induced steatosis J. Lipid Res., November 1, 2009; 50(11): 2193 - 2202. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Tojcic, M.-O. Benoit-Biancamano, M. H. Court, R. J. Straka, P. Caron, and C. Guillemette In Vitro Glucuronidation of Fenofibric Acid by Human UDP-Glucuronosyltransferases and Liver Microsomes Drug Metab. Dispos., November 1, 2009; 37(11): 2236 - 2243. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. C. Chan, G. F. Watts, E. M.M. Ooi, K.-A. Rye, J. Ji, A. G. Johnson, and P. H. R. Barrett Regulatory Effects of Fenofibrate and Atorvastatin on Lipoprotein A-I and Lipoprotein A-I:A-II Kinetics in the Metabolic Syndrome Diabetes Care, November 1, 2009; 32(11): 2111 - 2113. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. J. Chapman, W. Le Goff, M. Guerin, and A. Kontush Cholesteryl ester transfer protein: at the heart of the action of lipid-modulating therapy with statins, fibrates, niacin, and cholesteryl ester transfer protein inhibitors Eur. Heart J., October 12, 2009; (2009) ehp399v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. SERTZNIG, T. DUNLOP, M. SEIFERT, W. TILGEN, and J. REICHRATH Cross-talk between Vitamin D Receptor (VDR)- and Peroxisome Proliferator-activated Receptor (PPAR)-signaling in Melanoma Cells Anticancer Res, September 1, 2009; 29(9): 3647 - 3658. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Simo and C. Hernandez Advances in the Medical Treatment of Diabetic Retinopathy Diabetes Care, August 1, 2009; 32(8): 1556 - 1562. [Full Text] [PDF]
|
|
|
|
 |
|
 H. Wang and R. H. Eckel Lipoprotein lipase: from gene to obesity Am J Physiol Endocrinol Metab, August 1, 2009; 297(2): E271 - E288. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Ohta, N. Masutomi, N. Tsutsui, T. Sakairi, M. Mitchell, M. V. Milburn, J. A. Ryals, K. D. Beebe, and L. Guo Untargeted Metabolomic Profiling as an Evaluative Tool of Fenofibrate-Induced Toxicology in Fischer 344 Male Rats Toxicol Pathol, June 1, 2009; 37(4): 521 - 535. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Okada, F. Sano, I. Ikeda, J. Sugimoto, S. Takagi, H. Sakai, and T. Yanai Fenofibrate-Induced Muscular Toxicity Is Associated with a Metabolic Shift Limited to Type-1 Muscles in Rats Toxicol Pathol, June 1, 2009; 37(4): 517 - 520. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. A. Gyamfi and Y.-J. Y. Wan Mechanisms of Resistance of Hepatocyte Retinoid X Receptor {alpha}-Null Mice to WY-14,643-induced Hepatocyte Proliferation and Cholestasis J. Biol. Chem., April 3, 2009; 284(14): 9321 - 9330. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Nakajima, N. Tanaka, H. Kanbe, A. Hara, Y. Kamijo, X. Zhang, F. J. Gonzalez, and T. Aoyama Bezafibrate at Clinically Relevant Doses Decreases Serum/Liver Triglycerides via Down-Regulation of Sterol Regulatory Element-Binding Protein-1c in Mice: A Novel Peroxisome Proliferator-Activated Receptor {alpha}-Independent Mechanism Mol. Pharmacol., April 1, 2009; 75(4): 782 - 792. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G Magee and P C Sharpe Paradoxical decreases in high-density lipoprotein cholesterol with fenofibrate: a quite common phenomenon J. Clin. Pathol., March 1, 2009; 62(3): 250 - 253. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Seth Loomba and R. Arora Fibrates: where are we now? Therapeutic Advances in Cardiovascular Disease, February 1, 2009; 3(1): 91 - 96. [Abstract] [PDF]
|
|
|
|
|
|
G. R. Hajer, T. W. van Haeften, and F. L.J. Visseren Adipose tissue dysfunction in obesity, diabetes, and vascular diseases Eur. Heart J., December 2, 2008; 29(24): 2959 - 2971. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Nishimura, Y. Dewa, T. Okamura, M. Jin, Y. Saegusa, M. Kawai, T. Umemura, M. Shibutani, and K. Mitsumori Role of Nrf2 and Oxidative stress on Fenofibrate-Induced Hepatocarcinogenesis in Rats Toxicol. Sci., December 1, 2008; 106(2): 339 - 349. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. C. Chan, G. F. Watts, E. M.M. Ooi, J. Ji, A. G. Johnson, and P. H. R. Barrett Atorvastatin and Fenofibrate Have Comparable Effects on VLDL-Apolipoprotein C-III Kinetics in Men With the Metabolic Syndrome Arterioscler Thromb Vasc Biol, October 1, 2008; 28(10): 1831 - 1837. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Z. Chen, M. C. Gropler, J. Norris, J. C. Lawrence Jr, T. E. Harris, and B. N. Finck Alterations in Hepatic Metabolism in fld Mice Reveal a Role for Lipin 1 in Regulating VLDL-Triacylglyceride Secretion Arterioscler Thromb Vasc Biol, October 1, 2008; 28(10): 1738 - 1744. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Doi, T. Sakoda, T. Akagami, T. Naka, Y. Mori, T. Tsujino, T. Masuyama, and M. Ohyanagi Aldosterone induces interleukin-18 through endothelin-1, angiotensin II, Rho/Rho-kinase, and PPARs in cardiomyocytes Am J Physiol Heart Circ Physiol, September 1, 2008; 295(3): H1279 - H1287. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Biscetti and R. Pola Endothelial Progenitor Cells and Angiogenesis Join the PPARty Circ. Res., July 3, 2008; 103(1): 7 - 9. [Full Text] [PDF]
|
|
|
|
|
|
M. Adiels, S.-O. Olofsson, M.-R. Taskinen, and J. Boren Overproduction of Very Low-Density Lipoproteins Is the Hallmark of the Dyslipidemia in the Metabolic Syndrome Arterioscler Thromb Vasc Biol, July 1, 2008; 28(7): 1225 - 1236. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Montoudis, E. Seidman, F. Boudreau, J.-F. Beaulieu, D. Menard, M. Elchebly, G. Mailhot, A.-T. Sane, M. Lambert, E. Delvin, et al. Intestinal fatty acid binding protein regulates mitochondrion {beta}-oxidation and cholesterol uptake J. Lipid Res., May 1, 2008; 49(5): 961 - 972. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Clemenz, N. Frost, M. Schupp, S. Caron, A. Foryst-Ludwig, C. Bohm, M. Hartge, R. Gust, B. Staels, T. Unger, et al. Liver-Specific Peroxisome Proliferator-Activated Receptor {alpha} Target Gene Regulation by the Angiotensin Type 1 Receptor Blocker Telmisartan Diabetes, May 1, 2008; 57(5): 1405 - 1413. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Tsunoda, N. Kobayashi, T. Ide, M. Utsumi, M. Nagasawa, and K. Murakami A novel PPAR{alpha} agonist ameliorates insulin resistance in dogs fed a high-fat diet Am J Physiol Endocrinol Metab, May 1, 2008; 294(5): E833 - E840. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Biscetti, E. Gaetani, A. Flex, T. Aprahamian, T. Hopkins, G. Straface, G. Pecorini, E. Stigliano, R. C. Smith, F. Angelini, et al. Selective Activation of Peroxisome Proliferator-Activated Receptor (PPAR){alpha} and PPAR{gamma} Induces Neoangiogenesis Through a Vascular Endothelial Growth Factor-Dependent Mechanism Diabetes, May 1, 2008; 57(5): 1394 - 1404. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Zhao, Y.-Q. Chen, T. M. Bonacci, D. S. Bredt, S. Li, W. R. Bensch, D. E. Moller, M. Kowala, R. J. Konrad, and G. Cao Identification and Characterization of a Major Liver Lysophosphatidylcholine Acyltransferase J. Biol. Chem., March 28, 2008; 283(13): 8258 - 8265. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Kadereit, P. Kumar, W.-J. Wang, D. Miranda, E. L. Snapp, N. Severina, I. Torregroza, T. Evans, and D. L. Silver Evolutionarily conserved gene family important for fat storage PNAS, January 8, 2008; 105(1): 94 - 99. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Pedro-Botet Review: The role of fenofibrate in reducing cardiovascular risk in type 2 diabetes The British Journal of Diabetes & Vascular Disease, January 1, 2008; 8(1): 22 - 27. [Abstract] [PDF]
|
|
|
|
|
|
P. J. Barter and K.-A. Rye Is There a Role for Fibrates in the Management of Dyslipidemia in the Metabolic Syndrome? Arterioscler Thromb Vasc Biol, January 1, 2008; 28(1): 39 - 46. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. J. Bajwa, A. Alioua, J. W. Lee, D. S. Straus, L. Toro, and C. Lytle Fenofibrate inhibits intestinal Cl secretion by blocking basolateral KCNQ1 K+ channels Am J Physiol Gastrointest Liver Physiol, December 1, 2007; 293(6): G1288 - G1299. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. R. Babaev, H. Ishiguro, L. Ding, P. G. Yancey, D. E. Dove, W. J. Kovacs, C. F. Semenkovich, S. Fazio, and M. F. Linton Macrophage Expression of Peroxisome Proliferator Activated Receptor-{alpha} Reduces Atherosclerosis in Low-Density Lipoprotein Receptor Deficient Mice Circulation, September 18, 2007; 116(12): 1404 - 1412. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Bays, J. McElhattan, and B. S Bryzinski A double-blind, randomised trial of tesaglitazar versus pioglitazone in patients with type 2 diabetes mellitus Diabetes and Vascular Disease Research, September 1, 2007; 4(3): 181 - 193. [Abstract] [PDF]
|
|
|
|
|
|
J. P. Wilding, I. Gause-Nilsson, and A. Persson Tesaglitazar, as add-on therapy to sulphonylurea, dose-dependently improves glucose and lipid abnormalities in patients with type 2 diabetes Diabetes and Vascular Disease Research, September 1, 2007; 4(3): 194 - 203. [Abstract] [PDF]
|
|
|
|
|
|
B. Goke, I. Gause-Nilsson, and A. Persson The effects of tesaglitazar as add-on treatment to metformin in patients with poorly controlled type 2 diabetes Diabetes and Vascular Disease Research, September 1, 2007; 4(3): 204 - 213. [Abstract] [PDF]
|
|
|
|
 |
|
 R. R. Almon, D. C. DuBois, Z. Yao, E. P. Hoffman, S. Ghimbovschi, and W. J. Jusko Microarray analysis of the temporal response of skeletal muscle to methylprednisolone: comparative analysis of two dosing regimens Physiol Genomics, August 20, 2007; 30(3): 282 - 299. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. M. Singh, M. H. Shishehbor, and B. J. Ansell High-Density Lipoprotein as a Therapeutic Target: A Systematic Review JAMA, August 15, 2007; 298(7): 786 - 798. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. C. van der Hoogt, W. de Haan, M. Westerterp, M. Hoekstra, G. M. Dallinga-Thie, J. A. Romijn, H. M. G. Princen, J. W. Jukema, L. M. Havekes, and P. C. N. Rensen Fenofibrate increases HDL-cholesterol by reducing cholesteryl ester transfer protein expression J. Lipid Res., August 1, 2007; 48(8): 1763 - 1771. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. R. Cha, X. Zhang, Y. Zhang, J. Wu, D. Su, J. Y. Han, X. Fang, B. Yu, M. D. Breyer, and Y. Guan Peroxisome Proliferator Activated Receptor {alpha}/{gamma} Dual Agonist Tesaglitazar Attenuates Diabetic Nephropathy in db/db Mice Diabetes, August 1, 2007; 56(8): 2036 - 2045. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Blanco-Rivero, I. Marquez-Rodas, F. E. Xavier, R. Aras-Lopez, I. Arroyo-Villa, M. Ferrer, and G. Balfagon Long-term fenofibrate treatment impairs endothelium-dependent dilation to acetylcholine by altering the cyclooxygenase pathway Cardiovasc Res, July 15, 2007; 75(2): 398 - 407. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Luci, B. Giemsa, H. Kluge, and K. Eder Clofibrate causes an upregulation of PPAR-{alpha} target genes but does not alter expression of SREBP target genes in liver and adipose tissue of pigs Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2007; 293(1): R70 - R77. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Pozzi, M. R. Ibanez, A. E. Gatica, S. Yang, S. Wei, S. Mei, J. R. Falck, and J. H. Capdevila Peroxisomal Proliferator-activated Receptor-{alpha}-dependent Inhibition of Endothelial Cell Proliferation and Tumorigenesis J. Biol. Chem., June 15, 2007; 282(24): 17685 - 17695. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Okada, Y. Inoue, M. Ube, F. Sano, I. Ikeda, J. Sugimoto, and S. Takagi Skeletal Muscle Susceptibility to Clofibrate Induction of Lesions in Rats Toxicol Pathol, June 1, 2007; 35(4): 517 - 520. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Tanaka, J. M. Ordovas, J. Delgado-Lista, F. Perez-Jimenez, C. Marin, P. Perez-Martinez, P. Gomez, and J. Lopez-Miranda Peroxisome proliferator-activated receptor {alpha} polymorphisms and postprandial lipemia in healthy men J. Lipid Res., June 1, 2007; 48(6): 1402 - 1408. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. A. Hegele and R. L. Pollex Apolipoprotein A-V Genetic Variation and Plasma Lipoprotein Response to Fibrates Arterioscler Thromb Vasc Biol, June 1, 2007; 27(6): 1224 - 1227. [Full Text] [PDF]
|
|
|
|
|
|
C.-Q. Lai, D. K. Arnett, D. Corella, R. J. Straka, M. Y. Tsai, J. M. Peacock, X. Adiconis, L. D. Parnell, J. E. Hixson, M. A. Province, et al. Fenofibrate Effect on Triglyceride and Postprandial Response of Apolipoprotein A5 Variants: The GOLDN Study Arterioscler Thromb Vasc Biol, June 1, 2007; 27(6): 1417 - 1425. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Nishimura, Y. Dewa, M. Muguruma, Y. Kuroiwa, H. Yasuno, T. Shima, M. Jin, M. Takahashi, T. Umemura, and K. Mitsumori Effect of Fenofibrate on Oxidative DNA Damage and on Gene Expression Related to Cell Proliferation and Apoptosis in Rats Toxicol. Sci., May 1, 2007; 97(1): 44 - 54. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Zhu, G. Su, and Q. H. Meng Inhibitory Effects of Micronized Fenofibrate on Carotid Atherosclerosis in Patients with Essential Hypertension Clin. Chem., November 1, 2006; 52(11): 2036 - 2042. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Boulanger, R. Mansouri, J. F. Gautier, and D. Glotz Are peroxisome proliferator-activated receptors new therapeutic targets in diabetic and non-diabetic nephropathies? Nephrol. Dial. Transplant., October 1, 2006; 21(10): 2696 - 2702. [Full Text] [PDF]
|
|
|
|
|
|
T. Kooistra, L. Verschuren, J. de Vries-van der Weij, W. Koenig, K. Toet, H.M.G. Princen, and R. Kleemann Fenofibrate Reduces Atherogenesis in ApoE*3Leiden Mice: Evidence for Multiple Antiatherogenic Effects Besides Lowering Plasma Cholesterol Arterioscler Thromb Vasc Biol, October 1, 2006; 26(10): 2322 - 2330. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. Mezei, Y. Li, E. Mullen, J. S. Ross-Viola, and N. F. Shay Dietary isoflavone supplementation modulates lipid metabolism via PPAR{alpha}-dependent and -independent mechanisms Physiol Genomics, September 14, 2006; 26(1): 8 - 14. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Werle-Schneider, A. Wolfelschneider, M. C. von Brevern, J. Scheel, T. Storck, D. Muller, R. Glockner, H. Bartsch, and M. Bartelmann Gene Expression Profiles in Rat Liver Slices Exposed to Hepatocarcinogenic Enzyme Inducers, Peroxisome Proliferators, and 17{alpha}-Ethinylestradiol International Journal of Toxicology, September 1, 2006; 25(5): 379 - 395. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M J. Chapman The effects of fibrates on lipid metabolism and inflammation in type 2 diabetes Diabetes and Vascular Disease Research, September 1, 2006; 3(1_suppl): S6 - S9. [Abstract] [PDF]
|
|
|
|
|
|
P. F. Pilch and N. Bergenhem Pharmacological Targeting of Adipocytes/Fat Metabolism for Treatment of Obesity and Diabetes Mol. Pharmacol., September 1, 2006; 70(3): 779 - 785. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Serisier, F. Briand, K. Ouguerram, B. Siliart, T. Magot, and P. Nguyen Fenofibrate Lowers Lipid Parameters in Obese Dogs J. Nutr., July 1, 2006; 136(7): 2037S - 2040S. [Full Text] [PDF]
|
|
|
|
 |
|
 A. Benigni, C. Zoja, S. Tomasoni, M. Campana, D. Corna, C. Zanchi, E. Gagliardini, E. Garofano, D. Rottoli, T. Ito, et al. Transcriptional Regulation of Nephrin Gene by Peroxisome Proliferator-Activated Receptor-{gamma} Agonist: Molecular Mechanism of the Antiproteinuric Effect of Pioglitazone J. Am. Soc. Nephrol., June 1, 2006; 17(6): 1624 - 1632. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Grabacka, P. M. Plonka, K. Urbanska, and K. Reiss Peroxisome Proliferator-Activated Receptor {alpha} Activation Decreases Metastatic Potential of Melanoma Cells In vitro via Down-Regulation of Akt. Clin. Cancer Res., May 15, 2006; 12(10): 3028 - 3036. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Cuzzocrea, E. Mazzon, R. Di Paola, A. Peli, A. Bonato, D. Britti, T. Genovese, C. Muia, C. Crisafulli, and A. P. Caputi The role of the peroxisome proliferator-activated receptor-{alpha} (PPAR-{alpha}) in the regulation of acute inflammation J. Leukoc. Biol., May 1, 2006; 79(5): 999 - 1010. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Liu, C. Zang, M. H. Fenner, D. Liu, K. Possinger, H. P. Koeffler, and E. Elstner Growth inhibition and apoptosis in human Philadelphia chromosome-positive lymphoblastic leukemia cell lines by treatment with the dual PPAR{alpha}/{gamma} ligand TZD18 Blood, May 1, 2006; 107(9): 3683 - 3692. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Tenkanen, M. Manttari, P. T. Kovanen, H. Virkkunen, and V. Manninen Gemfibrozil in the Treatment of Dyslipidemia: An 18-Year Mortality Follow-up of the Helsinki Heart Study. Arch Intern Med, April 10, 2006; 166(7): 743 - 748. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Bilz, V. Samuel, K. Morino, D. Savage, C. S. Choi, and G. I. Shulman Activation of the farnesoid X receptor improves lipid metabolism in combined hyperlipidemic hamsters Am J Physiol Endocrinol Metab, April 1, 2006; 290(4): E716 - E722. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Paumelle, C. Blanquart, O. Briand, O. Barbier, C. Duhem, G. Woerly, F. Percevault, J.-C. Fruchart, D. Dombrowicz, C. Glineur, et al. Acute Antiinflammatory Properties of Statins Involve Peroxisome Proliferator-Activated Receptor-{alpha} via Inhibition of the Protein Kinase C Signaling Pathway Circ. Res., February 17, 2006; 98(3): 361 - 369. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Di Paola, E. Mazzon, D. Maiere, D. Zito, D. Britti, M. De Majo, T. Genovese, and S. Cuzzocrea Rosiglitazone Reduces the Evolution of Experimental Periodontitis in the Rat Journal of Dental Research, February 1, 2006; 85(2): 156 - 161. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C.-H. Lee and J. Plutzky Liver X Receptor Activation and High-Density Lipoprotein Biology: A Reversal of Fortune? Circulation, January 3, 2006; 113(1): 5 - 8. [Full Text] [PDF]
|
|
|
|
|
|
Evolving treatment paradigms for vascular risk reduction in type 2 diabetes: Report of an international symposium held in Barcelona, Spain, January 27-29, 2006 The British Journal of Diabetes & Vascular Disease, January 1, 2006; 6(1_suppl): S1 - S12. [PDF]
|
|
|
|
|
|
F. Blaschke, Y. Takata, E. Caglayan, R. E. Law, and W. A. Hsueh Obesity, Peroxisome Proliferator-Activated Receptor, and Atherosclerosis in Type 2 Diabetes Arterioscler Thromb Vasc Biol, January 1, 2006; 26(1): 28 - 40. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Chinetti-Gbaguidi, E. Rigamonti, L. Helin, A. L. Mutka, M. Lepore, J. C. Fruchart, V. Clavey, E. Ikonen, S. Lestavel, and B. Staels Peroxisome proliferator-activated receptor {alpha} controls cellular cholesterol trafficking in macrophages J. Lipid Res., December 1, 2005; 46(12): 2717 - 2725. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. C. Martinsen, I. Bakke, D. Chen, A. K. Sandvik, K. Zahlsen, T. Aamo, and H. L. Waldum Ciprofibrate stimulates the gastrin-producing cell by acting luminally on antral PPAR-{alpha} Am J Physiol Gastrointest Liver Physiol, December 1, 2005; 289(6): G1052 - G1060. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. L. Ruel, B. Lamarche, J.-F. Mauger, K. O. Badellino, J. S. Cohn, M. Marcil, and P. Couture Effect of Fenofibrate on Plasma Lipoprotein Composition and Kinetics in Patients With Complete Hepatic Lipase Deficiency Arterioscler Thromb Vasc Biol, December 1, 2005; 25(12): 2600 - 2607. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Fletcher, K. Berra, P. Ades, L. T. Braun, L. E. Burke, J. L. Durstine, J. M. Fair, G. F. Fletcher, D. Goff, L. L. Hayman, et al. Managing Abnormal Blood Lipids: A Collaborative Approach Circulation, November 15, 2005; 112(20): 3184 - 3209. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. F. Cariello, E. H. Romach, H. M. Colton, H. Ni, L. Yoon, J. G. Falls, W. Casey, D. Creech, S. P. Anderson, G. R. Benavides, et al. Gene Expression Profiling of the PPAR-alpha Agonist Ciprofibrate in the Cynomolgus Monkey Liver Toxicol. Sci., November 1, 2005; 88(1): 250 - 264. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Claudel, B. Staels, and F. Kuipers The Farnesoid X Receptor: A Molecular Link Between Bile Acid and Lipid and Glucose Metabolism Arterioscler Thromb Vasc Biol, October 1, 2005; 25(10): 2020 - 2030. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. D. Ashen and R. S. Blumenthal Low HDL Cholesterol Levels N. Engl. J. Med., September 22, 2005; 353(12): 1252 - 1260. [Full Text] [PDF]
|
|
|
|
|
|
C. Kjorholt, M. C. Akerfeldt, T. J. Biden, and D. R. Laybutt Chronic Hyperglycemia, Independent of Plasma Lipid Levels, Is Sufficient for the Loss of {beta}-Cell Differentiation and Secretory Function in the db/db Mouse Model of Diabetes Diabetes, September 1, 2005; 54(9): 2755 - 2763. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P.J. Barter Antiatherogenic Properties of Fibrates Arterioscler Thromb Vasc Biol, June 1, 2005; 25(6): 1095 - 1096. [Full Text] [PDF]
|
|
|
|
 |
|
 A. Reifel-Miller, K. Otto, E. Hawkins, R. Barr, W. R. Bensch, C. Bull, S. Dana, K. Klausing, J.-A. Martin, R. Rafaeloff-Phail, et al. A Peroxisome Proliferator-Activated Receptor {alpha}/{gamma} Dual Agonist with a Unique in Vitro Profile and Potent Glucose and Lipid Effects in Rodent Models of Type 2 Diabetes and Dyslipidemia Mol. Endocrinol., June 1, 2005; 19(6): 1593 - 1605. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Arakawa, N. Tamehiro, T. Nishimaki-Mogami, K. Ueda, and S. Yokoyama Fenofibric Acid, an Active Form of Fenofibrate, Increases Apolipoprotein A-I-Mediated High-Density Lipoprotein Biogenesis by Enhancing Transcription of ATP-Binding Cassette Transporter A1 Gene in a Liver X Receptor-Dependent Manner Arterioscler Thromb Vasc Biol, June 1, 2005; 25(6): 1193 - 1197. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G D Kolovou, K K Anagnostopoulou, and D V Cokkinos Pathophysiology of dyslipidaemia in the metabolic syndrome Postgrad. Med. J., June 1, 2005; 81(956): 358 - 366. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Wagner, P. J. Larson, S. Weiss, J. L. Miller, T. W. Doebber, M. S. Wu, D. E. Moller, and K. M. Gottesdiener Individual and Combined Effects of Peroxisome Proliferator-Activated Receptor and {gamma} Agonists, Fenofibrate and Rosiglitazone, on Biomarkers of Lipid and Glucose Metabolism in Healthy Nondiabetic Volunteers J. Clin. Pharmacol., May 1, 2005; 45(5): 504 - 513. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Li, K. Chen, N. Sinha, X. Zhang, Y. Wang, A. K. Sinha, F. Romeo, and J. L. Mehta The effects of PPAR-{gamma} ligand pioglitazone on platelet aggregation and arterial thrombus formation Cardiovasc Res, March 1, 2005; 65(4): 907 - 912. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A.-M. Paradis, B. Fontaine-Bisson, Y. Bosse, J. Robitaille, S. Lemieux, H. Jacques, B. Lamarche, A. Tchernof, P. Couture, and M.-C. Vohl The peroxisome proliferator-activated receptor {alpha} Leu162Val polymorphism influences the metabolic response to a dietary intervention altering fatty acid proportions in healthy men Am. J. Clinical Nutrition, February 1, 2005; 81(2): 523 - 530. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Sheena, R. Hertz, J. Nousbeck, I. Berman, J. Magenheim, and J. Bar-Tana Transcriptional regulation of human microsomal triglyceride transfer protein by hepatocyte nuclear factor-4{alpha} J. Lipid Res., February 1, 2005; 46(2): 328 - 341. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. V. Erbe, S. Wang, Y.-L. Zhang, K. Harding, L. Kung, M. Tam, L. Stolz, Y. Xing, S. Furey, A. Qadri, et al. Ertiprotafib Improves Glycemic Control and Lowers Lipids via Multiple Mechanisms Mol. Pharmacol., January 1, 2005; 67(1): 69 - 77. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. C. McCarthy, P. T. Pollak, E. A. Hanniman, and C. J. Sinal Disruption of Hepatic Lipid Homeostasis in Mice after Amiodarone Treatment Is Associated with Peroxisome Proliferator-Activated Receptor-{alpha}Target Gene Activation J. Pharmacol. Exp. Ther., December 1, 2004; 311(3): 864 - 873. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Okapcova and D. Gabor The Levels of Soluble Adhesion Molecules in Diabetic and Nondiabetic Patients with Combined Hyperlipoproteinemia and the Effect of Ciprofibrate Therapy Angiology, November 1, 2004; 55(6): 629 - 639. [Abstract] [PDF]
|
|
|
|
|
|
Y. Guan Peroxisome Proliferator-Activated Receptor Family and Its Relationship to Renal Complications of the Metabolic Syndrome J. Am. Soc. Nephrol., November 1, 2004; 15(11): 2801 - 2815. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Walcher and N. Marx Insulin resistance and cardiovascular disease: the role of PPAR{gamma} activators beyond their anti-diabetic action Diabetes and Vascular Disease Research, October 1, 2004; 1(2): 76 - 81. [Abstract] [PDF]
|
|
|
|
 |
|
 T. Kino and G. P. Chrousos Combating Atherosclerosis With LXR{alpha} And PPAR{alpha} Agonists: Is Rational Multitargeted Polypharmacy the Future of Therapeutics in Complex Diseases? Mol. Interv., October 1, 2004; 4(5): 254 - 257. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Normen, J. Frohlich, J. Montaner, M. Harris, T. Elliott, and G. Bondy Combination Therapy With Fenofibrate and Rosiglitazone Paradoxically Lowers Serum HDL Cholesterol Diabetes Care, September 1, 2004; 27(9): 2241 - 2242. [Full Text] [PDF]
|
|
|
|
|
|
G. Boden and M. Laakso Lipids and Glucose in Type 2 Diabetes: What is the cause and effect? Diabetes Care, September 1, 2004; 27(9): 2253 - 2259. [Full Text] [PDF]
|
|
|
|
 |
|
 B. D. Hegarty, S. M. Furler, N. D. Oakes, E. W. Kraegen, and G. J. Cooney Peroxisome Proliferator-Activated Receptor (PPAR) Activation Induces Tissue-Specific Effects on Fatty Acid Uptake and Metabolism in Vivo--A Study Using the Novel PPAR{alpha}/{gamma} Agonist Tesaglitazar Endocrinology, July 1, 2004; 145(7): 3158 - 3164. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. P. Beyer, R. J. Schmidt, P. Foxworthy, Y. Zhang, J. Dai, W. R. Bensch, R. F. Kauffman, H. Gao, T. P. Ryan, X.-C. Jiang, et al. Coadministration of a Liver X Receptor Agonist and a Peroxisome Proliferator Activator Receptor-{alpha} Agonist in Mice: Effects of Nuclear Receptor Interplay on High-Density Lipoprotein and Triglyceride Metabolism in Vivo J. Pharmacol. Exp. Ther., June 1, 2004; 309(3): 861 - 868. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Marx, H. Duez, J.-C. Fruchart, and B. Staels Peroxisome Proliferator-Activated Receptors and Atherogenesis: Regulators of Gene Expression in Vascular Cells Circ. Res., May 14, 2004; 94(9): 1168 - 1178. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T.B. Twickler, G.M. Dallinga-Thie, J.S. Cohn, and M.J. Chapman Elevated Remnant-Like Particle Cholesterol Concentration: A Characteristic Feature of the Atherogenic Lipoprotein Phenotype Circulation, April 27, 2004; 109(16): 1918 - 1925. [Full Text] [PDF]
|
|
|
|
|
|
K. Goya, S. Sumitani, X. Xu, T. Kitamura, H. Yamamoto, S. Kurebayashi, H. Saito, H. Kouhara, S. Kasayama, and I. Kawase Peroxisome Proliferator-Activated Receptor {alpha} Agonists Increase Nitric Oxide Synthase Expression in Vascular Endothelial Cells Arterioscler Thromb Vasc Biol, April 1, 2004; 24(4): 658 - 663. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. M. Post, M. Groenendijk, K. Solaas, P. C. N. Rensen, and H. M. G. Princen Cholesterol 7{alpha}-Hydroxylase Deficiency in Mice on an APOE*3-Leiden Background Impairs Very-Low-Density Lipoprotein Production Arterioscler Thromb Vasc Biol, April 1, 2004; 24(4): 768 - 774. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Ricote, A. F. Valledor, and C. K. Glass Decoding Transcriptional Programs Regulated by PPARs and LXRs in the Macrophage: Effects on Lipid Homeostasis, Inflammation, and Atherosclerosis Arterioscler Thromb Vasc Biol, February 1, 2004; 24(2): 230 - 239. [Abstract] [Full Text]
|
|
|
|
|
|
M. C. Sugden and M. J. Holness Potential Role of Peroxisome Proliferator-Activated Receptor-{alpha} in the Modulation of Glucose-Stimulated Insulin Secretion Diabetes, February 1, 2004; 53(90001): S71 - 81. [Abstract] [Full Text]
|
|
|
|
 |
|
 W. A. Hsueh and D. Bruemmer Peroxisome Proliferator-Activated Receptor {gamma}: Implications for Cardiovascular Disease Hypertension, February 1, 2004; 43(2): 297 - 305. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Bilz, S. Wagner, M. Schmitz, A. Bedynek, U. Keller, and T. Demant Effects of atorvastatin versus fenofibrate on apoB-100 and apoA-I kinetics in mixed hyperlipidemia J. Lipid Res., January 1, 2004; 45(1): 174 - 185. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||