(Circulation. 2001;103:357.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Pravastatin and the Development of Diabetes Mellitus
Evidence for a Protective Treatment Effect in the West of Scotland Coronary Prevention Study
From the Department of Biological Sciences (D.J.F.), University of Durham, Durham, UK; Robertson Centre for Biostatistics (J.N., I.F.), University of Glasgow, Glasgow, UK; Department of Pathological Biochemistry (N.S., C.J.P., J.S., A.G.), Glasgow Royal Infirmary University NHS Trust, Glasgow, UK; Department of Clinical Biochemistry (R.D.G.N.), Dryburn Hospital, North Durham Healthcare NHS Trust, Durham, UK; Department of Medical Cardiology (S.M.C., A.R.L., P.W.M.), Glasgow Royal Infirmary, Glasgow, UK; Department of Medicine (C.I.), Dumfries and Galloway Royal Infirmary, Dumfries, UK; and University Department of Medicine (J.H.M.), Glasgow Royal Infirmary, Glasgow, UK.
Correspondence to Dr Allan Gaw, Department of Pathological Biochemistry, Glasgow Royal Infirmary University NHS Trust, Glasgow G31 2ER, UK.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionAppendix 1References |
|---|
Background—We examined the development of new diabetes mellitus in men aged 45 to 64 years during the West of Scotland Coronary Prevention Study.
Methods and Results—Our
definition of diabetes mellitus was based on the American Diabetic
Association threshold of a blood glucose level of 
7.0 mmol/L.
Subjects who self-reported diabetes at baseline or had a baseline
glucose level of 7.0 mmol/L were excluded from the analyses. A total
of 5974 of the 6595 randomized subjects were included in the analysis,
and 139 subjects became diabetic during the study. The baseline
predictors of the transition from normal glucose control to diabetes
were studied. In the univariate model, body mass index, log
triglyceride, log white blood cell count, systolic blood pressure,
total and HDL cholesterol, glucose, and randomized treatment assignment
to pravastatin were significant predictors. In a multivariate model,
body mass index, log triglyceride, glucose, and pravastatin therapy
were retained as predictors of diabetes in this
cohort.
Conclusions—We concluded that the assignment to pravastatin therapy resulted in a 30% reduction (P=0.042) in the hazard of becoming diabetic. By lowering plasma triglyceride levels, pravastatin therapy may favorably influence the development of diabetes, but other explanations, such as the anti-inflammatory properties of this drug in combination with its endothelial effects, cannot be excluded with these analyses.
Key Words: diabetes mellitus • prevention • lipids • trials • risk factors
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
|---|
Factors that influence the development of diabetes mellitus have been the subject of considerable research.1 2 3 4 Blood lipid and lipoprotein levels have been confirmed as important predictors of this pathology,4 5 and more recently, markers of low-grade inflammation have been shown to predict the occurrence of type 2 diabetes.4 Interestingly, despite these strong associations, there have been very few investigations into the effects of drugs that influence the blood lipid profile or that have anti-inflammatory actions on the development of diabetes. One such drug that exhibits potentially beneficial pleiotropic effects on both plasma lipids and the inflammatory response is pravastatin.
Pravastatin is an HMG Co-A reductase inhibitor that has significant effects on the plasma lipid and lipoprotein profile, lowering total and LDL cholesterol and triglyceride levels and raising HDL cholesterol levels.6 7 8 In addition to these lipid effects, pravastatin has been shown to have a range of other antiatherothrombotic effects, including the restoration of endothelial function9 and anti-inflammatory effects.10
Pravastatin therapy has been shown unequivocally to reduce cardiovascular risk in a series of large-scale, randomized, controlled clinical trials.6 7 8 In a diabetic/glucose-intolerant subgroup analysis of one study, pravastatin significantly reduced coronary events, but no attempt was made to examine the effects of pravastatin on glucose control over time.11
The West of Scotland Coronary Prevention Study (WOSCOPS)
database provided an opportunity to study prospectively the effects of
pravastatin therapy on the risk of developing diabetes in subjects with
follow-up ranging from 3.5 to 6.1
years.6 We used the American
Diabetes Association (ADA) definition of diabetes mellitus (fasting
blood glucose level of 7.0
mmol/L)12 and were able to
study the major baseline predictors of the loss of glucose control in
this patient group. In addition, we examined whether pravastatin
influenced the subsequent development of diabetes
mellitus.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
|---|
Subjects
All study subjects were participants in WOSCOPS, and their characteristics have been summarized in detail elsewhere.6 13 Briefly, these subjects were all men aged 45 to 64 (mean age 55.2 years) with a mean baseline plasma total cholesterol level of 7.0 mmol/L (SD 0.6), LDL cholesterol level of 5.0 mmol/L (SD 0.4), HDL cholesterol level of 1.1 mmol/L (SD 0.3), and triglyceride level of 1.9 mmol/L (SD 0.8). They also had normal renal and hepatic function with no history of myocardial infarction or organ transplantation. With the exception of plasma cholesterol levels and the absence of a history of myocardial infarction, unstable angina, or coronary revascularization, the study recruits had a similar risk factor profile and demographic distribution as the group of 81 000 screenees from which they were selected.13
Laboratory Methods
Glucose was measured according to an automated
enzymatic method, and plasma lipids and lipoproteins were measured
according to the protocols of the Lipid Research
Clinics.14 Blood counts,
including white blood cell count (WBC), were performed with a Coulter
STKR or S+1 automated cell counter.
Definition of Diabetes
Fasting venous blood glucose measurements were
performed at baseline and at 6-month intervals throughout WOSCOPS. We
used the ADA definition of diabetes mellitus, which requires a fasting
blood glucose level of 7.0 mmol/L. Two important additional criteria
were imposed. Although all glucose measurements were intended to be
performed on fasting samples in WOSCOPS, inevitably in such a large
group during 5 years, some patients may have failed to fast. Because a
single, nonfasting glucose measurement may result in the
misclassification of a subject as diabetic, a minimum of 2 glucose
measurements of 7.0 mmol/L were required. In addition, because we
were primarily interested in examining subjects who experienced
significant deterioration in their glucose control, a further restraint
was incorporated into the definition, whereby one glucose measurement
must be 2.0 mmol/L above baseline. The value of 2.0 mmol/L was chosen
to represent an average increment from a normal glucose of 
5.0
mmol/L to a diabetic value of 7.0 mmol/L.
Inevitably, this strategy restricted the number of subjects classified as newly diabetic but increased our level of confidence that the subjects labeled in this study as newly diabetic were truly thus. In addition, individuals who had been newly prescribed hypoglycemic agents (oral hypoglycemic agents or insulin) during the study were accepted as having become diabetic.
Importantly, because this analysis was designed to examine
the development of new diabetes, subjects who were self-reported
diabetics at baseline (76 subjects) or had baseline glucose level of
7.0 mmol/L (an additional 72 subjects) were excluded. In addition,
473 subjects with insufficient on-treatment glucose measurements to
allow classification of diabetes according to the above definitions
were excluded.
Statistical Methods
Data are summarized as mean (SD) for continuous
variables and number of subjects (percent) for categorical variables.
Cox proportional hazards models were fitted to identify predictors of
transition to diabetes, both univariately and
multivariately.15 Subjects’
time to becoming glucose intolerant was taken as the 6-month visit at
which they first had 2 postrandomization glucose measurements of
7.0 mmol/L and 1 postrandomization glucose measurement of >2.0
mmol/L above the baseline glucose level or as the postrandomization
visit at which they first indicated taking hypoglycemic drugs. Due to
nonattendance at visits or end of study (with varying length of
follow-up), subjects’ time to becoming glucose intolerant was censored
at the last 6-monthly visit at which their glucose level was measured.
Lifestyle, lipids, and other coronary heart disease risk factors at
baseline were considered. The multivariate model contained all of the
covariates, regardless of statistical significance, to allow the effect
of each covariate in the presence of all other, possibly confounding,
covariates to be assessed. Glucose was modeled after transformation
into quintiles, and plasma triglyceride and WBC were log
transformed.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
|---|
Study Subjects
The WOSCOPS cohort consisted of 6595 men, of whom 5974 had
2 postrandomization blood glucose measurements and were neither
self-reported diabetics nor had elevated fasting blood glucose levels
(7.0 mmol/L) at baseline
(Table 1
). With the definition of diabetes outlined
in Methods, 139 of the 5974 subjects included were classified as having
a transition from normal glucose control to overt diabetes mellitus
during the study.
|
Univariate Predictors of Diabetes
As shown in
Table 2, body mass index (BMI), HDL cholesterol, log
triglyceride, total cholesterol, log WBC, baseline glucose, and
systolic blood pressure were all univariate predictors of the
development of diabetes. Age, alcohol intake, and smoking status were
not significant predictors of development of diabetes. Interestingly,
pravastatin treatment itself significantly influenced development of
diabetes (hazard ratio 0.70, 95% CI 0.50 to 0.98;
P=0.036).
|
When baseline blood glucose levels were divided into 5
quintiles as shown in
Table 2
, highly significant differences in the risk of
developing diabetes mellitus were observed among these. As might be
expected, baseline glucose is a strong predictor of developing new
diabetes with levels in the top quintile (>5.0 mmol/L) conferring a
13-fold greater risk than the bottom quintile in the univariate
analysis and an almost 10-fold greater risk in the multivariate
analyses.
Kaplan-Meier plots of the development of diabetes according
to median baseline glucose, BMI, log triglyceride, and treatment
assignment are shown in the
Figure.
|
Multivariate Predictors of Diabetes
In the multivariate Cox model, baseline BMI, log
triglyceride, and baseline glucose remained significant predictors, but
systolic blood pressure and log WBC were no longer statistically
significant
(Table 2). Pravastatin therapy also remained a significant
predictor with a multivariate hazard ratio of 0.70 (95% CI 0.50 to
0.99,
P=0.042).
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
|---|
The principal findings of this study are that with a definition based on serial fasting glucose measurements and the ADA criteria, we were able to confirm well-recognized predictors of loss of glucose control such as BMI and plasma triglyceride level. In addition to establishing these variables as independent predictors, we identified for the first time a clinically important association between pravastatin therapy and a reduced risk of developing diabetes. It should be noted that these analyses were not predefined as part of WOSCOPS and as such should be interpreted cautiously. Nevertheless, they raise important new clinical possibilities, which should now be explored in further studies.
The definition of diabetes mellitus according to the ADA
requires a fasting blood glucose of 7.0 mmol/L. We have used this
cutoff to define diabetes, but to avoid the mislabeling of patients as
diabetic on the basis of single nonfasting samples, we used more
rigorous additional criteria by requiring two blood glucose levels of
7.0 mmol/L and one level of 2.0 mmol/L than baseline. The finding
that BMI and plasma triglyceride, both well-recognized risk factors for
insulin resistance and glucose
intolerance,5 were strong
independent predictors of the loss of glucose control in this group is
reassuring.
In our multivariate analysis, baseline WBC failed to reach
statistical significance
(P=0.063) as a predictor of the
loss of glucose control. The importance of baseline WBC as a predictor
of the loss of glucose control has, however, been established by
others4 and potentially lies
in its association with low-grade chronic inflammation. Only very
recently has it been appreciated that inflammatory markers linked with
insulin resistance associate with the development of diabetes in
adults.4 16 The
mechanism by which inflammation leads to glucose intolerance and
ultimately diabetes is unknown, but proinflammatory cytokines, such as
tumor necrosis factor (TNF)-
, and leptin may produce insulin
resistance by influencing the function of the insulin
receptor17 18 or
impairing insulin action and inhibiting insulin
secretion.19
Previous investigations into the effects of pravastatin on glucose tolerance have been equivocal. Most studies have been performed in small groups for a short duration and have yielded inconclusive results.20 21 In the present study, the benefits associated with pravastatin therapy are long term, and it should be noted that the subjects studied in WOSCOPS, on average, had normal triglyceride levels at baseline. The beneficial effects of pravastatin on glucose-intolerant subjects have been shown in a subgroup analysis of the CARE trial,11 in which significant reductions were observed in cardiovascular risk. The mechanism by which pravastatin may reduce a subject’s risk of developing diabetes mellitus is not clear from these analyses. One possibility that cannot be discounted with the present analysis is the impact of pravastatin on vascular events that lead to a secondary reduction in the need for the use of cardiovascular drugs that influence glucose control, such as thiazide diuretics and ß-blockers. The WOSCOPS database has information on concomitant medication but has insufficient resolution with respect to specific drugs to answer this question. Drug use at baseline was virtually identical between the placebo and pravastatin groups, and it may be argued that active treatment would actually increase the use of drugs such as thiazides and ß-blockers by reducing the fatal event rate in the study.
We may, however, speculate that three known effects of pravastatin therapy may play a primary role, either individually or in concert in the development of diabetes.
First, the triglyceride-lowering effect of pravastatin therapy may be important over the long term in reducing the risk of the development of insulin resistance. It has been known for many years that elevated triglyceride levels are associated with the development of diabetes.5 In WOSCOPS, pravastatin therapy reduced triglycerides by an average of 12%.6 Interestingly, when the on-treatment triglyceride values were put into the stepwise multivariate model, pravastatin therapy was no longer a statistically significant, independent predictor (data not shown). This, however, cannot be interpreted as necessarily explaining the pravastatin effect. On-treatment triglyceride levels, calculated as the average of the 6- and 12-month postrandomization values, are not independent of pravastatin therapy. Indeed, as stated earlier, pravastatin significantly decreases the plasma triglyceride level. The data are therefore compatible with a treatment effect mediated through a change in plasma triglyceride levels but are not necessarily explained by this. It should also be noted that other lipid-lowering drugs, such as fibric acid derivatives, which have a greater lowering effect on plasma triglyceride than do statins, do not appear to improve insulin resistance.22 This would suggest that triglyceride lowering per se does not explain the observed effect.
Second, the anti-inflammatory effects of pravastatin may be
key. Pravastatin has been shown to reduce circulating levels of the
cytokines interleukin-6 and
TNF-.23 TNF- and
interleukin-6 are known to inhibit lipoprotein lipase
activity24 and to stimulate
lipolysis in adipose
tissue.25 Indeed, it has
been postulated that these cytokines, derived in part from adipose
tissue, may be possibly responsible for the metabolic syndrome
associated with insulin
resistance.16 The
anti-inflammatory properties of pravastatin may therefore interrupt the
natural progression from central obesity to insulin resistance mediated
by the adipose tissue–derived cytokines.
Finally, another effect of pravastatin that has been consistently demonstrated is the effect on endothelial function.9 26 27 This may be explained in part by the lipid-lowering effects of this statin, as dyslipidemia is known to impair endothelium-mediated vasodilatation.28 Impaired endothelial function has recently been shown to result in diminished capillary recruitment and in turn to correlate with the degree of insulin resistance.29 By restoring endothelial function, pravastatin may significantly influence selective tissue perfusion and thereby beneficially affect glucose and insulin transport.
These 3 mechanisms may all be operative, and together they may explain this important new finding that pravastatin therapy may reduce the propensity of subjects within WOSCOPS to develop diabetes. However, there may be other direct or indirect effects of pravastatin therapy on glucose control that have yet to be unraveled. Regardless of the mechanism or mechanisms, the prevention or delay of the onset of diabetes may contribute significantly to the observed cardiovascular benefits of pravastatin therapy.
These findings are generated from a post hoc analysis of WOSCOPS. As such, we must emphasize that our results should be treated as hypothesis generating and should now be confirmed in a prospective manner in other statin trials, such as the ongoing Prospective Study of Pravastatin in the Elderly at Risk (PROSPER).30
|
Appendix 1 |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
|---|
WOSCOPS Group
Executive Committee
James Shepherd (chairman), Stuart M. Cobbe, A. Ross Lorimer, James H. McKillop, Ian Ford, Christopher J. Packard, Peter W. Macfarlane, Christopher Isles.
Data and Safety Monitoring Committee
Michael F. Oliver (chairman), Anthony F. Lever, Byron
W. Brown, John G.G. Ledingham, Stuart J. Pocock, Basil M.
Rifkind.
Cardiovascular End-Points Committee
Stuart M. Cobbe (chairman), Barry D. Vallance, Peter
W. Macfarlane.
Adverse Events Review Board
A. Ross Lorimer, James H. McKillop, David
Ballantyne.
Data Center Staff
Liz Anderson, David Duncan, Sharon Kean, Audrey
Lawrence, June McGrath, Vivette Montgomery, John
Norrie.
Population Screening
Melvyn Percy.
Clinical Coordination, Monitoring, and
Administration
Elspeth Pomphrey, Andrew Whitehouse, Patricia
Cameron, Pamela Parker, Fiona Porteous, Leslie Fletcher, Christine
Kilday.
Computerized ECG Analysis
David Shoat (deceased), Shahid Latif, Julie
Kennedy.
Laboratory Operations
M. Anne Bell, Robert Birrell.
Company Liaison and General Support
Margot Mellies, Joseph Meyer, Wendy
Campbell.
|
Acknowledgments |
|---|
We gratefully acknowledge the financial support of an educational grant from Bristol-Myers Squibb Co. Research. In addition, we acknowledge financial support from the Scottish Home and Health Department (grant K/MRS/50/C2310), the Medical Research Funds Committee of the University of Glasgow, and the British Hyperlipidaemia Association Research Awards.
|
Footnotes |
|---|
Drs Shepherd, Packard, Cobbe, Gaw, Ford, and Macfarlane have received grants from Bristol-Myers Squibb, as well as other organizations, and serve as ad hoc consultants to Bristol-Myers Squibb and other entities. Dr Isles serves as an ad hoc consultant to Bristol-Myers Squibb and various other organizations.
Received May 25, 2000; revision received August 3, 2000; accepted August 8, 2000.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
|---|
1. Wilson PW, McGee DL, Kannel WB. Obesity, very low density lipoproteins, and glucose intolerance over fourteen years: the Framingham Study. Am J Epidemiol. 1981;114:697–704.
2. Kadowaki T, Miyake Y, Hagura R, et al. Risk factors for worsening to diabetes in subjects with impaired glucose tolerance. Diabetologia. 1984;26:44–49.[Medline] [Order article via Infotrieve]
3.
Meigs JB, Nathan
DM, Wilson PWF, et al. Metabolic risk factors worsen continuously
across the spectrum of nondiabetic glucose tolerance.
Ann Intern Med. 1998;128:524–533.
4. Schmidt MI, Duncan BB, Sharrett AR, et al. Markers of inflammation and prediction of diabetes mellitus in adults (Atherosclerosis Risk in Communities study): a cohort study. Lancet. 1999;353:1649–1652.[Medline] [Order article via Infotrieve]
5.
Haffner SM, Stern
MP, Hazuda HP, et al. Cardiovascular risk factors in confirmed
prediabetic individuals: does the clock for coronary disease start
ticking before the onset of clinical diabetes?
JAMA. 1990;263:2893–2898.
6.
Shepherd J, Cobbe
SM, Ford I, et al. Prevention of coronary heart disease with
pravastatin in men with hypercholesterolemia.
N Engl J Med. 1995;333:1301–1307.
7.
Sacks FM, Pfeffer
MA, Moye LA, et al. The effect of pravastatin on coronary events after
myocardial infarction in patients with average cholesterol levels.
N Engl J Med. 1996;335:1001–1009.
8.
LIPID Study Group.
Prevention of cardiovascular events and death with pravastatin in
patients with coronary heart disease and a broad range of cholesterol
levels. N Engl J Med. 1998;339:1349–1357.
9.
Egashira K, Hirooka
Y, Kai H, et al. Reduction in serum cholesterol with pravastatin
improves endothelium-dependent coronary vasomotion in patients with
hypercholesterolemia.
Circulation. 1994;89:2519–2524.
10.
Kobashigawa J,
Katznelson S, Laks H, et al. Effect of pravastatin on outcomes after
cardiac transplantation. N Engl
J Med. 1995;333:621–627.
11.
Goldberg RB,
Mellies MJ, Sacks FM, et al. Cardiovascular events and their reduction
with pravastatin in diabetic and glucose-intolerant myocardial
infarction survivors with average cholesterol levels. Subgroup analyses
in the Cholesterol and Recurrent Events (CARE) trial.
Circulation. 1998;98:2513–2519.
12. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care. 1997;20;1183–1197.
13. WOSCOPS Study Group. Screening experience and baseline characteristics in the West of Scotland Study. Am J Cardiol. 1995;76:485–491.[Medline] [Order article via Infotrieve]
14. Lipid Research Clinics Program. Lipid and Lipoprotein Analysis. Manual of Laboratory Operations. Vol 1. Bethesda, Md: National Institutes of Health, Department of Health, Education, and Welfare; 1974: publication No. 75-628.
15. Collett D. Modelling Survival Data in Medical Research. London, UK: Chapman and Hall; 1994.
16.
Yudkin JS,
Stehouwer CDA, Emeis JJ, et al. C-reactive protein in healthy subjects:
associations with obesity, insulin resistance, and endothelial
dysfunction. Arterioscler Thromb Vasc
Biol. 1999;19:972–978.
17.
Uysal KT,
Wiesbrock SM, Marino MW, et al. Protection from obesity-induced insulin
resistance in mice lacking TNF- function.
Nature. 1997;389:610–614.[Medline]
[Order article via Infotrieve]
18. Hotamisligil GS, Peraldi P, Budavari A, et al. IRS-1 mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity- induced insulin resistance. Science. 1996;271:665–668.[Abstract]
19. Girard J. Is leptin the link between obesity and insulin resistance? Diabetes Metab. 1997;23(suppl 3):16–24.
20. Sheu WHH, Shieh SM, Shen DDC, et al. Effect of pravastatin treatment on glucose, insulin, and lipoprotein metabolism in patients with hypercholesterolemia. Am Heart J. 1994;127:331–336.[Medline] [Order article via Infotrieve]
21. Baba T, Kodama T, Yajima Y, et al. Effects of pravastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, on glucose tolerance in patients with essential hypertension. Diabetes Care. 1993;16:402–404.
22. Sane T, Knudsen P, Vuorinen-Markkola H, et al. Decreasing triglyceride by gemfibrozil therapy does not affect the glucoregulatory or antilipolytic effect of insulin in non-diabetic subjects with mild hypertriglyceridemia. Metabolism. 1995;44:589–596.[Medline] [Order article via Infotrieve]
23. Rosenson RS, Tangney CC, Casey LC. Inhibition of proinflammatory cytokine production by pravastatin. Lancet. 1999;353:983–984.[Medline] [Order article via Infotrieve]
24. Kawakami M, Pekala PH, Lane MD, et al. Lipoprotein lipase suppression in 3T3-L1 cells by an endotoxin-induced mediator from exudate cells. Proc Natl Acad Sci U S A. 1982;82:912–916.
25. Hardardóttir I, Grünfeld C, Feingold KR. Effects of endotoxins and cytokines on lipid metabolism. Curr Opin Lipidol. 1994;5:207–215.[Medline] [Order article via Infotrieve]
26. Muramatsu J, Kobayashi A, Hasegawa N, et al. Hemodynamic changes associated with reduction in total cholesterol by treatment with the HMG-CoA reductase inhibitor pravastatin. Atherosclerosis. 1997;130:179–182.[Medline] [Order article via Infotrieve]
27.
Williams JK,
Sukhova GK, Herrington DM, et al. Pravastatin has cholesterol-lowering
independent effects on the artery wall of atherosclerotic monkeys.
J Am Coll Cardiol. 1998;31:684–691.
28. Leung WH, Lau CP, Wong CK. Beneficial effect of cholesterol lowering therapy on coronary endothelium-dependent relaxation in hypercholesterolaemic patients. Lancet. 1993;341:1496–1500.[Medline] [Order article via Infotrieve]
29.
Serné EH,
Stehouwer CDA, ter Maaten JC, et al. Microvascular function relates to
insulin sensitivity and blood pressure in normal subjects.
Circulation. 1999;99:896–902.
30. Shepherd J, Blauw GJ, Murphy MB, et al. The design of a prospective study of pravastatin in the elderly at risk (PROSPER). Am J Cardiol. 1999;84:1192–1197. [Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  D. S. Grimes History of the cholesterol hypothesis in Britain QJM, June 1, 2009; 102(6): 436 - 438. [Full Text] [PDF]
|
|
|
|
 |
|
 N. Nacasch and Z. Korzets Worsening of hyperglycemia due to atorvastatin in a renal transplant patient NDT Plus, May 18, 2009; (2009) sfp058v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. M Ridker The JUPITER Trial: Results, Controversies, and Implications for Prevention Circ Cardiovasc Qual Outcomes, May 1, 2009; 2(3): 279 - 285. [Full Text] [PDF]
|
|
|
|
 |
|
 B. G. Drew, S. J. Duffy, M. F. Formosa, A. K. Natoli, D. C. Henstridge, S. A. Penfold, W. G. Thomas, N. Mukhamedova, B. de Courten, J. M. Forbes, et al. High-Density Lipoprotein Modulates Glucose Metabolism in Patients With Type 2 Diabetes Mellitus Circulation, April 21, 2009; 119(15): 2103 - 2111. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. T Nurmohamed and B. A C Dijkmans Dyslipidaemia, statins and rheumatoid arthritis Ann Rheum Dis, April 1, 2009; 68(4): 453 - 455. [Full Text] [PDF]
|
|
|
|
 |
|
 F. J. Al Badarin, I. J. Kullo, S. L. Kopecky, and R. J. Thomas Impact of Ezetimibe on Atherosclerosis: Is the Jury Still Out? Mayo Clin. Proc., April 1, 2009; 84(4): 353 - 361. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S S Jick, H Choi, L Li, I B McInnes, and N Sattar Hyperlipidaemia, statin use and the risk of developing rheumatoid arthritis Ann Rheum Dis, April 1, 2009; 68(4): 546 - 551. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Szendroedi, C. Anderwald, M. Krssak, M. Bayerle-Eder, H. Esterbauer, G. Pfeiler, A. Brehm, P. Nowotny, A. Hofer, W. Waldhausl, et al. Effects of High-Dose Simvastatin Therapy on Glucose Metabolism and Ectopic Lipid Deposition in Nonobese Type 2 Diabetic Patients Diabetes Care, February 1, 2009; 32(2): 209 - 214. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Sathyapalan, E. S. Kilpatrick, A.-M. Coady, and S. L. Atkin The Effect of Atorvastatin in Patients with Polycystic Ovary Syndrome: A Randomized Double-Blind Placebo-Controlled Study J. Clin. Endocrinol. Metab., January 1, 2009; 94(1): 103 - 108. [Abstract] [Full Text] [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]
|
|
|
|
 |
|
 C. Cramer, M. N. Haan, S. Galea, K. M. Langa, and J. D. Kalbfleisch Use of statins and incidence of dementia and cognitive impairment without dementia in a cohort study Neurology, July 29, 2008; 71(5): 344 - 350. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Abe, M. Matsuda, H. Kobayashi, Y. Miyata, Y. Nakayama, R. Komuro, A. Fukuhara, and I. Shimomura Effects of Statins on Adipose Tissue Inflammation: Their Inhibitory Effect on MyD88-Independent IRF3/IFN-{beta} Pathway in Macrophages Arterioscler. Thromb. Vasc. Biol., May 1, 2008; 28(5): 871 - 877. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. M. Witteles and M. B. Fowler Insulin-Resistant Cardiomyopathy: Clinical Evidence, Mechanisms, and Treatment Options J. Am. Coll. Cardiol., January 15, 2008; 51(2): 93 - 102. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. W. McEvoy, R. Margey, G. J. Blake, M. Tsubokura, M. Kami, A. P. DeFilippis, S. Bansal, R. S. Blumenthal, I. Ford, H. Murray, et al. Long-Term Follow-up of the West of Scotland Coronary Prevention Study N. Engl. J. Med., January 10, 2008; 358(2): 193 - 195. [Full Text] [PDF]
|
|
|
|
 |
|
 D. Preiss and N. Sattar Metabolic syndrome, dysglycaemia and vascular disease: making sense of the evidence Heart, December 1, 2007; 93(12): 1493 - 1496. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Schindler Review: The metabolic syndrome as an endocrine disease: is there an effective pharmacotherapeutic strategy optimally targeting the pathogenesis? Therapeutic Advances in Cardiovascular Disease, October 1, 2007; 1(1): 7 - 26. [Abstract] [PDF]
|
|
|
|
 |
|
 M. Hao, W. S. Head, S. C. Gunawardana, A. H. Hasty, and D. W. Piston Direct Effect of Cholesterol on Insulin Secretion: A Novel Mechanism for Pancreatic {beta}-Cell Dysfunction Diabetes, September 1, 2007; 56(9): 2328 - 2338. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Ashrafian, M. P. Frenneaux, and L. H. Opie Metabolic Mechanisms in Heart Failure Circulation, July 24, 2007; 116(4): 434 - 448. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. I. Frisard, A. Broussard, S. S. Davies, L. J. Roberts II, J. Rood, L. d. Jonge, X. Fang, S. M. Jazwinski, W. A. Deutsch, E. Ravussin, et al. Aging, Resting Metabolic Rate, and Oxidative Damage: Results From the Louisiana Healthy Aging Study J. Gerontol. A Biol. Sci. Med. Sci., July 1, 2007; 62(7): 752 - 759. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Sattar The metabolic syndrome: setting the scene. The cons Diabetes and Vascular Disease Research, June 1, 2007; 4(2_suppl): S4 - S6. [Abstract] [PDF]
|
|
|
|
 |
|
 M. Yano, T. Matsumura, T. Senokuchi, N. Ishii, Y. Murata, K. Taketa, H. Motoshima, T. Taguchi, K. Sonoda, D. Kukidome, et al. Statins Activate Peroxisome Proliferator-Activated Receptor {gamma} Through Extracellular Signal-Regulated Kinase 1/2 and p38 Mitogen-Activated Protein Kinase-Dependent Cyclooxygenase-2 Expression in Macrophages Circ. Res., May 25, 2007; 100(10): 1442 - 1451. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. J. Dzau, E. M. Antman, H. R. Black, D. L. Hayes, J. E. Manson, J. Plutzky, J. J. Popma, and W. Stevenson The Cardiovascular Disease Continuum Validated: Clinical Evidence of Improved Patient Outcomes: Part I: Pathophysiology and Clinical Trial Evidence (Risk Factors Through Stable Coronary Artery Disease) Circulation, December 19, 2006; 114(25): 2850 - 2870. [Full Text] [PDF]
|
|
|
|
 |
|
 J. I. Barzilay, B. R. Davis, J. A. Cutler, S. L. Pressel, P. K. Whelton, J. Basile, K. L. Margolis, S. T. Ong, L. S. Sadler, J. Summerson, et al. Fasting Glucose Levels and Incident Diabetes Mellitus in Older Nondiabetic Adults Randomized to Receive 3 Different Classes of Antihypertensive Treatment: A Report From the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). Arch Intern Med, November 13, 2006; 166(20): 2191 - 2201. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Umeji, S. Umemoto, S. Itoh, M. Tanaka, S. Kawahara, T. Fukai, and M. Matsuzaki Comparative effects of pitavastatin and probucol on oxidative stress, Cu/Zn superoxide dismutase, PPAR-{gamma}, and aortic stiffness in hypercholesterolemia Am J Physiol Heart Circ Physiol, November 1, 2006; 291(5): H2522 - H2532. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Costa, M. Borges, C. David, and A. Vaz Carneiro Efficacy of lipid lowering drug treatment for diabetic and non-diabetic patients: meta-analysis of randomised controlled trials BMJ, May 13, 2006; 332(7550): 1115 - 1124. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. B. Meigs, C. J. O'Donnell, G. H. Tofler, E. J. Benjamin, C. S. Fox, I. Lipinska, D. M. Nathan, L. M. Sullivan, R. B. D'Agostino, and P. W.F. Wilson Hemostatic Markers of Endothelial Dysfunction and Risk of Incident Type 2 Diabetes: The Framingham Offspring Study Diabetes, February 1, 2006; 55(2): 530 - 537. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. E. Hansen, J. P. Hildebrand, E. E. Ferguson, and J. H. Stein Outcomes in 45 Patients With Statin-Associated Myopathy Arch Intern Med, December 12, 2005; 165(22): 2671 - 2676. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Kawai, M. Tokui, O. Funae, S. Meguro, S. Yamada, M. Tabata, and A. Shimada Efficacy of Pitavastatin, a New HMG-CoA Reductase Inhibitor, on Lipid and Glucose Metabolism in Patients With Type 2 Diabetes Diabetes Care, December 1, 2005; 28(12): 2980 - 2981. [Full Text] [PDF]
|
|
|
|
|
|
J. G. Robinson, B. Smith, N. Maheshwari, and H. Schrott Pleiotropic Effects of Statins: Benefit Beyond Cholesterol Reduction?: A Meta-Regression Analysis J. Am. Coll. Cardiol., November 15, 2005; 46(10): 1855 - 1862. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Tenenbaum, M. Motro, E. Z. Fisman, Y. Adler, J. Shemesh, D. Tanne, J. Leor, V. Boyko, E. Schwammenthal, and S. Behar Effect of bezafibrate on incidence of type 2 diabetes mellitus in obese patients Eur. Heart J., October 1, 2005; 26(19): 2032 - 2038. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. J. Milionis, I. F. Gazi, T. D. Filippatos, V. Tzovaras, G. Chasiotis, J. Goudevenos, K. Seferiadis, and M. S. Elisaf Starting with Rosuvastatin in Primary Hyperlipidemia--: Is There More Than Lipid Lowering? Angiology, September 1, 2005; 56(5): 585 - 592. [Abstract] [PDF]
|
|
|
|
|
|
P. A. Tataranni and E. Ortega A Burning Question: Does an Adipokine-Induced Activation of the Immune System Mediate the Effect of Overnutrition on Type 2 Diabetes? Diabetes, April 1, 2005; 54(4): 917 - 927. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Rossi, E. Cioni, A. Nuzzo, G. Origliani, and M. G. Modena Endothelial-Dependent Vasodilation and Incidence of Type 2 Diabetes in a Population of Healthy Postmenopausal Women Diabetes Care, March 1, 2005; 28(3): 702 - 707. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Padwal, S. R. Majumdar, J. A. Johnson, J. Varney, and F. A. McAlister A Systematic Review of Drug Therapy to Delay or Prevent Type 2 Diabetes Diabetes Care, March 1, 2005; 28(3): 736 - 744. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Curtis and C. Wilson Preventing Type 2 Diabetes Mellitus J Am Board Fam Med, January 1, 2005; 18(1): 37 - 43. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. S. Daskalopoulou, D. P. Mikhailidis, and M. Elisaf Prevention and Treatment of the Metabolic Syndrome Angiology, November 1, 2004; 55(6): 589 - 612. [Abstract] [PDF]
|
|
|
|
|
|
N. Sattar, O. Scherbakova, I. Ford, D. St. J. O'Reilly, A. Stanley, E. Forrest, P. W. MacFarlane, C. J. Packard, S. M. Cobbe, and J. Shepherd Elevated Alanine Aminotransferase Predicts New-Onset Type 2 Diabetes Independently of Classical Risk Factors, Metabolic Syndrome, and C-Reactive Protein in the West of Scotland Coronary Prevention Study Diabetes, November 1, 2004; 53(11): 2855 - 2860. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. S. Skyler Effects of Glycemic Control on Diabetes Complications and on the Prevention of Diabetes Clin. Diabetes, October 1, 2004; 22(4): 162 - 166. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. K. Shetty, P. A. Economides, E. S. Horton, C. S. Mantzoros, and A. Veves Circulating Adiponectin and Resistin Levels in Relation to Metabolic Factors, Inflammatory Markers, and Vascular Reactivity in Diabetic Patients and Subjects at Risk for Diabetes Diabetes Care, October 1, 2004; 27(10): 2450 - 2457. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Yu, K. Ohmori, Y. Chen, C. Sato, H. Kiyomoto, K. Shinomiya, H. Takeuchi, K. Mizushige, and M. Kohno Effects of pravastatin on progression of glucose intolerance and cardiovascular remodeling in a type II diabetes model J. Am. Coll. Cardiol., August 18, 2004; 44(4): 904 - 913. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. M. Witteles, W. H. W. Tang, A. H. Jamali, J. W. Chu, G. M. Reaven, and M. B. Fowler Insulin resistance in idiopathic dilated cardiomyopathy: A possible etiologic link J. Am. Coll. Cardiol., July 7, 2004; 44(1): 78 - 81. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Janatuinen, J. Knuuti, J. O. Toikka, M. Ahotupa, P. Nuutila, T. Ronnemaa, and O. T. Raitakari Effect of Pravastatin on Low-Density Lipoprotein Oxidation and Myocardial Perfusion in Young Adults With Type 1 Diabetes Arterioscler. Thromb. Vasc. Biol., July 1, 2004; 24(7): 1303 - 1308. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Davignon Beneficial Cardiovascular Pleiotropic Effects of Statins Circulation, June 15, 2004; 109(23_suppl_1): III-39 - III-43. [Abstract] [Full Text]
|
|
|
|
|
|
I. Moussa, M. B. Leon, D. S. Baim, W. W. O'Neill, J. J. Popma, M. Buchbinder, J. Midwall, C. A. Simonton, E. Keim, P. Wang, et al. Impact of Sirolimus-Eluting Stents on Outcome in Diabetic Patients: A SIRIUS (SIRolImUS-coated Bx Velocity balloon-expandable stent in the treatment of patients with de novo coronary artery lesions) Substudy Circulation, May 18, 2004; 109(19): 2273 - 2278. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. G. Futterman and L. Lemberg STATIN PLEIOTROPY: FACT OR FICTION? Am. J. Crit. Care., May 1, 2004; 13(3): 244 - 249. [Full Text] [PDF]
|
|
|
|
|
|
A. Ceriello and E. Motz Is Oxidative Stress the Pathogenic Mechanism Underlying Insulin Resistance, Diabetes, and Cardiovascular Disease? The Common Soil Hypothesis Revisited Arterioscler. Thromb. Vasc. Biol., May 1, 2004; 24(5): 816 - 823. [Abstract] [Full Text]
|
|
|
|
 |
|
 J. B. Meigs, F. B. Hu, N. Rifai, and J. E. Manson Biomarkers of Endothelial Dysfunction and Risk of Type 2 Diabetes Mellitus JAMA, April 28, 2004; 291(16): 1978 - 1986. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Mohlig, H. Boeing, J. Spranger, M. Osterhoff, A. Kroke, E. Fisher, M. M. Bergmann, M. Ristow, K. Hoffmann, and A. F. H. Pfeiffer Body Mass Index and C-174G Interleukin-6 Promoter Polymorphism Interact in Predicting Type 2 Diabetes J. Clin. Endocrinol. Metab., April 1, 2004; 89(4): 1885 - 1890. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. J. Shrot, F. M. Sahebzamani, and H. J. Brownlee Jr. Case Study: Screening and Treatment of Pre-Diabetes in Primary Care Clin. Diabetes, April 1, 2004; 22(2): 98 - 100. [Full Text] [PDF]
|
|
|
|
 |
|
 L. M. Prisant Preventing Type II Diabetes Mellitus J. Clin. Pharmacol., April 1, 2004; 44(4): 406 - 413. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. C. Pickup Inflammation and Activated Innate Immunity in the Pathogenesis of Type 2 Diabetes Diabetes Care, March 1, 2004; 27(3): 813 - 823. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. B. Hu, J. B. Meigs, T. Y. Li, N. Rifai, and J. E. Manson Inflammatory Markers and Risk of Developing Type 2 Diabetes in Women Diabetes, March 1, 2004; 53(3): 693 - 700. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P L Sanchez, J L Morinigo, P Pabon, F Martin, I Piedra, I F Palacios, and C Martin-Luengo Prognostic relations between inflammatory markers and mortality in diabetic patients with non-ST elevation acute coronary syndrome Heart, March 1, 2004; 90(3): 264 - 269. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. K. Meier-Ewert, P. M. Ridker, N. Rifai, M. M. Regan, N. J. Price, D. F. Dinges, and J. M. Mullington Effect of sleep loss on C-Reactive protein, an inflammatory marker of cardiovascular risk J. Am. Coll. Cardiol., February 18, 2004; 43(4): 678 - 683. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. A. Golomb, M. H. Criqui, H. White, and J. E. Dimsdale Conceptual Foundations of the UCSD Statin Study: A Randomized Controlled Trial Assessing the Impact of Statins on Cognition, Behavior, and Biochemistry Arch Intern Med, January 26, 2004; 164(2): 153 - 162. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. C. Tong, K.-F. Lee, W.-Y. So, M. H. Ng, W.-B. Chan, M. K. Lo, N. N. Chan, and J. C. Chan White Blood Cell Count Is Associated With Macro- and Microvascular Complications in Chinese Patients With Type 2 Diabetes Diabetes Care, January 1, 2004; 27(1): 216 - 222. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. T. Hurst and R. W. Lee Increased Incidence of Coronary Atherosclerosis in Type 2 Diabetes Mellitus: Mechanisms and Management Ann Intern Med, November 18, 2003; 139(10): 824 - 834. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Gadsby Review: Diabetic dyslipidaemia -- the case for using statins The British Journal of Diabetes & Vascular Disease, November 1, 2003; 3(6): 402 - 407. [Abstract] [PDF]
|
|
|
|
|
|
J. Buse Statin Treatment in Diabetes Mellitus Clin. Diabetes, October 1, 2003; 21(4): 168 - 172. [Full Text] [PDF]
|
|
|
|
|
|
F. B. Hu and M. J. Stampfer Is Type 2 Diabetes Mellitus a Vascular Condition? Arterioscler. Thromb. Vasc. Biol., October 1, 2003; 23(10): 1715 - 1716. [Full Text] [PDF]
|
|
|
|
|
|
A. Keech, D. Colquhoun, J. Best, A. Kirby, R. J. Simes, D. Hunt, W. Hague, E. Beller, M. Arulchelvam, J. Baker, et al. Secondary Prevention of Cardiovascular Events With Long-Term Pravastatin in Patients With Diabetes or Impaired Fasting Glucose: Results from the LIPID trial Diabetes Care, October 1, 2003; 26(10): 2713 - 2721. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Z. T. Bloomgarden The Endocrine Society Meeting: Topics in Insulin Sensitivity and Hypertension Diabetes Care, September 1, 2003; 26(9): 2679 - 2688. [Full Text] [PDF]
|
|
|
|
|
|
J. B. Meigs, P. W.F. Wilson, D. M. Nathan, R. B. D'Agostino Sr., K. Williams, and S. M. Haffner Prevalence and Characteristics of the Metabolic Syndrome in the San Antonio Heart and Framingham Offspring Studies Diabetes, August 1, 2003; 52(8): 2160 - 2167. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Sattar, A. Gaw, O. Scherbakova, I. Ford, D. St.J. O'Reilly, S. M. Haffner, C. Isles, P. W. Macfarlane, C. J. Packard, S. M. Cobbe, et al. Metabolic Syndrome With and Without C-Reactive Protein as a Predictor of Coronary Heart Disease and Diabetes in the West of Scotland Coronary Prevention Study Circulation, July 29, 2003; 108(4): 414 - 419. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. E. Friday Aggressive Lipid Management for Cardiovascular Prevention: Evidence from Clinical Trials Experimental Biology and Medicine, July 1, 2003; 228(7): 769 - 778. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M. Fernandez-Real and W. Ricart Insulin Resistance and Chronic Cardiovascular Inflammatory Syndrome Endocr. Rev., June 1, 2003; 24(3): 278 - 301. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Rizos, E. Bairaktari, A. Kostoula, G. Hasiotis, A. Achimastos, E. Ganotakis, M. Elisaf, and D. P. Mikhailidis The Combination of Nebivolol plus Pravastatin is Associated with a More Beneficial Metabolic Profile Compared to that of Atenolol plus Pravastatin in Hypertensive Patients with Dyslipidemia: A Pilot Study Journal of Cardiovascular Pharmacology and Therapeutics, June 1, 2003; 8(2): 127 - 134. [Abstract] [PDF]
|
|
|
|
|
|
P. Dandona, A. Aljada, A. Chaudhuri, and A. Bandyopadhyay The Potential Influence of Inflammation and Insulin Resistance on the Pathogenesis and Treatment of Atherosclerosis-Related Complications in Type 2 Diabetes J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2422 - 2429. [Full Text] [PDF]
|
|
|
|
 |
|
 C. J. Lyon, R. E. Law, and W. A. Hsueh Minireview: Adiposity, Inflammation, and Atherogenesis Endocrinology, June 1, 2003; 144(6): 2195 - 2200. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M.-E. Roehrich, V. Mooser, V. Lenain, J. Herz, J. Nimpf, S. Azhar, M. Bideau, A. Capponi, P. Nicod, J.-A. Haefliger, et al. Insulin-secreting beta -Cell Dysfunction Induced by Human Lipoproteins J. Biol. Chem., May 9, 2003; 278(20): 18368 - 18375. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Durrington Clinical trials of lipid-lowering medication in diabetes The British Journal of Diabetes & Vascular Disease, May 1, 2003; 3(3): 217 - 220. [Abstract] [PDF]
|
|
|
|
 |
|
 G. Wolf and E. Ritz Diabetic Nephropathy in Type 2 Diabetes Prevention and Patient Management J. Am. Soc. Nephrol., May 1, 2003; 14(5): 1396 - 1405. [Full Text] [PDF]
|
|
|
|
|
|
G. G. L. Biondi-Zoccai, A. Abbate, G. Liuzzo, and L. M. Biasucci Atherothrombosis, inflammation, and diabetes J. Am. Coll. Cardiol., April 2, 2003; 41(7): 1071 - 1077. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. B. Marks The Daily Walk or the Daily Pill? Clin. Diabetes, April 1, 2003; 21(2): 51 - 52. [Full Text] [PDF]
|
|
|
|
|
|
S. E. Inzucchi and R. S. Sherwin Applying the Lessons of the DPP to Clinical Practice Clin. Diabetes, April 1, 2003; 21(2): 91 - 92. [Full Text] [PDF]
|
|
|
|
|
|
S. H. Golden, N.-Y. Wang, M. J. Klag, L. A. Meoni, and F. L. Brancati Blood Pressure in Young Adulthood and the Risk of Type 2 Diabetes in Middle Age Diabetes Care, April 1, 2003; 26(4): 1110 - 1115. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Z. T. Bloomgarden American Association of Clinical Endocrinologists (AACE) Consensus Conference on the Insulin Resistance Syndrome: 25-26 August 2002, Washington, DC Diabetes Care, April 1, 2003; 26(4): 1297 - 1303. [Full Text] [PDF]
|
|
|
|
|
|
R. S. Weinstock Treating Type 2 Diabetes Mellitus: A Growing Epidemic Mayo Clin. Proc., April 1, 2003; 78(4): 411 - 413. [PDF]
|
|
|
|
|
|
M. Wolf, L. Sandler, K. Hsu, K. Vossen-Smirnakis, J. L. Ecker, and R. Thadhani First-Trimester C-Reactive Protein and Subsequent Gestational Diabetes Diabetes Care, March 1, 2003; 26(3): 819 - 824. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. J. Blake and P. M. Ridker C-reactive protein and other inflammatory risk markers in acute coronary syndromes J. Am. Coll. Cardiol., February 19, 2003; 41(4_Suppl_S): 37S - 42S. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Z. T. Bloomgarden Pharmacologic Treatment of Type 2 Diabetes Diabetes Care, February 1, 2003; 26(2): 526 - 533. [Full Text] [PDF]
|
|
|
|
|
|
P. P. Simonen, H. Gylling, and T. A. Miettinen Diabetes and Cholesterol Metabolism: The succinate hypothesis Diabetes Care, February 1, 2003; 26(2): 550 - 550. [Full Text]
|
|
|
|
 |
|
 B. P. Leung, N. Sattar, A. Crilly, M. Prach, D. W. McCarey, H. Payne, R. Madhok, C. Campbell, J. A. Gracie, F. Y. Liew, et al. A Novel Anti-Inflammatory Role for Simvastatin in Inflammatory Arthritis J. Immunol., February 1, 2003; 170(3): 1524 - 1530. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Freemark Pharmacologic Approaches to the Prevention of Type 2 Diabetes in High Risk Pediatric Patients J. Clin. Endocrinol. Metab., January 1, 2003; 88(1): 3 - 13. [Full Text] [PDF]
|
|
|
|
|
|
N. Sattar, C. G Perry, and J. R Petrie Type 2 diabetes as an inflammatory disorder The British Journal of Diabetes & Vascular Disease, January 1, 2003; 3(1): 36 - 41. [Abstract] [PDF]
|
|
|
|
|
|
R. A Defronzo Impaired glucose tolerance: do pharmacological therapies correct the underlying metabolic disturbance? The British Journal of Diabetes & Vascular Disease, January 1, 2003; 3(1_suppl): S24 - S40. [Abstract] [PDF]
|
|
|
|
|
|
T. S. Han, N. Sattar, K. Williams, C. Gonzalez-Villalpando, M. E.J. Lean, and S. M. Haffner Prospective Study of C-Reactive Protein in Relation to the Development of Diabetes and Metabolic Syndrome in the Mexico City Diabetes Study Diabetes Care, November 1, 2002; 25(11): 2016 - 2021. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. K. Plenge, T. L. Hernandez, K. M. Weil, P. Poirier, G. K. Grunwald, S. M. Marcovina, and R. H. Eckel Simvastatin Lowers C-Reactive Protein Within 14 Days: An Effect Independent of Low-Density Lipoprotein Cholesterol Reduction Circulation, September 17, 2002; 106(12): 1447 - 1452. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. J Krentz Type 2 diabetes and atherosclerotic cardiovascular disease: do they share common antecedents? The British Journal of Diabetes & Vascular Disease, September 1, 2002; 2(5): 370 - 378. [Abstract] [PDF]
|
|
|
|
|
|
C. Mcdougall and M. Fisher Prevention of diabetes in cardiovascular studies: implications for the aetiology of type 2 diabetes The British Journal of Diabetes & Vascular Disease, September 1, 2002; 2(5): 384 - 389. [Abstract] [PDF]
|
|
|
|
|
|
S. M. Haffner, A. S. Greenberg, W. M. Weston, H. Chen, K. Williams, and M. I. Freed Effect of Rosiglitazone Treatment on Nontraditional Markers of Cardiovascular Disease in Patients With Type 2 Diabetes Mellitus Circulation, August 6, 2002; 106(6): 679 - 684. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. C. Chan, G. F. Watts, P. H. R. Barrett, L. J. Beilin, T. G. Redgrave, and T. A. Mori Regulatory Effects of HMG CoA Reductase Inhibitor and Fish Oils on Apolipoprotein B-100 Kinetics in Insulin-Resistant Obese Male Subjects With Dyslipidemia Diabetes, August 1, 2002; 51(8): 2377 - 2386. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.A. Paniagua, J. Lopez-Miranda, A. Escribano, F.J. Berral, C. Marin, D. Bravo, E. Paz-Rojas, P. Gomez, M. Barcos, J.A. Moreno, et al. Cerivastatin Improves Insulin Sensitivity and Insulin Secretion in Early-State Obese Type 2 Diabetes Diabetes, August 1, 2002; 51(8): 2596 - 2603. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A.D. Pradhan and P.M. Ridker Do atherosclerosis and type 2 diabetes share a common inflammatory basis? Eur. Heart J., June 1, 2002; 23(11): 831 - 834. [Full Text] [PDF]
|
|
|
|
 |
|
 D. C. Chan, G. F. Watts, P. H. R. Barrett, L. J. Beilin, and T. A. Mori Effect of Atorvastatin and Fish Oil on Plasma High-Sensitivity C-Reactive Protein Concentrations in Individuals with Visceral Obesity Clin. Chem., June 1, 2002; 48(6): 877 - 883. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. J. Freeman, J. Norrie, M. J. Caslake, A. Gaw, I. Ford, G. D.O. Lowe, D. St. J. O'Reilly, C. J. Packard, and N. Sattar C-Reactive Protein Is an Independent Predictor of Risk for the Development of Diabetes in the West of Scotland Coronary Prevention Study Diabetes, May 1, 2002; 51(5): 1596 - 1600. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||