(Circulation. 2000;102:42.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Chronic Subclinical Inflammation as Part of the Insulin Resistance Syndrome
The Insulin Resistance Atherosclerosis Study (IRAS)
From the Department of Medicine, Division of Clinical Epidemiology, University of Texas Health Science Center at San Antonio (A.F., L.M., S.M.H.); Department of Public Health Sciences, Wake Forest University School of Medicine, Winston Salem, NC (R.D’A., G.H.); and Laboratory for Clinical Biochemistry Research, Department of Pathology, University of Vermont College of Medicine, Burlington (R.P.T.).
Correspondence to Andreas Festa, MD, University of Texas Health Science Center at San Antonio, Mail Code 7873, 7703 Floyd Curl Dr, San Antonio, TX 78228-3900. E-mail festa{at}magnet.at
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Abstract |
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Background—Inflammation has been suggested as a risk factor for the development of atherosclerosis. Recently, some components of the insulin resistance syndrome (IRS) have been related to inflammatory markers. We hypothesized that insulin insensitivity, as directly measured, may be associated with inflammation in nondiabetic subjects.
Methods and Results—We studied the relation of C-reactive protein (CRP), fibrinogen, and white cell count to components of IRS in the nondiabetic population of the Insulin Resistance Atherosclerosis Study (IRAS) (n=1008; age, 40 to 69 years; 33% with impaired glucose tolerance), a multicenter, population-based study. None of the subjects had clinical coronary artery disease. Insulin sensitivity (SI) was measured by a frequently sampled intravenous glucose tolerance test, and CRP was measured by a highly sensitive competitive immunoassay. All 3 inflammatory markers were correlated with several components of the IRS. Strong associations were found between CRP and measures of body fat (body mass index, waist circumference), SI, and fasting insulin and proinsulin (all correlation coefficients >0.3, P<0.0001). The associations were consistent among the 3 ethnic groups of the IRAS. There was a linear increase in CRP levels with an increase in the number of metabolic disorders. Body mass index, systolic blood pressure, and SI were related to CRP levels in a multivariate linear regression model.
Conclusions—We suggest that chronic subclinical inflammation is part of IRS. CRP, a predictor of cardiovascular events in previous reports, was independently related to SI. These findings suggest potential benefits of anti-inflammatory or insulin-sensitizing treatment strategies in healthy individuals with features of IRS.
Key Words: inflammation • proteins • insulin resistance syndrome • insulin • atherosclerosis
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Introduction |
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Arelationship between C-reactive protein (CRP), a sensitive marker of inflammation, and the development of atherosclerotic disease has been observed in experimental1 2 3 4 and epidemiological studies.5 6 7 8 It is still unknown, however, whether elevated CRP levels merely reflect an epi-phenomenon accompanying established atherosclerotic disease or whether the protein itself is involved in the initiation and/or progression of atherosclerosis.
Previous reports suggest a positive association between components of the insulin resistance syndrome (IRS) and markers of the acute-phase response, including CRP6 8 9 10 11 12 and fibrinogen.13 CRP levels were associated with body mass index (BMI),6 8 9 10 12 serum lipids,6 8 9 10 12 and fasting glucose.9 Elevated levels of inflammatory markers (including CRP) were also found in type 2 diabetic patients with features of IRS.11
The nature of the association of CRP with IRS, however, is poorly understood. We hypothesized that insulin insensitivity and/or hyperinsulinemia may be associated with circulating CRP levels. Such an association would potentially provide insights into the role of CRP in atherosclerotic disease and further clarify the association of hyperinsulinemia with cardiovascular disease.14
We studied the relation of inflammatory markers (CRP, fibrinogen, white cell count) and components of IRS, including insulin sensitivity, as directly measured by a frequently sampled intravenous glucose tolerance test. Furthermore, we sought to investigate whether CRP levels were independently related to insulin (or its precursors), insulin sensitivity, or both. The analyses were restricted to nondiabetic subjects without clinical coronary artery disease to avoid possible confounding by preexisting cardiovascular disease. It has been shown previously that patients with type 2 diabetes present with higher levels of inflammatory markers8 11 and a high prevalence of atherosclerosis, including clinically undetected disease.15
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Methods |
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Study Subjects
The Insulin Resistance Atherosclerosis Study (IRAS) is a multicenter, population-based epidemiological study exploring relationships between insulin resistance, cardiovascular risk factors, and cardiovascular disease across different ethnic groups and various states of glucose tolerance. A full description of the design and methods of the IRAS has been published.16 The IRAS protocol was approved by local institutional review committees, and all subjects gave informed consent.
A total of 1088 nondiabetic individuals participated in the IRAS. Subjects with a current acute illness (including clinically significant infectious disease) were excluded from IRAS examination. Subjects with clinically overt coronary artery disease, defined as past myocardial infarction, PTCA or CABG, or ECG evidence of ischemic heart disease, were excluded from the present analyses. This report includes data on 1008 nondiabetic subjects in whom CRP and fibrinogen levels were measured. Cigarette smoking was dichotomized into "never" and "ever" (including past and current) by use of a standard questionnaire. BMI (weight/height2 [kg/m2]) was used as an estimate of overall adiposity. Waist circumference (estimate of visceral fat) was measured at the natural indentation between the 10th rib and the iliac crest (minimum waist).
A standard 75-g oral glucose tolerance test was performed. Glucose tolerance status was based on World Health Organization criteria.17
Laboratory Measurements
Plasma glucose was measured with the glucose oxidase technique
on an automated autoanalyzer (Yellow Springs Equipment Co).
Insulin was measured with the dextran-charcoal
radioimmunoassay.18 This insulin assay cross-reacts with
proinsulin. Fasting serum intact proinsulin and 32–33 split proinsulin
were determined at the Department of Clinical Biochemistry at
Addenbrook’s Hospital, Cambridge, UK (Professor C.N. Hales), by means
of highly specific 2-site monoclonal antibody–based immunoradiometric
assays.19
Insulin sensitivity was assessed by a frequently sampled intravenous glucose tolerance test20 with minimal model analysis.21 Two modifications of the original protocol were used: (1) an injection of regular insulin, rather than tolbutamide, to ensure adequate plasma insulin levels for the accurate computation of insulin sensitivity across a broad range of glucose tolerance22 and (2) the reduced sampling protocol23 because of the large number of subjects. Insulin sensitivity, expressed as the insulin sensitivity index (SI), was calculated by mathematical modeling methods (MINMOD, version 3.0, 1994).
Plasma lipoprotein measurements were obtained from fasting single fresh plasma samples through Lipid Research Clinic methods at the central IRAS laboratory at Medlantic Research Institute, Washington, DC (Professor B.V. Howard).
CRP was measured by in-house ultrasensitive competitive immunoassay (antibodies and antigens from Calbiochem) with an interassay coefficient of variation of 8.9%.24 Fibrinogen was measured in citrated plasma with a modified clot-rate assay by use of the Diagnostica STAGO ST4 instrument, as described previously.25 Complete blood cell counts were performed with standard techniques.
Statistical Analysis
Statistical analyses were performed with the SAS
statistical software system. Descriptive statistics (mean±SE) and
number/percent are shown on Table 1
. CRP levels differed by sex and
ethnicity in the present population, and age and smoking were
determinants of CRP levels in previous reports; therefore,
multivariate models (partial Spearman correlations,
multiple linear regression analysis) were tailored to account
for these possible confounders. Partial Spearman correlations
(adjusting for age, sex, ethnicity, clinic, and smoking status) for
inflammatory markers with components of the IRS were estimated for the
overall population (Table 2) and
stratified by ethnicity and glucose tolerance status (normal [NGT]
versus impaired [IGT] glucose tolerance). In these models, we also
tested for interactions between the independent variables of
interest (BMI, fasting glucose, insulin, proinsulin, split proinsulin,
and SI) and ethnicity and glucose tolerance
status, respectively. The distribution of CRP levels was highly skewed.
Logarithmically transformed values of CRP (log CRP) were used because
the distribution of the residuals from the fitted models became
normally distributed after log transformation. Thus, mean values of log
CRP (adjusted for age, sex, ethnicity, clinic, and smoking status) in
relation to the number of metabolic disorders were
calculated by ANCOVA (Figure 1).
Furthermore, we calculated (unadjusted) mean values of log CRP by
tertile for SI, BMI, and
triglycerides and for hypertension (Figure 2).
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75th percentile for waist circumferences: men=103.0 cm and
women=99.3 cm), (3) insulin resistance (<25th percentile for
SI: <0.88x10-4 min-1 ·
µU-1 · mL-1 or in 47 subjects without
frequently sampled intravenous glucose tolerance test,
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Stepwise linear regression models were fit for log CRP as a dependent
variable, including all variables of interest at the same time
as independent variables to demonstrate the relative contribution
of each of these variables to the outcome variable. After age,
sex, ethnicity, clinic, and smoking status were forced into the model,
the following independent variables were considered for the model:
BMI, diastolic and systolic blood pressures,
fasting glucose, SI, fasting insulin, and
proinsulin (intact). Only variables that had a P
0.05
were considered in the final fitted model (Table 3). A value of P<0.05
(2-sided) was considered statistically significant.
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Results |
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Table 1
shows descriptive data. All 3 inflammatory markers
were correlated with several components of IRS (Table 2). The
associations were generally stronger for CRP than for white cell count
and fibrinogen. Strong associations (correlation coefficients >0.3)
were found between CRP and measures of body fat (BMI, waist
circumference), SI, fasting insulin, and
proinsulin. There was a linear increase in CRP levels with an increase
in the number of metabolic disorders
(dyslipidemia, upper body adiposity, insulin resistance,
hypertension; Figure 1). The respective mean log of CRP levels
(±SE) were 0.075±0.06, 0.511±0.06, 0.845±0.07, 1.34±0.10, and
1.39±0.17 in the presence of 0, 1, 2, 3, or 4 metabolic
disorders. The percentage of subjects presenting with 0, 1, 2, 3,
and 4 disorders was 30.3%, 32.7%, 22.7%, 10.4%, and 4.0%,
respectively. When mean values of log CRP were analyzed by
tertiles of SI, BMI, and
triglycerides and by hypertension (Figure 2), higher
levels of log CRP were found in the lower tertiles of
SI (indicating a relation of higher CRP levels
with higher insulin resistance), in the higher tertiles of BMI, in the
highest tertile of triglycerides, and in hypertensive
subjects. Furthermore, the distribution curves of log CRP values showed
a shift to the right for hypertensive subjects and for increasing
tertiles of BMI and triglycerides or a shift to the left
for increasing tertiles of SI.
The associations as shown in the overall population (Table 2)
were also consistent among the 3 ethnic groups. Correlation
coefficients for CRP in non-Hispanic whites (n=399), blacks (n=267),
and Hispanics (n=342) were 0.43, 0.43, and 0.38 (BMI); 0.43, 0.46, and
0.39 (waist); 0.35, 0.29, and 0.36 (fasting insulin); 0.30, 0.31, and
0.29 (intact proinsulin); 0.38, 0.28, and 0.29 (split proinsulin); and
-0.41, -0.33, and -0.38 (SI), respectively
(all P<0.0001). The correlation coefficient of CRP with
fasting glucose was 0.16 (P<0.005) in non-Hispanic whites,
0.12 (P=NS) in blacks, and 0.25 (P<0.0001) in
Hispanics. The association of fasting insulin with CRP and fibrinogen
was less pronounced in blacks compared with non-Hispanic whites and
Hispanics (P<0.005 and P<0.05 for interaction
terms), respectively, although the associations were clearly in the
same direction and, for CRP, highly significant in all 3 ethnic groups.
All other interaction terms were not statistically significant.
The associations were also consistently seen in subjects with NGT and IGT. Correlation coefficients for CRP in subjects with NGT and IGT were 0.34 and 0.41 (BMI), 0.37 and 0.40 (waist), 0.32 and 0.23 (fasting insulin), 0.23 and 0.29 (intact proinsulin), 0.25 and 0.31 (split proinsulin), and -0.35 and -0.26 (SI), respectively (all P<0.0001). The correlation of CRP with fasting glucose was weak in NGT (r=0.11, P<0.05) and not significant in IGT (r=0.09). The association of fasting insulin with CRP was stronger in subjects with NGT than with IGT (P<0.0001 for interaction term). All other interaction terms were not statistically significant.
Multivariate linear regression analyses showed
that BMI, systolic blood pressure, and SI
(inversely) were independently associated with log CRP levels in the
overall population (Table 3).
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Discussion |
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In the present study, we have shown that in healthy, nondiabetic subjects, CRP, a sensitive marker of inflammation that has previously been associated with cardiovascular disease,5 6 7 8 was independently related to insulin sensitivity. Chronic subclinical inflammation emerged as part of IRS. The findings were consistent across the 3 ethnic groups of the IRAS (non-Hispanic whites, blacks, and Hispanics) and in subjects with NGT and IGT.
Previously, in various populations, CRP levels were associated with
BMI,6 8 9 10 12 triglyceride
level,6 8 9 10 12 HDL cholesterol level
(inversely),9 10 12 total cholesterol
level,9 and blood pressure.8 12 Mendall et
al9 found an association between CRP levels and fasting
glucose, confirmed by Tracy et al10 in the elderly but
only in a nonsmoking subset. However, information about the association
of serum levels of inflammatory markers with insulinemia and insulin
sensitivity, hallmarks of the IRS, is scarce. Recently, we have
reported from the IRAS associations of fibrinogen and
plasminogen activator-1 with several components
of IRS, including insulin, proinsulin, and
SI.26 In 3 other studies, fibrinogen
levels were independently associated with fasting insulin levels in
nondiabetic subjects.13 27 28 In 107 nondiabetic subjects,
CRP levels were related to insulin resistance, as calculated with the
homeostasis model assessment model.12 The present
study clearly corroborates and extends these results, indicating that
chronic, subclinical inflammation is part of IRS. We have shown that
various components of IRS were correlated to inflammatory markers
(Table 2 and Figure 2) and that an increasing number of
components of IRS (dyslipidemia, abdominal obesity, low
SI, and hypertension) paralleled increasing
levels of CRP (Figure 1). The results were consistent
across a variety of ethnic groups that differ in insulin
sensitivity,29 indicating that the relations found in our
study apply to populations with high and low
SI.
There are several possible explanations for these findings, which are
not necessarily exclusive. First, it is possible that chronic
inflammation may represent a triggering factor in the origin of
IRS, and eventually type 2 diabetes, as previously discussed by Pickup
and Crook.30 According to this hypothesis, stimuli such as
overnutrition would result in cytokine hypersecretion and
eventually lead to insulin resistance and diabetes in genetically or
metabolically predisposed individuals. Cytokines,
mainly interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-
,
exert major stimulatory effects on hepatic synthesis of acute-phase
proteins.31
Second, clustering of cardiovascular risk factors as typically encountered in subjects with the IRS may yield cardiovascular disease (yet undetected), and elevated CRP levels thus would be the result of preexisting atherosclerosis.32 Previous cross-sectional analyses show an association between CRP levels and atherosclerotic disease.6 9 CRP was also elevated in elderly women with subclinical atherosclerosis in the Cardiovascular Health Study7 ; however, in a larger cohort from the same population, no significant association of CRP with carotid intimal-medial thickness was found.10 Atherosclerosis starts very early in life, and insulin resistance potentially accelerates this process.33 Therefore, it is highly likely that in our "healthy" middle-aged population, atherosclerosis prevails, particularly in those with features of IRS. However, the degree and extent of atherosclerosis operative in increasing CRP levels is unknown; therefore, even relatively sensitive methods of assessing preclinical atherosclerosis (such as carotid ultrasound) may lack accuracy in this respect.
Third, decreased insulin sensitivity may lead to enhanced CRP expression by counteracting the physiological effect of insulin on hepatic acute-phase protein synthesis.34 Clamp studies in normal subjects showed that insulin exerts selective effects on hepatic protein synthesis, with an increase in albumin synthesis and a decrease in fibrinogen synthesis,35 the inverse of the picture typically seen during the acute-phase response.36 Resistance to this effect would then lead to increased synthesis of acute-phase proteins, such as fibrinogen and CRP.
Finally, the effect could be indirect via body fat; we observed a
strong and independent association of CRP levels with measures of body
fat and triglycerides. This is in accordance with results
of previous cross-sectional analyses.6 8 9 10 12 In
a previous interventional study, the synthesis of proinflammatory
cytokines by peripheral monocytes (TNF-, IL-1)
was suppressed by dietary fish oil supplementation,37
suggesting an effect of dietary fat on cytokine
production.38 Another (speculative at this time)
mechanism would be a generally enhanced adipose tissue–derived
cytokine expression (TNF-, IL-6). Accordingly, weight loss
was associated with a decrease in CRP in the Women’s Healthy Lifestyle
Project (E. Meilahn, personal communication, 1996), also supporting
an association of body fat and chronic inflammation.
We found a strong and independent association of elevations in inflammatory markers, namely CRP, with decreased SI. The association of low SI (indicating high insulin resistance) with elevated CRP levels found in the present study could potentially explain the association of hyperinsulinemia (another indicator of insulin resistance) with cardiovascular disease.14 Several experimental studies suggest a direct role of CRP in the initiation and/or progression of atherosclerotic lesions. CRP has been shown to (1) be a potent stimulator of tissue factor production by macrophages4 ; (2) activate the complement system in vivo39 ; (3) accumulate in early atherosclerotic lesions in human aorta2 and coronary arteries3 ; (4) bind to lipoproteins, such as LDL and VLDL, thus inducing their aggregation1 ; and (5) be expressed by monocytes.40 In epidemiological studies, CRP levels in the upper normal range have consistently been predictive of cardiovascular disease in various populations.5 6 7 8 Moreover, sensitive assays and the biological properties of CRP (such as its stable half-life41 ) make this protein a clinically useful marker of chronic subclinical inflammation.
The results of the present study are potentially clinically important. As previously shown, treatment of several components of IRS (adiposity, dyslipidemia, hypertension) may have beneficial effects in terms of preventing type 2 diabetes42 and cardiovascular disease.43 44 Therefore, if subclinical inflammation is indeed another facet of the IRS, anti-inflammatory treatment may also be beneficial. Accordingly, it has been suggested that the effects of aspirin may, at least partly, be mediated through its anti-inflammatory rather than its antiplatelet properties.5 Furthermore, treatment aiming at improving insulin resistance, whether nonpharmacological, such as exercise and weight reduction, or pharmacological, such as metformin and thiazolidinediones, may lower CRP levels and thus provide additional therapeutic benefits beyond mere glucose lowering. Alternatively, if elevated CRP levels were merely a marker of prevalent or developing atherosclerosis, these treatment strategies would then be clinically fruitless. Prospective studies are clearly needed to address these issues.
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Acknowledgments |
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This work was supported by the National Heart, Lung and Blood Institute (grants HL-47887, HL-47889, HL-47890, HL-47892, HL-47902, HL-55208, and R01-HL-58329) and the General Clinic Research Centers Program (grants NCRR GCRC, M01 RR431, and M01 RR01346).
Received August 30, 1999; revision received January 21, 2000; accepted February 2, 2000.
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R. B. Goldberg Cytokine and Cytokine-Like Inflammation Markers, Endothelial Dysfunction, and Imbalanced Coagulation in Development of Diabetes and Its Complications J. Clin. Endocrinol. Metab., September 1, 2009; 94(9): 3171 - 3182. [Abstract] [Full Text] [PDF]
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K. Tanigaki, C. Mineo, I. S. Yuhanna, K. L. Chambliss, M. J. Quon, E. Bonvini, and P. W. Shaul C-Reactive Protein Inhibits Insulin Activation of Endothelial Nitric Oxide Synthase via the Immunoreceptor Tyrosine-Based Inhibition Motif of Fc{gamma}RIIB and SHIP-1 Circ. Res., June 5, 2009; 104(11): 1275 - 1282. [Abstract] [Full Text] [PDF]
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G. Hu, P. Jousilahti, J. Tuomilehto, R. Antikainen, J. Sundvall, and V. Salomaa Association of Serum C-Reactive Protein Level with Sex-Specific Type 2 Diabetes Risk: A Prospective Finnish Study J. Clin. Endocrinol. Metab., June 1, 2009; 94(6): 2099 - 2105. [Abstract] [Full Text] [PDF]
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Z. T. Bloomgarden American College of Endocrinology Pre-Diabetes Consensus Conference: Part Three Diabetes Care, December 1, 2008; 31(12): 2404 - 2409. [Full Text] [PDF]
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A. Cartier, I. Lemieux, N. Almeras, A. Tremblay, J. Bergeron, and J.-P. Despres Visceral Obesity and Plasma Glucose-Insulin Homeostasis: Contributions of Interleukin-6 and Tumor Necrosis Factor-{alpha} in Men J. Clin. Endocrinol. Metab., May 1, 2008; 93(5): 1931 - 1938. [Abstract] [Full Text] [PDF]
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W. Otter, M. Winter, W. Doering, E. Standl, and O. Schnell C-Reactive Protein in Diabetic and Nondiabetic Patients With Acute Myocardial Infarction Diabetes Care, December 1, 2007; 30(12): 3080 - 3082. [Full Text] [PDF]
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J. Evans, M. Collins, C. Jennings, L. van der Merwe, I. Soderstrom, T. Olsson, N. S Levitt, E. V Lambert, and J. H Goedecke The association of interleukin-18 genotype and serum levels with metabolic risk factors for cardiovascular disease Eur. J. Endocrinol., November 1, 2007; 157(5): 633 - 640. [Abstract] [Full Text] [PDF]
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J. Westerbacka, M. Kolak, T. Kiviluoto, P. Arkkila, J. Siren, A. Hamsten, R. M. Fisher, and H. Yki-Jarvinen Genes Involved in Fatty Acid Partitioning and Binding, Lipolysis, Monocyte/Macrophage Recruitment, and Inflammation Are Overexpressed in the Human Fatty Liver of Insulin-Resistant Subjects Diabetes, November 1, 2007; 56(11): 2759 - 2765. [Abstract] [Full Text] [PDF]
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K. Takebayashi, M. Suetsugu, S. Wakabayashi, Y. Aso, and T. Inukai Retinol Binding Protein-4 Levels and Clinical Features of Type 2 Diabetes Patients J. Clin. Endocrinol. Metab., July 1, 2007; 92(7): 2712 - 2719. [Abstract] [Full Text] [PDF]
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S. M. Haffner Abdominal obesity, insulin resistance, and cardiovascular risk in pre-diabetes and type 2 diabetes Eur. Heart J. Suppl., May 1, 2006; 8(suppl_B): B20 - B25. [Abstract] [Full Text] [PDF]
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L. E. Bernstein, J. Berry, S. Kim, B. Canavan, and S. K. Grinspoon Effects of Etanercept in Patients With the Metabolic Syndrome. Arch Intern Med, April 24, 2006; 166(8): 902 - 908. [Abstract] [Full Text] [PDF]
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A. Festa, K. Williams, R. P. Tracy, L. E. Wagenknecht, and S. M. Haffner Progression of Plasminogen Activator Inhibitor-1 and Fibrinogen Levels in Relation to Incident Type 2 Diabetes Circulation, April 11, 2006; 113(14): 1753 - 1759. [Abstract] [Full Text] [PDF]
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A. Oberbach, A. Tonjes, N. Kloting, M. Fasshauer, J. Kratzsch, M. W Busse, R. Paschke, M. Stumvoll, and M. Bluher Effect of a 4 week physical training program on plasma concentrations of inflammatory markers in patients with abnormal glucose tolerance. Eur. J. Endocrinol., April 1, 2006; 154(4): 577 - 585. [Abstract] [Full Text] [PDF]
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R. P Raghavan, D. W Laight, K. M Shaw, and M. H Cummings Review: Aspirin and diabetes The British Journal of Diabetes & Vascular Disease, March 1, 2006; 6(2): 74 - 82. [Abstract] [PDF]
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M. Mohlig, M. Freudenberg, T. Bobbert, M. Ristow, H. Rochlitz, M. O. Weickert, A. F. H. Pfeiffer, and J. Spranger Acetylsalicylic Acid Improves Lipid-Induced Insulin Resistance in Healthy Men J. Clin. Endocrinol. Metab., March 1, 2006; 91(3): 964 - 967. [Abstract] [Full Text] [PDF]
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K. Lobner, A. Knopff, A. Baumgarten, U. Mollenhauer, S. Marienfeld, M. Garrido-Franco, E. Bonifacio, and A.-G. Ziegler Predictors of Postpartum Diabetes in Women With Gestational Diabetes Mellitus Diabetes, March 1, 2006; 55(3): 792 - 797. [Abstract] [Full Text] [PDF]
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M. Soinio, J. Marniemi, M. Laakso, S. Lehto, and T. Ronnemaa High-Sensitivity C-Reactive Protein and Coronary Heart Disease Mortality in Patients With Type 2 Diabetes: A 7-year follow-up study Diabetes Care, February 1, 2006; 29(2): 329 - 333. [Abstract] [Full Text] [PDF]
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C. Gubern, A. Lopez-Bermejo, J. Biarnes, J. Vendrell, W. Ricart, and J. M. Fernandez-Real Natural Antibiotics and Insulin Sensitivity: The Role of Bactericidal/Permeability-Increasing Protein Diabetes, January 1, 2006; 55(1): 216 - 224. [Abstract] [Full Text] [PDF]
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J. F. Navarro and C. Mora Role of inflammation in diabetic complications Nephrol. Dial. Transplant., December 1, 2005; 20(12): 2601 - 2604. [Full Text] [PDF]
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A. Tsuchida, T. Yamauchi, S. Takekawa, Y. Hada, Y. Ito, T. Maki, and T. Kadowaki Peroxisome Proliferator-Activated Receptor (PPAR){alpha} Activation Increases Adiponectin Receptors and Reduces Obesity-Related Inflammation in Adipose Tissue: Comparison of Activation of PPAR{alpha}, PPAR{gamma}, and Their Combination Diabetes, December 1, 2005; 54(12): 3358 - 3370. [Abstract] [Full Text] [PDF]
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H. Koyama, T. Shoji, H. Yokoyama, K. Motoyama, K. Mori, S. Fukumoto, M. Emoto, T. Shoji, H. Tamei, H. Matsuki, et al. Plasma Level of Endogenous Secretory RAGE Is Associated With Components of the Metabolic Syndrome and Atherosclerosis Arterioscler Thromb Vasc Biol, December 1, 2005; 25(12): 2587 - 2593. [Abstract] [Full Text] [PDF]
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A. J.G. Hanley, K. Williams, A. Festa, L. E. Wagenknecht, R. B. D'Agostino Jr, and S. M. Haffner Liver Markers and Development of the Metabolic Syndrome: The Insulin Resistance Atherosclerosis Study Diabetes, November 1, 2005; 54(11): 3140 - 3147. [Abstract] [Full Text] [PDF]
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L. Kalra, C. Rambaran, P. Chowienczyk, D. Goss, I. Hambleton, J. Ritter, A. Shah, R. Wilks, and T. Forrester Ethnic Differences in Arterial Responses and Inflammatory Markers in Afro-Caribbean and Caucasian Subjects Arterioscler Thromb Vasc Biol, November 1, 2005; 25(11): 2362 - 2367. [Abstract] [Full Text] [PDF]
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the Diabetes Prevention Program Research Group Lipid, Lipoproteins, C-Reactive Protein, and Hemostatic Factors at Baseline in the Diabetes Prevention Program Diabetes Care, October 1, 2005; 28(10): 2472 - 2479. [Abstract] [Full Text] [PDF]
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