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The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 8 3773-3776
Copyright © 2003 by The Endocrine Society

Elevated Plasma High-Sensitivity C-Reactive Protein Concentrations in Asian Indians Living in the United States

Manisha Chandalia, Alberto V. Cabo-Chan, Jr, Sridevi Devaraj, Ishwarlal Jialal, Scott M. Grundy and Nicola Abate

Center for Human Nutrition (M.C., A.V.C.-C., S.M.G., N.A.), Department of Internal Medicine (M.C., A.V.C.-C., S.M.G., N.A.), Division of Endocrinology and Metabolism (M.C., A.V.C.-C., N.A.), University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-9169; and Laboratory for Atherosclerosis and Metabolic Research (S.D., I.J.), University of California, Davis Medical Center, Davis, California 95616

Address all correspondence and requests for reprints to: Nicola Abate, M.D., 6011 Harry Hines Boulevard, Dallas, Texas 75390-9169. E-mail: Nicola.Abate{at}UTSouthwestern.edu.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Proinflammatory state may contribute to the excessive prevalence of type 2 diabetes and cardiovascular disease observed in populations originating from the Indian subcontinent (Asian Indians). This study was conducted to evaluate whether nondiabetic Asian Indian men living in the United States manifest a proinflammatory state when compared with Caucasians of similar age and body fat content. We also compared the relationships between plasma high-sensitivity C-reactive protein (hs-CRP), a marker of low-grade inflammation, and various parameters of body composition and fat distribution and insulin sensitivity in Asian Indians and Caucasians. For this purpose, plasma hs-CRP, oral glucose tolerance test, and anthropometric measurements were conducted in 82 Asian Indian men and 55 Caucasian men of similar age. The two groups had similar body fat content and truncal skinfolds thickness. Asian Indians had higher insulin areas under the curve during oral glucose tolerance tests, indicating a greater insulin resistance. Asian Indians also manifested a significant elevation of plasma hs-CRP. We conclude that young, overtly healthy Asian Indian men have both greater insulin resistance and higher hs-CRP levels than do Caucasians. This difference cannot be explained by greater adiposity in Asian Indians and suggests that many Asian Indians have an underlying proinflammatory state that may contribute to their increased risk for both type 2 diabetes and cardiovascular disease.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
A PROINFLAMMATORY STATE appears to be associated with increased risk for both cardiovascular disease (CVD) and diabetes (1, 2, 3, 4, 5, 6, 7, 8, 9, 10). Several reports indicate that populations at risk have high plasma levels of both cytokines and acute phase reactants (7, 8). Among the latter is an elevation of high-sensitivity C-reactive protein (hs-CRP). One population at high risk for both CVD and diabetes includes persons originating from the Indian subcontinent (Asian Indians) (11, 12, 13, 14, 15, 16). An important question therefore is whether Asian Indians exhibit a proinflammatory state. This possibility exists because their high risk for CVD cannot be explained by established risk factors; moreover, type 2 diabetes often develops in the presence of only mild obesity. Although high levels of hs-CRP have been reported for Asian Indians (17, 18), not all studies have confirmed these findings (19), and data in Asian Indians living in the United States is scanty. The present study therefore was carried out to determine whether hs-CRP levels are significantly different between Asian Indian men and Caucasian men who have similar age and body fat content.

Previous reports indicate that hs-CRP levels are correlated with body mass index (BMI) (10) and body fat distribution (20, 21). One mechanism for elevation of plasma hs-CRP in obese persons could be a high production of cytokines, e.g. IL-6 and TNF{alpha} by excess adipose tissue, which could induce higher hs-CRP production by the liver. The presence of visceral obesity in particular has been reported to raise hs-CRP levels. One study (18) implicates this mechanism as the cause of higher CRP levels in Asian Indians. In the present study, therefore, we examined whether Asian Indians and Caucasians differ in hs-CRP relationships to different parameters of body fat content and distribution.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Subjects

Subjects were recruited through public advertisement and were screened for hematological and blood chemistry abnormalities. The study was approved by the Institutional Review Board of the University of Texas Southwestern Medical Center at Dallas (Dallas, TX). All subjects signed a written informed consent. Subjects with diabetes mellitus and other endocrine disorders, coronary heart disease, liver function test abnormalities, and those receiving any form of therapies, including aspirin, cyclooxygenase-2 inhibitors and statins, were excluded from the study. At the time of enrollment, each volunteer was administered a health history questionnaire. Height, weight, and blood pressure measurements were taken for all subjects. Fasting blood samples were collected in all the subjects.

The general characteristics of Asian Indian men are compared with those of the Caucasian men in Table 1Go. Eighty-two Asian Indian males and 55 Caucasian males participated in this study. The Asian Indian group included 20 Muslims and 62 Hindus. Of the Muslims, 19 originated from Pakistan and one was from Bangladesh. All Hindus were originating from India. The two groups were of similar age and all were healthy without any acute or chronic illness. Only six Asian Indian and four Caucasian subjects reported a smoking habit. Asian Indians had lower mean BMI than Caucasians. However, percentage of body fat, truncal skinfolds thickness, and peripheral skinfolds thickness were similar for the two groups. Despite these similarities, Asian Indians had significantly smaller waist and hip circumferences than Caucasians.


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  		TABLE 1. General characteristics of Asian Indians and Caucasians

 
Biochemical analyses

Plasma glucose concentration was assayed using a glucose oxidase method. Plasma insulin was determined by immunoassay at the Linco Research Inc. (St. Louis, MO). The plasma concentrations of hs-CRP were measured by a highly sensitive nephelometric assay using a monoclonal antibody to CRP coated on polyesterene beads (Dade Behring, Newark, DE). Both interassay and intraassay coefficient of variation were less than 0.5%. The lower sensitivity of the hs-CRP assay was 0.2 mg/liter. Five subjects from each study group had a measured hs-CRP lower than 0.2 mg/liter.

Oral glucose tolerance test (OGTT)

After 12-h fasting, subjects had an iv catheter placed in a forearm vein to collect blood. A solution containing 75 g glucose was administered orally to the subjects (Tru-Glu 100, Fisher Scientific, Pittsburgh, PA). Blood was collected at time -30, -15, 0, 30, 60, 90, 120, 150, and 180 min for measurement of glucose and insulin concentrations. Results at times -30, -15, and 0 min were averaged as baseline measurements for analysis.

Anthropometry

Anthropometric measurements were done in all subjects. Height and weight were measured by standard procedures. Waist circumference was measured at the umbilical level. The average of two measurements was used for analysis. Skinfolds thickness was measured at nine different anatomical sites (subscapular diagonal and vertical, chest, mid-axillary, abdominal horizontal and vertical, supra iliac diagonal, and vertical, triceps, biceps, thigh, and calf) using a Lange skinfold caliper (Cambridge Scientific Instruments Inc., Cambridge, MD), as previously reported (22). Body density was calculated from measurements of body volume determined by hydrostatic weighing with adjustment for residual volume measured by helium dilution during the underwater weighing. Percentage of body fat was calculated using the Siri equation (23) assuming a fat free density of 1.10 g/cc for men and 1.097 g/cc for women.

Statistical analysis

A target sample of 100 subjects per study group was chosen to have 90% power to detect difference of 0.5 mg/liter in hs-CRP between the two study groups. Complete studies could be performed in 60 Caucasians and 90 Asian Indians. We excluded five Asian Indians and one Caucasian from the analysis because of diagnosis of diabetes based on the fasting plasma glucose above 126 mg/dl (7 mmol/liter). Another three Asian Indians and four Caucasians were excluded because of hs-CRP above 10 mg/liter. The final sample size used for analysis was of 82 Asian Indians and 55 Caucasians. The area under the curve (AUC) during OGTT was calculated for glucose and insulin using the trapezoidal rule. Wilcoxon rank sum tests were used to compare the Asian Indian and Caucasian groups in Table 1Go. For skewed variables (hs-CRP and insulin AUC), the data were log transformed before analysis. The data on hs-CRP and insulin AUC are reported as geometric mean. Adjusted means were derived using analysis of covariance models. Spearman correlation coefficients were used to assess the association between continuous variables. Statistical analysis was performed using SAS version 8.2 (SAS Institute, Cary, NC).


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
Asian Indians in this study had significantly higher concentrations of hs-CRP than did Caucasians (the geometric means were 0.94 and 0.63 mg/liter, respectively; P = 0.036 (Fig. 1Go). Asian Indians also had higher AUCs for insulin than Caucasians [the geometric means were 13,337 µU·min/ml (92.6 nmol·min/liter) and 8,872 µU·min/ml (61.6 nmol·min/liter), respectively; P < 0.0001]. However, the two groups had similar plasma glucose levels during OGTTs [mean and SD of AUCs were 22,716 ± 4,884 mg·min/dl (1,261 ± 271 mmol·min/liter) and 21,279 ± 2,869 mg·min/dl (1,181 ± 159 mmol·min/liter), for Asian Indians and Caucasians, respectively]. In Table 2Go, differences in hs-CRP and insulin AUC are shown after adjustment for total fat mass and for waist circumference. The data indicate that the level of statistical significance for the differences between Asian Indians and Caucasians was even greater after these adjustments. Significant difference in plasma hs-CRP between the two study groups was observed when statistical adjustment included total fat mass, waist, and insulin AUC (P = 0.02).



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  		FIG. 1. Geometric means for plasma hs-CRP concentrations and insulin AUC during OGTT in Asian Indians ({blacksquare}) and Caucasians ({square}). Wilcoxon rank sum tests were used to compare the Asian Indian and the Caucasian groups after log transformation due to skewed variables. Systeme Internationale conversion factor for insulin is 0.6945 pmol/liter.

 

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  		TABLE 2. Differences in hs-CRP and insulin AUC between Asian Indians and Caucasians after adjustment for body fat and waist circumference

 
Table 3Go shows the relationship between body fat and parameters of fat distribution with plasma concentrations of hs-CRP and insulin AUC for the two ethnic groups. In both groups, increasing adiposity was accompanied by higher levels of hs-CRP. However, the difference in the intercepts of the correlation lines between Asian Indians and Caucasians was not significantly different (data not shown). In general, correlation coefficients were higher for Caucasians than for Asian Indians. This finding suggests that hs-CRP and insulin AUC are more tightly correlated with body fat parameters in Caucasians than Asian Indians. This apparent difference, however, was more striking for total body fat than for measures of fat distribution.


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  		TABLE 3. Relationship between body composition and fat distribution with hs-CRP and insulin AUC

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
Nonobese Asian Indians in general are more insulin resistant than are nonobese Caucasians. This difference has been demonstrated in several previous studies including our own (23, 24, 25). Because higher waist-to-hip ratio has been reported in Asian Indians living in United Kingdom compared with the local Caucasian population, a predisposition to abdominal fat distribution has been suggested as a possible explanation for the excessive insulin resistance in the Asian Indians (24, 25). In the current study, despite similar age, body fat content, and lower waist circumference than Caucasians, the Asian Indian men had significantly higher AUCs for plasma insulin following an oral glucose challenge. Nonetheless, in both Asian Indians and Caucasians, the insulin AUC was significantly correlated with body fat measures—percentage of body fat, total fat mass, waist circumference, and skinfolds thickness. As we have previously reported (26), the highest correlations between body fat measures of insulin sensitivity are observed with truncal skinfolds thickness. The correlation between truncal skinfolds thickness and insulin AUC was independent of total body fat content (P = 0.02 after adjustment for body fat mass). Nonetheless, for every level of body fat, Asian Indians were more insulin resistant than Caucasians.

The primary new finding of the present study was that hs-CRP differences between the two ethnic groups paralleled changes in insulin sensitivity. Asian Indians as a group had significantly higher plasma hs-CRP levels than Caucasians. This difference was even more highly statistically significant when hs-CRP concentrations were adjusted for total body fat and waist circumference. Importantly, the difference could not be explained by any excess body fat or abdominal obesity in Asian Indians beyond what was revealed by BMI. Nonetheless, in both Asian Indians and Caucasians, hs-CRP concentrations were positively correlated with body fat estimates—percentage of body fat, total fat mass, waist circumference, and truncal skinfolds thickness. The present results thus are in accord with previous studies that reported that hs-CRP levels are correlated with body fat content (10, 20, 21). For several of the body fat measures, correlation coefficients with hs-CRP levels were higher for Caucasians, suggesting a tighter relationship with body fat. Nevertheless, the intercepts of the correlation lines were not different in the two groups, indicating a similar overall relationship of adiposity on hs-CRP levels. Even so, for similar degree of adiposity, Asian Indians had higher levels of hs-CRP than Caucasians.

The parallel relationships between insulin sensitivity and hs-CRP concentrations for the two groups raise the interesting question of possible cause and effect. Several studies point out that high levels of cytokines can impair insulin signaling and otherwise will promote development of insulin resistance (7, 8). Some investigators speculate that the greater insulin resistance accompanying increasing adiposity can be explained in part by high levels of circulating cytokines (27, 28, 29, 30). In the current study, an increase in body fat compartments contributed to higher hs-CRP levels in both groups. Nonetheless, in Asian Indians, hs-CRP concentrations were elevated out of proportion to those of Caucasians with similar level of adiposity. If these higher concentrations of an acute phase reactant are truly indicative of higher cytokine levels, the latter could contribute to lower insulin sensitivity in Asian Indians. Presumably a greater insulin resistance in Asian Indians is responsible in large part for their propensity to developing type 2 diabetes. In addition, Asian Indians with insulin resistance are at increased risk for CVD. In fact, the increase in CVD risk in this population appears to be out of proportion to levels of established risk factors (11, 12, 13, 14). On the other hand, recent studies indicate that Caucasian subjects with elevated hs-CRP carry an increased risk for coronary heart disease, again independently of established risk factors (1, 2, 3). These workers speculate that a proinflammatory state also may be a proatherogenic state. If Asian Indians do indeed carry a greater inflammatory background than do Caucasians, this too could contribute to their higher risk for coronary heart disease.

In summary, this study documents that young, overtly healthy Asian Indian men have both greater insulin resistance and higher hs-CRP levels than do Caucasians. This difference cannot be explained by greater adiposity in Asian Indians, although hs-CRP levels were correlated with body fat parameters in both ethnic groups. The findings of this study thus suggest that many Asian Indians have an underlying proinflammatory state that may contribute to their increased risk for both type 2 diabetes and CVD.


   Acknowledgments
 
We thank Marjorie Whelan, Rincy Varughese, and Munira Abbas for technical assistance; Mary Tenison for help in manuscript preparation; the nursing and dietetic services of the General Clinical Research Center; and Beverley Adams-Huet for biostatistical assistance. We are grateful to Dr. R. Munford for helpful discussions during the preparation of the manuscript and to Dr. P. Snell for assisting with underwater weighing. (All are from UT Southwestern Medical Center, Dallas, TX).


   Footnotes
 
This work was supported by National Institutes of Health Grants K23-RR16075, MO1-RR-00633, and K24-AT-00596.

Abbreviations: AUC, Area under the curve; BMI, body mass index; CVD, cardiovascular disease; hs-CRP, high-sensitivity C-reactive protein; OGTT, oral glucose tolerance test.

Received February 21, 2003.

Accepted May 12, 2003.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

  1. Ridker PM, Rifai N, Rose L, Buring JE, Cook NR 2002 Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N Engl J Med 347:1557–1565[Abstract/Free Full Text]
  2. Ridker PM, Buring JE, Cook NR, Rifai N 2003 C-reactive protein, the metabolic syndrome, and risk of incident cardiovascular events: an 8-year follow-up of 14,719 initially healthy American women. Circulation 107:391–397[Abstract/Free Full Text]
  3. Albert CM, Ma J, Rifai N, Stampfer MJ, Ridker PM 2002 Prospective study of C-reactive protein, homocysteine, and plasma lipid levels as predictors of sudden cardiac death. Circulation 105:2595–2599[Abstract/Free Full Text]
  4. Koenig W, Sund M, Frohlich M, Fischer HG, Lowel H, Doring A, Hutchinson WL, Pepys MB 1999 C-reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men: results from the MONICA (monitoring trends and determinants in cardiovascular disease) Augsburg Cohort Study, 1984 to 1992. Circulation 99:237–242[Abstract/Free Full Text]
  5. Mendall MA, Strachan DP, Butland BK, Ballam L, Morris J, Sweetnam PM, Elwood PC 2000 C-reactive protein: relation to total mortality, cardiovascular mortality and cardiovascular risk factors in men. Eur Heart J 21:1584–1590[Abstract/Free Full Text]
  6. Rost NS, Wolf PA, Kase CS, Kelly-Hayes M, Silbershatz H, Massaro JM, D’Agostino RB, Franzblau C, Wilson PW 2001 Plasma concentration of C-reactive protein and risk of ischemic stroke and transient ischemic attack: the Framingham study. Stroke 32:2575–2579[Abstract/Free Full Text]
  7. Festa A, D’Agostino Jr R, Tracy RP, Haffner SM 2002 Elevated levels of acute-phase proteins and plasminogen activator inhibitor-1 predict the development of type 2 diabetes: the insulin resistance atherosclerosis study. Diabetes 51:1131–1137[Abstract/Free Full Text]
  8. Leinonen E, Hurt-Camejo E, Wiklund O, Hulten LM, Hiukka A, Taskinen MR 2003 Insulin resistance and adiposity correlate with acute-phase reaction and soluble cell adhesion molecules in type 2 diabetes. Atherosclerosis 166:387–394[CrossRef][Medline]
  9. Wu T, Dorn JP, Donahue RP, Sempos CT, Trevisan M 2002 Associations of serum C-reactive protein with fasting insulin, glucose, and glycosylated hemoglobin: the Third National Health and Nutrition Examination Survey, 1988–1994. Am J Epidemiol 155:65–71[Abstract/Free Full Text]
  10. Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM 2001 C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA 286:327–334[Abstract/Free Full Text]
  11. Hughes K 1989 Mortality from cardiovascular diseases in Chinese, Malays and Indians in Singapore, in comparison with England and Wales, USA and Japan. Ann Acad Med Singapore 18:642–645[Medline]
  12. Balarajan R 1991 Ethnic differences in mortality from ischaemic heart disease and cerebrovascular disease in England and Wales. BMJ 302:560–564
  13. Anand SS, Yusuf S, Vuksan V, Devanesen S, Teo KK, Montague PA, Kelemen L, Yi C, Lonn E, Gerstein H, Hegele RA, McQueen M 2000 Differences in risk factors, atherosclerosis, and cardiovascular disease between ethnic groups in Canada: the Study of Health Assessment and Risk in Ethnic groups (SHARE). Lancet 356:279–284[CrossRef][Medline]
  14. Lee J, Heng D, Chia KS, Chew SK, Tan BY, Hughes K 2001 Risk factors and incident coronary heart disease in Chinese, Malay and Asian Indian males: the Singapore Cardiovascular Cohort Study. Int J Epidemiol 30:983–988[Abstract/Free Full Text]
  15. Chandalia M, Deedwania PC 2001 Coronary heart disease and risk factors in Asian Indians. Adv Exp Med Biol 498:27–34[Medline]
  16. Kamath SK, Hussain EA, Amin D, Mortillaro E, West B, Peterson CT, Aryee F, Murillo G, Alekel DL 1999 Cardiovascular disease risk factors in 2 distinct ethnic groups: Indian and Pakistani compared with American premenopausal women. Am J Clin Nutr 69:621–631[Abstract/Free Full Text]
  17. Chambers JC, Eda S, Bassett P, Karim Y, Thompson SG, Gallimore JR, Pepys MB, Kooner JS 2001 C-reactive protein, insulin resistance, central obesity, and coronary heart disease risk in Indian Asians from the United Kingdom compared with European whites. Circulation 104:145–150[Abstract/Free Full Text]
  18. Forouhi NG, Sattar N, McKeigue PM 2001 Relation of C-reactive protein to body fat distribution and features of the metabolic syndrome in Europeans and South Asians. Int J Obes Relat Metab Disord 25:1327–1331[CrossRef][Medline]
  19. Chatha K, Anderson NR, Gama R 2002 Ethnic variation in C-reactive protein: UK resident Indo-Asians compared with Caucasians. J Cardiovasc Risk 9:139–141[CrossRef][Medline]
  20. Lemieux I, Pascot A, Prud’homme D, Almeras N, Bogaty P, Nadeau A, Bergeron J, Despres JP 2001 Elevated C-reactive protein: another component of the atherothrombotic profile of abdominal obesity. Arterioscler Thromb Vasc Biol 21:961–967[Abstract/Free Full Text]
  21. Weyer C, Yudkin JS, Stehouwer CD, Schalkwijk CG, Pratley RE, Tataranni PA 2002 Humoral markers of inflammation and endothelial dysfunction in relation to adiposity and in vivo insulin action in Pima Indians. Atherosclerosis 161:233–242[CrossRef][Medline]
  22. Chandalia M, Abate N, Garg A, Stray-Gundersen J, Grundy SM 1999 Relationship between generalized and upper body obesity to insulin resistance in Asian Indian men. J Clin Endocrinol Metab 84:2329–2335[Abstract/Free Full Text]
  23. Siri WE 1961 Techniques for measuring body composition. In: Borzek J, Hanschel A, eds. Body composition from fluid spaces and density. Washington, DC: National Academy of Sciences; 223–224
  24. McKeigue PM, Pierpoint T, Ferrie JE, Marmot MG 1992 Relationship of glucose intolerance and hyperinsulinemia to body fat pattern in south Asians and Europeans. Diabetologia 35:785–791[Medline]
  25. McKeigue PM, Shah B, Marmot MG 1991 Relation of central obesity and insulin resistance with high diabetes prevalence and cardiovascular risk in South Asians. Lancet 337:382–386[CrossRef][Medline]
  26. Abate N, Garg A, Peshock RM, Stray-Gundersen J, Grundy SM 1995 Relationships of generalized and regional adiposity to insulin sensitivity in men. J Clin Invest 96:88–98
  27. McLaughlin T, Abbasi F, Lamendola C, Liang L, Reaven G, Schaaf P, Reaven P 2002 Differentiation between obesity and insulin resistance in the association with C-reactive protein. Circulation 106:2908–2912[Abstract/Free Full Text]
  28. Grimble RF 2002 Inflammatory status and insulin resistance. Curr Opin Clin Nutr Metab Care 5:551–559[CrossRef][Medline]
  29. Yudkin JS, Stehouwer CD, Emeis JJ, Coppack SW 1999 C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol 19:972–978[Abstract/Free Full Text]
  30. Festa A, D’Agostino Jr R, Howard G, Mykkanen L, Tracy RP, Haffner SM 2000 Chronic subclinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS). Circulation 102:42–47[Abstract/Free Full Text]



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