Skip to main content
  • More from ADA
    • Diabetes
    • Clinical Diabetes
    • Diabetes Spectrum
    • ADA Standards of Medical Care
    • ADA Scientific Sessions Abstracts
    • BMJ Open Diabetes Research & Care
  • Subscribe
  • Log in
  • Log out
  • My Cart
  • Follow ada on Twitter
  • RSS
  • Visit ada on Facebook
Diabetes Care

Advanced Search

Main menu

  • Home
  • Current
    • Current Issue
    • Online Ahead of Print
    • Special Article Collections
    • ADA Standards of Medical Care
  • Browse
    • By Topic
    • Issue Archive
    • Saved Searches
    • Special Article Collections
    • ADA Standards of Medical Care
  • Info
    • About the Journal
    • About the Editors
    • ADA Journal Policies
    • Instructions for Authors
    • Guidance for Reviewers
  • Reprints/Reuse
  • Advertising
  • Subscriptions
    • Individual Subscriptions
    • Institutional Subscriptions and Site Licenses
    • Access Institutional Usage Reports
    • Purchase Single Issues
  • Alerts
    • E­mail Alerts
    • RSS Feeds
  • Podcasts
    • Diabetes Core Update
    • Special Podcast Series: Therapeutic Inertia
    • Special Podcast Series: Influenza Podcasts
    • Special Podcast Series: SGLT2 Inhibitors
    • Special Podcast Series: COVID-19
  • Submit
    • Submit a Manuscript
    • Journal Policies
    • Instructions for Authors
    • ADA Peer Review
  • More from ADA
    • Diabetes
    • Clinical Diabetes
    • Diabetes Spectrum
    • ADA Standards of Medical Care
    • ADA Scientific Sessions Abstracts
    • BMJ Open Diabetes Research & Care

User menu

  • Subscribe
  • Log in
  • Log out
  • My Cart

Search

  • Advanced search
Diabetes Care
  • Home
  • Current
    • Current Issue
    • Online Ahead of Print
    • Special Article Collections
    • ADA Standards of Medical Care
  • Browse
    • By Topic
    • Issue Archive
    • Saved Searches
    • Special Article Collections
    • ADA Standards of Medical Care
  • Info
    • About the Journal
    • About the Editors
    • ADA Journal Policies
    • Instructions for Authors
    • Guidance for Reviewers
  • Reprints/Reuse
  • Advertising
  • Subscriptions
    • Individual Subscriptions
    • Institutional Subscriptions and Site Licenses
    • Access Institutional Usage Reports
    • Purchase Single Issues
  • Alerts
    • E­mail Alerts
    • RSS Feeds
  • Podcasts
    • Diabetes Core Update
    • Special Podcast Series: Therapeutic Inertia
    • Special Podcast Series: Influenza Podcasts
    • Special Podcast Series: SGLT2 Inhibitors
    • Special Podcast Series: COVID-19
  • Submit
    • Submit a Manuscript
    • Journal Policies
    • Instructions for Authors
    • ADA Peer Review
Epidemiology/Health Services Research

Understanding the High Prevalence of Diabetes in U.S. South Asians Compared With Four Racial/Ethnic Groups: The MASALA and MESA Studies

  1. Alka M. Kanaya1⇑,
  2. David Herrington2,
  3. Eric Vittinghoff1,
  4. Susan K. Ewing1,
  5. Kiang Liu3,
  6. Michael J. Blaha4,
  7. Swapna S. Dave3,
  8. Fareeha Qureshi1 and
  9. Namratha R. Kandula3
  1. 1University of California, San Francisco, San Francisco, CA
  2. 2Wake Forest University Medical Center, Winston-Salem, NC
  3. 3Northwestern University, Chicago, IL
  4. 4Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD
  1. Corresponding author: Alka M. Kanaya, alka.kanaya{at}ucsf.edu.
Diabetes Care 2014 Jun; 37(6): 1621-1628. https://doi.org/10.2337/dc13-2656
PreviousNext
  • Article
  • Figures & Tables
  • Info & Metrics
  • PDF
Loading

Abstract

OBJECTIVE We compared South Asians with four other racial/ethnic groups in the U.S. to determine whether sociodemographic, lifestyle, or metabolic factors could explain the higher diabetes prevalence and whether insulin resistance and β-cell dysfunction occurred at younger ages and/or lower adiposity levels compared with other groups.

RESEARCH DESIGN AND METHODS We performed a cross-sectional analysis of two community-based cohorts, the Mediators of Atherosclerosis in South Asians Living in America (MASALA) study and the Multi-Ethnic Study of Atherosclerosis (MESA); all participants had no known cardiovascular disease and were between 44 and 84 years of age. We compared 799 South Asians with 2,611 whites, 1,879 African Americans, 1,493 Latinos, and 801 Chinese Americans. Type 2 diabetes was classified by fasting plasma glucose ≥126 mg/dL or use of a diabetes medication. Insulin resistance was estimated by the homeostasis model assessment (HOMA) and β-cell function was measured by the HOMA-β model.

RESULTS South Asians had significantly higher age-adjusted prevalence of diabetes (23%) than the MESA ethnic groups (6% in whites, 18% in African Americans, 17% in Latinos, and 13% in Chinese Americans). This difference increased further after adjustment for potential confounders. HOMA of insulin resistance (HOMA-IR) levels were significantly higher and HOMA-β levels were lower among South Asians compared with all other racial/ethnic groups after adjustment for age and adiposity.

CONCLUSIONS The higher prevalence of diabetes in South Asians is not explained by traditionally measured risk factors. South Asians may have lower β-cell function and an inability to compensate adequately for higher glucose levels from insulin resistance.

Introduction

The prevalence of type 2 diabetes is increasing worldwide, with lifestyle and behavioral factors promoting obesity cited as the primary culprit (1). South Asians, including individuals originating from India, Pakistan, Nepal, Sri Lanka, and Bangladesh, have a very high prevalence of diabetes (2,3), and the South Asian subcontinent is forecast to have the greatest burden of diabetes worldwide by 2030 (4,5). Insulin resistance and abnormalities of insulin secretion in pancreatic β-cells are the main defects that lead to type 2 diabetes. South Asians have high rates of insulin resistance (6,7), but more recent studies have shown that South Asians may have an early decline in β-cell function as well (8,9), a phenomenon with more genetic underpinnings (10).

In a pilot study of a community-based population of Asian Indians, we previously reported that the prevalence of diabetes was higher than in other U.S. ethnic groups (11). Here we report the prevalence of impaired fasting glucose (IFG) and diabetes in a larger community-based South Asian population called the Mediators of Atherosclerosis in South Asians Living in America (MASALA) study. The MASALA study was created with similar methods and measurements as the Multi-Ethnic Study of Atherosclerosis (MESA) to make valid and efficient cross-ethnic comparisons (12). We sought to determine whether this higher diabetes prevalence in South Asians was explained by lifestyle factors, adiposity measures, or other metabolic covariates, including fasting insulin. We also examined the effect of age and adiposity on insulin resistance and β-cell function in South Asians compared with the four MESA racial/ethnic groups.

Research Design and Methods

MASALA Study Design and Setting

The MASALA study is a community-based cohort of South Asian men and women from two clinical sites (San Francisco Bay Area at the University of California, San Francisco [UCSF], and the greater Chicago area at Northwestern University [NWU]). The baseline examination was conducted from October 2010 through March 2013. The institutional review boards of UCSF and NWU approved the MASALA study protocol.

Eligibility Criteria

Study methods have been previously reported (12). In brief, to be eligible for the MASALA study, participants had to 1) self-identify to be of South Asian origin and have at least three grandparents born in one of the following countries: India, Pakistan, Bangladesh, Nepal, or Sri Lanka; 2) be between 40 and 84 years of age; and 3) have the ability to speak and/or read English, Hindi, or Urdu. We used identical exclusion criteria to MESA (13), which included having a physician-diagnosed heart attack, stroke, or transient ischemic attack, heart failure, angina, or use of nitroglycerin or those with a history of cardiovascular procedures such as coronary artery bypass graft surgery, angioplasty, valve replacement, pacemaker or defibrillator implantation, or any surgery on the heart or arteries. Those with current atrial fibrillation or in active treatment for cancer were excluded. Those with life expectancy <5 years due to a serious medical illness, with impaired cognitive ability as judged by the reviewer, planning to move out of the study region in the next 5 years, or living in a nursing home or on a waiting list were also excluded. Due to computed tomography scanner limitations, those weighing >300 lbs were excluded.

Clinical Measurements

All visits were conducted by trained bilingual study staff, and all consent forms were translated into Hindi and Urdu. We gathered information on participant demographic data, tobacco use, alcohol consumption, and medication use. Intentional exercise in metabolic equivalents (MET)-minutes per week was assessed using the Typical Week’s Physical Activity Questionnaire (14).

Seated resting blood pressure was measured three times using an automated blood pressure monitor (V100 Vital Signs Monitor; GE Medical Systems, Fairfield, CT), and the average of the last two readings was used for analysis. Hypertension was defined as self-reported treatment for hypertension or a systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg. Participant weight was measured on a standard balance beam scale or digital weighing scale and height using a stadiometer, and BMI was calculated as weight in kilograms divided by height in meters squared. Waist circumference was measured using a flexible tape measure tape at the site of maximum circumference midway between the lower ribs and the anterior superior iliac spine.

After a requested 12-h fast, blood tests were obtained. Fasting plasma glucose was measured by the glucose oxidase method; total cholesterol, triglycerides, and HDL cholesterol were measured by enzymatic methods (Quest, San Jose, CA, and Chicago, IL) and LDL cholesterol was calculated (15). Diabetes was classified if a participant was using a glucose-lowering medication or had a fasting plasma glucose ≥126 mg/dL. IFG was defined for those with fasting glucose between 100 and 125 mg/dL, and normal glucose was <100 mg/dL (16). Fasting serum samples were batched for insulin measured by the sandwich immunoassay method (Roche Elecsys 2010; Roche Diagnostics, Indianapolis, IN). The homeostasis model assessment of insulin resistance (HOMA-IR) was used to measure insulin resistance and calculated as insulin0 (µIU/mL) × glucose0 (mmol/L)/22.5, and HOMA-β was used to measure β-cell function and was calculated as 20 × insulin0 (µIU/mL)/glucose0 (mmol/L) − 3.5 (17). Individuals taking diabetes medications were excluded from the analyses of HOMA-IR and HOMA-β due to bias in the measurement with treatment effects.

MESA Study Methods

The study design, eligibility, and methods for MESA have been previously published (13). MESA includes individuals from four racial/ethnic groups (whites, African Americans, Latinos, and Chinese Americans). We used data from the baseline MESA examination (2000–2002) for this analysis. Identical questionnaires for sociodemographic characteristics and physical activity and protocols for seated blood pressure and anthropometry were used as described above for the MASALA study.

Serum glucose was measured from fasting samples by the glucose oxidase method (Ortho Clinical Diagnostics, Johnson & Johnson). Serum insulin was measured from baseline samples with the Beckman Access assay. To harmonize this insulin assay with newer-generation assays with the Roche Elecsys assay that were used in future MESA exams (as well as the MASALA study), a calibration study was performed to calculate a formula for serum insulin values that correlated with the Roche method. The calibration formula is as follows: calibrated insulin = 1.656 + [0.208 × (Beckman Access assay result × 6)].

Similar definitions were used for diabetes, impaired and normal fasting glucose, and HOMA-IR and HOMA-β. We excluded six MESA participants from this analysis who had fasting glucose levels <64 mg/dL and were not taking diabetes medications since HOMA-β could not be calculated.

To have a similar age range of participants from both the MASALA and MESA studies, individuals in the MASALA study <44 years of age were excluded from this analysis, leaving a total of 799 South Asians who were compared with the four MESA racial/ethnic groups (2,611 whites, 1,879 African Americans, 1,493 Latinos, and 801 Chinese Americans).

Statistical Analyses

Baseline characteristics of the MASALA participants and each of the MESA racial/ethnic groups were summarized using descriptive statistics as appropriate. The crude, age-/site-/sex-adjusted, and fully adjusted prevalence of normal, IFG, and diabetes within each race/ethnicity and for each sex was estimated using multinomial logistic regression models, followed by regression standardization (18). Fully adjusted models included age, sex, clinical site, educational attainment, family income, current smoking, alcohol use, exercise, BMI, waist circumference, HDL cholesterol, triglycerides, hypertension, and fasting insulin. We purposely did not adjust for HOMA-IR or HOMA-β because fasting glucose is a common component of these surrogate measures and the outcome of this analysis, complicating interpretation.

Average HOMA-IR and HOMA-β levels for each racial/ethnic group were estimated using linear models adjusting for age, sex, site, BMI, waist circumference, fasting glucose, smoking status, physical activity levels, and alcohol use. Because HOMA-IR and HOMA-β are right skewed, these measures were log transformed for analysis, and then the results were back transformed to the measured scale. Linear models adjusting for site and sex were also used to examine the association between the HOMA measures and age among participants not using diabetes medications within each racial/ethnic group. Specifically, we regressed log-transformed HOMA values on a three-knot restricted cubic spline in age and then plotted the back-transformed fitted values against age. We also used this approach to examine the associations between HOMA and BMI and waist circumference, by race/ethnicity and then by sex, adjusting for age and site. Tests for interaction were used to determine whether the associations between HOMA and age, BMI, and waist circumference differed by race/ethnicity or sex. Scatter plots were used to assess the potential influence of outliers.

All analyses were conducted in SAS version 9.3 (SAS Institute, Cary, NC) and Stata version 12.1 (Stata Corporation, College Station, TX).

Results

Table 1 shows the baseline characteristics of the MASALA and MESA participants by racial/ethnic group. South Asians were significantly younger than the MESA groups and had higher educational attainment and family income and less current tobacco use. South Asians also had lower physical activity levels than all of the MESA groups. The Chinese Americans had the lowest mean BMI and waist circumference, followed by the South Asians, whites, and Latinos, with African Americans having the highest BMI. South Asians had higher fasting median glucose and insulin values, higher HOMA-IR, lower HOMA-β, higher diabetes medication use, and significantly higher prevalence of IFG (24%) and diabetes (21%) than all four MESA racial/ethnic groups.

View this table:
  • View inline
  • View popup
  • Download powerpoint
Table 1

Baseline characteristics of MASALA and MESA participants by race/ethnicity

Table 2 shows the prevalence of diabetes comparing South Asians to each of the MESA racial/ethnic groups overall and by sex. After adjusting for age, sex, and study site, there was a larger difference in diabetes prevalence between the South Asians (23%) and the other groups. Further adjustment for potential explanatory variables that could explain the association between race/ethnicity and diabetes, including education, family income, smoking, alcohol use, exercise, BMI, waist circumference, HDL, triglycerides, hypertension, and fasting insulin, increased the adjusted prevalence of diabetes in South Asians (27%) and widened the differences between South Asians and each racial/ethnic group. In sex-stratified analyses, South Asian men had a significantly higher prevalence of IFG and diabetes than men and women in all other ethnic groups. In unadjusted analyses, South Asian women had a significantly higher prevalence of IFG than women in other ethnic groups, but had a similar prevalence of diabetes compared with African American, Latino, and Chinese American women. In fully adjusted analyses for women, South Asian women had a higher diabetes prevalence compared with all other groups except for African Americans. Within each racial/ethnic group, after full covariate adjustment, men had a significantly higher diabetes prevalence compared with women.

View this table:
  • View inline
  • View popup
  • Download powerpoint
Table 2

Prevalence of IFG and diabetes in five ethnic groups with sequential adjustment for covariates, MASALA and MESA studies

Figure 1 displays the adjusted medians for HOMA-IR and HOMA-β by racial/ethnic group among participants who were not taking diabetes medications. South Asians had a higher HOMA-IR and lower HOMA-β compared with the other racial/ethnic groups, and this difference persisted after adjusting for their main determinants, including fasting glucose value. The only adjusted interethnic comparison that was not significantly different was between South Asians and Chinese Americans for HOMA-IR outcome. Figure 2 shows the spline curves for insulin resistance (A) and β-cell function (B) over the age distribution for each racial/ethnic group, adjusted for sex and clinical site. Race/ethnicity significantly modified the association between age and insulin resistance (P for interaction =0.001), but the association between age and HOMA-β was similar for each racial/ethnic group (P for interaction =0.27). Additionally, in all ethnic groups, the association between age and HOMA-IR was stronger in men than in women (P for interaction =0.02). In contrast, although South Asians had the lowest levels of HOMA-β compared with all other groups, the gradual decline in β-cell function by age was common to all racial/ethnic groups and to both men and women.

Figure 1
  • Download figure
  • Open in new tab
  • Download powerpoint
Figure 1

Median (95% CI) HOMA-IR and HOMA-β values adjusted by sex, age, clinical site, fasting glucose level, BMI, waist circumference, physical activity levels, smoking, and alcohol use; excludes those on any diabetes medications; the MASALA and MESA studies. *P < 0.001 in comparison to South Asians.

Figure 2
  • Download figure
  • Open in new tab
  • Download powerpoint
Figure 2

Association between age and insulin resistance (A) and β-cell function (B) in the five racial/ethnic groups adjusted for sex and clinical site; excludes those on any diabetes medications; the MASALA and MESA studies.

The association between BMI and HOMA-IR showed a log-linear relationship in most racial/ethnic groups, but South Asians had a distinct nonlinear pattern, with faster increases in HOMA-IR in the region with BMI <30 kg/m2 but slower increases above that level (P for interaction <0.001) (Fig. 3A). On average, the trend in HOMA-IR was steepest for Chinese Americans. HOMA-β was lowest among South Asians at any given BMI (P for interaction <0.001) (Fig. 3B), and on average, the trend was steepest among Chinese Americans. These relationships were more significant in men than women in all racial/ethnic groups (P for interaction by sex <0.001). Plotting HOMA-IR and HOMA-β against waist circumference revealed similar results in the four MESA ethnic groups but somewhat different patterns in the South Asians (Fig. 3, lower panels). In particular, trends among South Asians in both metabolic measures accelerated across the range of waist circumference, in contrast to their decelerating trends in the region with BMI >30 kg/m2.

Figure 3
  • Download figure
  • Open in new tab
  • Download powerpoint
Figure 3

Association between BMI (A and B) and waist circumference (C and D) with insulin resistance (left panels) and β-cell function (right panels); adjusted for sex, age, and site; excludes those on any diabetes medications; MASALA and MESA studies. P for interaction <0.001 for each figure.

Conclusions

In a large community-based sample of South Asians without existing cardiovascular disease, we confirmed that South Asians have a significantly higher prevalence of prediabetes and diabetes than four other U.S. ethnic groups (11). Additionally, South Asian men have the highest diabetes prevalence overall, whereas South Asian women have a higher diabetes prevalence than white and Chinese American women but a similar prevalence to African American and Latino women. The broad disparity in diabetes among South Asians compared with the other ethnic groups was further widened after adjusting for all potential correlates of diabetes. South Asians have higher HOMA-IR levels and lower HOMA-β than all other ethnic groups after adjusting for age and adiposity. These findings suggest that South Asians may have lower β-cell function and are unable to compensate for higher glucose levels due to insulin resistance, which ultimately leads to the dramatically higher rates of type 2 diabetes.

South Asians are known for having high type 2 diabetes prevalence in native (19,20) and diaspora settings (2,21,22). Studies that have directly compared diabetes prevalence in South Asians with other ethnic groups in North America have found higher diabetes rates among South Asians than most other ethnic groups (23–25). Similarly, we found that middle- to older-aged South Asians in the U.S. with higher socioeconomic attainment than South Asians living in other Western countries still have a significantly higher IFG and diabetes prevalence compared with four other ethnic groups. Adjusting for sociodemographic, lifestyle, and metabolic covariates only enhanced the difference between South Asians and other ethnic groups, suggesting that other unmeasured factors, including biologic differences in the mechanisms of diabetes and a higher genetic burden (26), may be responsible.

We compared insulin resistance patterns by age and adiposity and found that South Asians have higher HOMA-IR levels compared with other ethnic groups. Although no prior studies have compared as many ethnic groups directly with South Asians, several have reported that South Asians have higher basal insulin levels and a higher insulin response to a glucose load than Europeans (27) and Chinese (28–30). Moreover, studies have found that a higher percentage of body fat and abdominal adiposity in South Asians (31) does not appear to explain these high levels of insulin resistance (32,33).

We also found that South Asians have lower β-cell function at all ages than other ethnic groups, although the decline with age appears to be similar to other groups. Whereas others have found reduced β-cell function in Asian Indians (9), others have noted that β-cell function declines more rapidly with age in Asian Indians than other ethnic groups (28). It is unclear whether there may be a genetic predisposition to lower β-cell mass and function, earlier β-cell loss from environmental factors, or quicker β-cell exhaustion from higher levels of insulin resistance or a complex combination of all of these factors among South Asians (34).

There was a notable difference in the spline curves between BMI and waist circumference for both HOMA-IR and HOMA-β that was observed only among South Asians. Increases in HOMA-IR and HOMA-β plateau in the region above BMI of 30 kg/m2, whereas both measures continue to increase across the range of waist circumference values. This inconsistency in the associations between these two surrogate measures of body adiposity may be due to sparse data with few South Asians having BMI >30 kg/m2, but also underscores the findings of early studies where central adiposity was much more closely linked to insulin resistance and diabetes than BMI in South Asians (35). This finding also provides further evidence that for assessing metabolic risk, waist circumference is a better measure of adiposity than BMI among South Asians.

Although we were able to compare glycemic status between South Asians and four other well-phenotyped U.S. ethnic groups, we were limited to using fasting glucose and insulin measures and did not have more sophisticated measures of insulin resistance or β-cell function. The cross-sectional design also limits us from comparing the relative strengths of insulin resistance or β-cell function as risk factors for diabetes. We also did not have comparable measures of dietary intake in both studies and were unable to determine whether diet may explain some of the ethnic differences in diabetes prevalence. Although the South Asians in MASALA are representative of middle-aged South Asians in the U.S. (12), the findings may not generalize to all South Asians in native or other diaspora settings with very different socioeconomic and environmental exposure.

In conclusion, South Asians have a significantly higher prediabetes and diabetes prevalence than other U.S. ethnic groups, which is not explained by known risk factors. South Asians have significantly higher insulin resistance and lower β-cell function than other ethnic groups. The biological and genetic mechanisms underlying these differences deserve further study. Prospective follow-up of the MASALA study cohort can assess whether insulin resistance and β-cell function explain the higher diabetes rates in South Asians.

Article Information

Funding. The MASALA study was supported by the National Institutes of Health (NIH) Grant 1R01-HL-093009. Data collection at UCSF was also supported by NIH/National Center for Research Resources UCSF-CTSI Grant UL1-RR-024131. The MESA study was funded by contracts N01-HC-95159, N01-HC-95169, and N01-HC-95166 from the National Heart, Lung, and Blood Institute.

The sponsors for both studies did not play a significant role in the analysis, interpretation, and presentation of these results.

Duality of Interest. No potential conflicts of interest relevant to this article were reported.

Author Contributions. A.M.K. conceived the project, researched data, and wrote the manuscript. D.H. contributed to the interpretation of the results and reviewed and edited the manuscript. E.V. supervised and contributed to the data analyses and reviewed and edited the manuscript. S.K.E. performed the data analysis and reviewed and edited the manuscript. K.L. and M.J.B. reviewed and edited the manuscript. S.S.D. and F.Q. collected data and reviewed and edited the manuscript. N.R.K. contributed to the interpretation of the results and reviewed and edited the manuscript. A.M.K. is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Prior Presentation. This study was presented as a moderated poster at the American Heart Association Epidemiology and Prevention/Nutrition, Physical Activity, and Metabolism 2014 Scientific Sessions, San Francisco, CA, 18–21 March 2014.

  • Received November 13, 2013.
  • Accepted February 5, 2014.
  • © 2014 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

References

  1. ↵
    1. Hu FB
    . Globalization of diabetes: the role of diet, lifestyle, and genes. Diabetes Care 2011;34:1249–1257pmid:21617109
    OpenUrlAbstract/FREE Full Text
  2. ↵
    1. Misra R,
    2. Patel T,
    3. Kotha P,
    4. et al
    . Prevalence of diabetes, metabolic syndrome, and cardiovascular risk factors in US Asian Indians: results from a national study. J Diabetes Complications 2009; 24:145–153pmid:19303333
    OpenUrlCrossRefPubMed
  3. ↵
    1. Nair M,
    2. Ali MK,
    3. Ajay VS,
    4. et al
    . CARRS Surveillance study: design and methods to assess burdens from multiple perspectives. BMC Public Health 2012;12:701pmid:22928740
    OpenUrlCrossRefPubMed
  4. ↵
    1. Shaw JE,
    2. Sicree RA,
    3. Zimmet PZ
    . Global estimates of the prevalence of diabetes for 2010 and 2030. Diabetes Res Clin Pract 2010;87:4–14pmid:19896746
    OpenUrlCrossRefPubMedWeb of Science
  5. ↵
    1. Wild S,
    2. Roglic G,
    3. Green A,
    4. Sicree R,
    5. King H
    . Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care 2004;27:1047–1053pmid:15111519
    OpenUrlAbstract/FREE Full Text
  6. ↵
    McKeigue PM. Metabolic consequences of obesity and body fat pattern: lessons from migrant studies. Ciba Found Symp 1996;201:54–64; discussion 64–67, 188–193
  7. ↵
    1. Gujral UP,
    2. Pradeepa R,
    3. Weber MB,
    4. Narayan KM,
    5. Mohan V
    . Type 2 diabetes in South Asians: similarities and differences with white Caucasian and other populations. Ann N Y Acad Sci 2013;1281:51–63pmid:23317344
    OpenUrlCrossRefPubMed
  8. ↵
    1. Mohan V,
    2. Amutha A,
    3. Ranjani H,
    4. et al
    . Associations of β-cell function and insulin resistance with youth-onset type 2 diabetes and prediabetes among Asian Indians. Diabetes Technol Ther 2013;15:315–322pmid:23484483
    OpenUrlCrossRefPubMed
  9. ↵
    1. Staimez LR,
    2. Weber MB,
    3. Ranjani H,
    4. et al
    . Evidence of reduced β-cell function in Asian Indians with mild dysglycemia. Diabetes Care 2013;36:2772–2778pmid:23596180
    OpenUrlAbstract/FREE Full Text
  10. ↵
    1. Florez JC
    . Newly identified loci highlight beta cell dysfunction as a key cause of type 2 diabetes: where are the insulin resistance genes? Diabetologia 2008;51:1100–1110pmid:18504548
    OpenUrlCrossRefPubMedWeb of Science
  11. ↵
    1. Kanaya AM,
    2. Wassel CL,
    3. Mathur D,
    4. et al
    . Prevalence and correlates of diabetes in South Asian Indians in the United States: findings from the Metabolic Syndrome and Atherosclerosis in South Asians Living in America study and the Multi-Ethnic Study of Atherosclerosis. Metab Syndr Relat Disord 2010;8:157–164pmid:19943798
    OpenUrlCrossRefPubMed
  12. ↵
    1. Kanaya AM,
    2. Kandula N,
    3. Herrington D,
    4. et al
    . Mediators of Atherosclerosis in South Asians Living in America (MASALA) Study: objectives, methods, and cohort description. Clin Cardiol. 5 November 2013 [Epub ahead of print]pmid:24194499
    OpenUrlPubMed
  13. ↵
    1. Bild DE,
    2. Bluemke DA,
    3. Burke GL,
    4. et al
    . Multi-ethnic study of atherosclerosis: objectives and design. Am J Epidemiol 2002;156:871–881pmid:12397006
    OpenUrlAbstract/FREE Full Text
  14. ↵
    1. Ainsworth BE,
    2. Irwin ML,
    3. Addy CL,
    4. Whitt MC,
    5. Stolarczyk LM
    . Moderate physical activity patterns of minority women: the Cross-Cultural Activity Participation Study. J Womens Health Gend Based Med 1999;8:805–813pmid:10495261
    OpenUrlCrossRefPubMedWeb of Science
  15. ↵
    1. Friedewald WTLR,
    2. Levy RI,
    3. Fredrickson DS
    . Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972;18:499–502pmid:4337382
    OpenUrlAbstract/FREE Full Text
  16. ↵
    1. American Diabetes Association
    . Diagnosis and classification of diabetes mellitus. Diabetes Care 2004;27(Suppl. 1):S5–S10pmid:14693921
    OpenUrlCrossRefPubMed
  17. ↵
    1. Matthews DR,
    2. Hosker JP,
    3. Rudenski AS,
    4. Naylor BA,
    5. Treacher DF,
    6. Turner RC
    . Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985;28:412–419pmid:3899825
    OpenUrlCrossRefPubMedWeb of Science
  18. ↵
    1. Lane PW,
    2. Nelder JA
    . Analysis of covariance and standardization as instances of prediction. Biometrics 1982;38:613–621pmid:7171691
    OpenUrlCrossRefPubMedWeb of Science
  19. ↵
    1. Mohan V,
    2. Deepa M,
    3. Deepa R,
    4. et al
    . Secular trends in the prevalence of diabetes and impaired glucose tolerance in urban South India—the Chennai Urban Rural Epidemiology Study (CURES-17). Diabetologia 2006;49:1175–1178pmid:16570158
    OpenUrlCrossRefPubMedWeb of Science
  20. ↵
    1. Ramachandran A,
    2. Mary S,
    3. Yamuna A,
    4. Murugesan N,
    5. Snehalatha C
    . High prevalence of diabetes and cardiovascular risk factors associated with urbanization in India. Diabetes Care 2008;31:893–898pmid:18310309
    OpenUrlAbstract/FREE Full Text
  21. ↵
    1. Tillin T,
    2. Hughes AD,
    3. Godsland IF,
    4. et al
    . Insulin resistance and truncal obesity as important determinants of the greater incidence of diabetes in Indian Asians and African Caribbeans compared with Europeans: the Southall And Brent REvisited (SABRE) cohort. Diabetes Care 2013;36:383–393pmid:22966089
    OpenUrlAbstract/FREE Full Text
  22. ↵
    1. Bhopal R,
    2. Hayes L,
    3. White M,
    4. et al
    . Ethnic and socio-economic inequalities in coronary heart disease, diabetes and risk factors in Europeans and South Asians. J Public Health Med 2002;24:95–105pmid:12141592
    OpenUrlAbstract/FREE Full Text
  23. ↵
    1. Karter AJ,
    2. Schillinger D,
    3. Adams AS,
    4. et al
    . Elevated rates of diabetes in Pacific Islanders and Asian subgroups: the Diabetes Study of Northern California (DISTANCE). Diabetes Care 2013;36:574–579pmid:23069837
    OpenUrlAbstract/FREE Full Text
    1. Lee JW,
    2. Brancati FL,
    3. Yeh HC
    . Trends in the prevalence of type 2 diabetes in Asians versus whites: results from the United States National Health Interview Survey, 1997-2008. Diabetes Care 2011;34:353–357pmid:21216863
    OpenUrlAbstract/FREE Full Text
  24. ↵
    1. Anand SS,
    2. Yusuf S,
    3. Vuksan V,
    4. et al
    . 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 2000;356:279–284pmid:11071182
    OpenUrlCrossRefPubMedWeb of Science
  25. ↵
    1. Khan NA,
    2. Wang H,
    3. Anand S,
    4. et al
    . Ethnicity and sex affect diabetes incidence and outcomes. Diabetes Care 2011;34:96–101pmid:20978094
    OpenUrlAbstract/FREE Full Text
  26. ↵
    1. Mohan V,
    2. Sharp PS,
    3. Cloke HR,
    4. Burrin JM,
    5. Schumer B,
    6. Kohner EM
    . Serum immunoreactive insulin responses to a glucose load in Asian Indian and European type 2 (non-insulin-dependent) diabetic patients and control subjects. Diabetologia 1986;29:235–237pmid:3519338
    OpenUrlCrossRefPubMedWeb of Science
  27. ↵
    1. Dowse GK,
    2. Qin H,
    3. Collins VR,
    4. Zimmet PZ,
    5. Alberti KG,
    6. Gareeboo H,
    7. The Mauritius NCD Study Group
    . Determinants of estimated insulin resistance and beta-cell function in Indian, Creole and Chinese Mauritians. Diabetes Res Clin Pract 1990;10:265–279pmid:2073874
    OpenUrlCrossRefPubMedWeb of Science
    1. Liew CF,
    2. Seah ES,
    3. Yeo KP,
    4. Lee KO,
    5. Wise SD
    . Lean, nondiabetic Asian Indians have decreased insulin sensitivity and insulin clearance, and raised leptin compared to Caucasians and Chinese subjects. Int J Obes Relat Metab Disord 2003;27:784–789pmid:12821962
    OpenUrlCrossRefPubMed
  28. ↵
    1. Hughes K,
    2. Aw TC,
    3. Kuperan P,
    4. Choo M
    . Central obesity, insulin resistance, syndrome X, lipoprotein(a), and cardiovascular risk in Indians, Malays, and Chinese in Singapore. J Epidemiol Community Health 1997;51:394–399pmid:9328546
    OpenUrlAbstract/FREE Full Text
  29. ↵
    1. Deurenberg P,
    2. Yap M,
    3. van Staveren WA
    . Body mass index and percent body fat: a meta analysis among different ethnic groups. Int J Obes Relat Metab Disord 1998;22:1164–1171pmid:9877251
    OpenUrlCrossRefPubMedWeb of Science
  30. ↵
    1. Chandalia M,
    2. Abate N,
    3. Garg A,
    4. Stray-Gundersen J,
    5. Grundy SM
    . Relationship between generalized and upper body obesity to insulin resistance in Asian Indian men. J Clin Endocrinol Metab 1999;84:2329–2335pmid:10404798
    OpenUrlCrossRefPubMedWeb of Science
  31. ↵
    1. Forouhi NG,
    2. Jenkinson G,
    3. Thomas EL,
    4. et al
    . Relation of triglyceride stores in skeletal muscle cells to central obesity and insulin sensitivity in European and South Asian men. Diabetologia 1999;42:932–935pmid:10491752
    OpenUrlCrossRefPubMedWeb of Science
  32. ↵
    1. Taylor R
    . Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause. Diabetologia 2008;51:1781–1789pmid:18726585
    OpenUrlCrossRefPubMedWeb of Science
  33. ↵
    1. McKeigue PM,
    2. Shah B,
    3. Marmot MG
    . Relation of central obesity and insulin resistance with high diabetes prevalence and cardiovascular risk in South Asians. Lancet 1991;337:382–386pmid:1671422
    OpenUrlCrossRefPubMedWeb of Science
PreviousNext
Back to top
Diabetes Care: 37 (6)

In this Issue

June 2014, 37(6)
  • Table of Contents
  • Table of Contents (PDF)
  • About the Cover
  • Index by Author
  • Masthead (PDF)
Sign up to receive current issue alerts
View Selected Citations (0)
Print
Download PDF
Article Alerts
Sign In to Email Alerts with your Email Address
Email Article

Thank you for your interest in spreading the word about Diabetes Care.

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Understanding the High Prevalence of Diabetes in U.S. South Asians Compared With Four Racial/Ethnic Groups: The MASALA and MESA Studies
(Your Name) has forwarded a page to you from Diabetes Care
(Your Name) thought you would like to see this page from the Diabetes Care web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
Understanding the High Prevalence of Diabetes in U.S. South Asians Compared With Four Racial/Ethnic Groups: The MASALA and MESA Studies
Alka M. Kanaya, David Herrington, Eric Vittinghoff, Susan K. Ewing, Kiang Liu, Michael J. Blaha, Swapna S. Dave, Fareeha Qureshi, Namratha R. Kandula
Diabetes Care Jun 2014, 37 (6) 1621-1628; DOI: 10.2337/dc13-2656

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Add to Selected Citations
Share

Understanding the High Prevalence of Diabetes in U.S. South Asians Compared With Four Racial/Ethnic Groups: The MASALA and MESA Studies
Alka M. Kanaya, David Herrington, Eric Vittinghoff, Susan K. Ewing, Kiang Liu, Michael J. Blaha, Swapna S. Dave, Fareeha Qureshi, Namratha R. Kandula
Diabetes Care Jun 2014, 37 (6) 1621-1628; DOI: 10.2337/dc13-2656
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • Abstract
    • Introduction
    • Research Design and Methods
    • Results
    • Conclusions
    • Article Information
    • References
  • Figures & Tables
  • Info & Metrics
  • PDF

Related Articles

Cited By...

More in this TOC Section

  • Comparisons of Polyexposure, Polygenic, and Clinical Risk Scores in Risk Prediction of Type 2 Diabetes
  • Quantifying Variation in Treatment Utilization for Type 2 Diabetes Across Five Major University of California Health Systems
  • Trends in Total and Out-of-pocket Payments for Noninsulin Glucose-Lowering Drugs Among U.S. Adults With Large-Employer Private Health Insurance From 2005 to 2018
Show more Epidemiology/Health Services Research

Similar Articles

Navigate

  • Current Issue
  • Standards of Care Guidelines
  • Online Ahead of Print
  • Archives
  • Submit
  • Subscribe
  • Email Alerts
  • RSS Feeds

More Information

  • About the Journal
  • Instructions for Authors
  • Journal Policies
  • Reprints and Permissions
  • Advertising
  • Privacy Policy: ADA Journals
  • Copyright Notice/Public Access Policy
  • Contact Us

Other ADA Resources

  • Diabetes
  • Clinical Diabetes
  • Diabetes Spectrum
  • Scientific Sessions Abstracts
  • Standards of Medical Care in Diabetes
  • BMJ Open - Diabetes Research & Care
  • Professional Books
  • Diabetes Forecast

 

  • DiabetesJournals.org
  • Diabetes Core Update
  • ADA's DiabetesPro
  • ADA Member Directory
  • Diabetes.org

© 2021 by the American Diabetes Association. Diabetes Care Print ISSN: 0149-5992, Online ISSN: 1935-5548.