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Interleukin-6, diabetes, and metabolic syndrome in a biracial cohort: the Reasons for Geographic and Racial Differences in Stroke cohort

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posted on 2024-01-18, 21:03 authored by Brittney J. Palermo, Katherine S. Wilkinson, Timothy B. Plante, Charles D. Nicoli, Suzanne E. Judd, Debora Kamin Mukaz, D. Leann Long, Nels C. Olson, Mary Cushman

Objective: Black Americans have a greater risk of type-2 diabetes than White Americans. The proinflammatory cytokine interleukin-6 (IL-6) is implicated in diabetes pathogenesis and is higher in Black people. This study investigated associations of IL-6 with incident diabetes and metabolic syndrome in a biracial cohort.

Research Design and Methods: The REasons for Geographic And Racial Differences in Stroke study enrolled 30,239 Black and White adults age 45+ in 2003-07, with a follow-up ~9.5 years later. Baseline plasma IL-6 was measured in 3,399 at risk for incident diabetes and 1,871 for metabolic syndrome. Modified Poisson regression estimated relative risk (RR) by IL-6 for both.

Results: Incident diabetes occurred in 14% and metabolic syndrome in 20%; both rose across IL-6 quartiles. There was a 3-way interaction of IL-6, race, and central adiposity for incident diabetes (p=8 x10-5). In Black participants with and without central adiposity RRs were 2.02 (95% CI 1.00-4.07) and 1.66 (1.00-2.75) for the 4th compared to 1st quartile of IL-6, respectively. The corresponding RRs were 1.73 (0.92-3.26) and 2.34 (1.17-4.66) in White participants. The pattern was similar for IL-6 and metabolic syndrome.

Conclusions: While IL-6 was higher in Black than White participants and those with central adiposity, associations of IL-6 with diabetes risk was only statistically significant among White participants without central adiposity. Associations with metabolic syndrome risk were similarly stronger in low-risk groups. Results support the concept of interventions to lower inflammation in diabetes prevention, but to reduce race disparities, better biomarkers are needed.

Funding

REGARDS is supported by cooperative agreement U01 NS041588 co-funded by the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (NIA), National Institutes of Health, Department of Health and Human Service. Additional support was from the Larner College of Medicine Dean’s Office (B.P.). This content is the sole responsibility of the authors and does not necessarily represent the official views of the National Institute of Neurological Disorders and Stroke, the National Institute of Health, the U.S. Department of Veterans Affairs, or the United States Government. We also appreciate the support and guidance of investigators from the Study Design and Molecular Epidemiology Core of the Vermont Center for Cardiovascular and Brain Health. Funding was provided by P20 GM135007 from the National Institute of General Medical Sciences (NIGMS) of NIH. Federal Employee Disclaimer (C.N.): The identification of specific products or scientific instrumentation is considered an integral part of the scientific endeavor and does not constitute endorsement or implied endorsement on the part of the author, Department of Defense (DoD), or any component agency. The views expressed in this manuscript are those of the author and do not reflect the official policy of the Department of Army/Navy/Air Force, DoD, or U.S. Government.

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