FRI660 Serum Lipids And Inflammatory Markers Reveal Race-associated Differences Between Diabetics And Non-diabetics

Disclosure: G. Pacheco Sanchez: None. M.L. Lopez: None. C. Jang: None. M.K. Evans: None. A.B. Zonderman: None. R. Kapadia: None. D.A. Nicholas: None. Health disparities (HD) disproportionately affect racial groups. One of the fastest growing HD worldwide with severe health consequences and high mortality rates is Type 2 Diabetes (T2D). T2D is an inflammatory disease associated with an increase in body mass index (BMI), a common obesity measurement, and clinically characterized by dysregulation of lipids or dyslipidemia. Reports suggest that compromised lipid metabolism can exacerbate chronic inflammation seen in T2D. Importantly, lipid metabolism can be impacted by systemic overabundance of lipids, a condition that has been reported to impact some racial groups, like African Americans (AA), in a disproportionate manner. Further, literature supports that elevated levels of inflammatory molecules correlate with excess of systemic lipids and impact the risk to develop T2D in AA women. Despite previous efforts, comprehensive biological information is still needed to determine the relationship of lipids and inflammation to the onset and/or progression of T2D. Here we show results from identified metabolic, and immunological features of serum and plasma samples derived from a cohort of AA and White individuals with and without T2D.Evaluation of clinical parameters related to metabolic state indicate that lipids measurements, such as blood concentrations of low-density cholesterol (LDL), high-density cholesterol (HDL), total cholesterol to HDL ratio, and triglycerides, are the main drivers of biological variability in our cohort, irrespective of diabetes status and race. Counterintuitively, Hemoglobin A1C and other glucose-related clinical standardized T2D measurements were not beneficial at addressing cohort variability. Based on results from our cytokine and chemokine analysis performed using a comprehensive 53-analytes Luminex panel we conclude that: : 1) Significant inflammatory molecules differences at a univariate level are seen when comparing AA and white in our total cohort, differences maintained irrespective of diabetes status; and 2) In a multivariate analysis, differential expression of a distinctive inflammatory cluster of cytokines and chemokines, composed of Eotaxin, IL6, IL18, IL27, IP10, MCP1, MDC and CXCL9, was identified between AA and whites, once again irrespective of diabetes status. Importantly, BMI had no major biological effect on any of the parameters we measured. Our results demonstrate a relation between lipids, not glucose, and the differential expression of inflammatory molecules, not conventionally reported for T2D, in a race-dependent manner. We anticipate this work to be the starting point for mechanistic studies addressing modulation of inflammatory responses by race-specific lipids profiles and components, for a better understanding of the immunometabolic contributors to HD. Presentation: Friday, June 16, 2023