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Obesity affects blacks, whites differently in prediabetes
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Modestly severe obesity has differential effects on the pathogenic mechanisms underlying glucose homeostasis and atherogenesis in Americans of white and black ethnicities with prediabetes, according to research published in Diabetes Care.
“We conclude that the regulation of glucose homeostasis and lipid/lipoprotein metabolism appears to differ in modestly severely obese African Americans and white Americans with prediabetes,” the researchers wrote.
Sara J. Healy, MD, of the Wexner Medical Center, The Ohio State University, and colleagues assessed 145 adults with prediabetes (mean age, 46.5 ± 11.2 years; mean BMI, 37.8 ± 6.3 kg/m2), including 61 whites and 84 blacks.
The investigators measured fasting levels of lipids, lipoproteins, inflammatory marker C-reactive protein (CRP), HDL functionality, oxidized LDL, adiponectin and interleukin-6; serum levels of glucose, insulin and C-peptide were measure during an oral glucose tolerance test.
The researchers obtained values for insulin sensitivity index, glucose effectiveness index, glucose effectiveness at zero insulin (GEZI) and acute insulin response to glucose (AIRg) through a frequently sampled IV glucose tolerance test, using MINMOD software.
Mean levels of fasting and incremental serum glucose, insulin and C-peptide were generally higher in whites than blacks. Mean Si did not differ in whites compared with blacks (2.6 ± 2.3 vs. 2.9 ± 3 x 10-4 x min-1 [µU/mL]-1)
Mean values for AIRg and disposition index, along with glucose effectiveness index and GEZI, were lower in whites than blacks. Higher serum triglyceride levels were also observed in whites vs. blacks (116.1 ± 55.5 mg/dL vs. 82.7 ± 44.2 mg/dL; P = .0002).
No significant differences were demonstrated between whites and blacks for mean levels of apolipoprotein A-I, HDL cholesterol, paraoxonase 1, oxidized LDL, CRP, adiponectin and IL-6.
“Longitudinal studies of underlying putative mechanisms and molecular targets for glucose homeostasis, lipid/lipoprotein metabolism, and HDL functionality in a large sample of obese African Americans and white Americans are warranted,” the researchers wrote.
Disclosure: The researchers report no relevant financial disclosures.
Perspective
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Stephen A. Brietzke, MD, FACP, FACE
The paper by Healy and colleagues identifying differences between white and African-Americans is interesting in that it seems to associate more severe insulin resistance in whites and, by comparison, more severe insulin secretory defect in African-Americans, during the prediabetes phase of dysglycemia. By contrast, measurable dyslipidemia (low HDLc and hypertriglyceridemia) was less frequent in African-Americans, in this study.
It is probable that ethnicity correlates with multiple genetic traits linked to insulin response, innate susceptibility or resistance to metabolic insults such as oxidative stress, endothelial dysfunction and glucolipotoxicity, and that like type 2 diabetes, prediabetes is a heterogeneous group of disorders characterized by measurable final common pathways to abnormal fasting and postprandial glucose.
The observations of the paper are undercut a bit by reporting mean fasting glucose below 100 mg/dL and mean HbA1c below 5.4% in the white group, as these levels are below the syndrome-defining cut points of fasting glucose between 100 and 125 mg/dl and HbA1c between 5.7% and 6.4%.
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