| Abstract
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Increasing evidence suggests that racial disparities in Type 2 Diabetes (T2D) may be associated with differences in body fat distribution. African-American women (AAW) tend to accumulate less visceral fat and more subcutaneous fat than Caucasian women (CAW) with similar body mass indexes (BMI). Recent studies in Pima Indians show that excessive subcutaneous fat may be linked with impaired adipocyte differentiation, which has been implicated in ectopic fat accumulation, deregulation of adipokines, and insulin resistance. Objective . A few studies show increased mid- thigh low density lean tissue (a marker of intramyocellular lipid (IMCL)) in AAW when compared to CAW. However, a racial difference in adipocyte differentiation in African-Americans has not been examined. Therefore the objective of this study was to determine if there were racial differences in adiopcyte differentiation in subcutaneous adipose tissue between a total of 58 obese, non-diabetic AAW and CAW with similar BMI. Research design and methods . We examined the expression of the following candidate genes: PPARγ2, AGPAT2, SCD1, FAT/CD36, ATGL, Lipin β, RBP4, and PEPCK via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). We also examined the expression of inflammatory genes that have been implicated in the inhibition of adipocyte differentiation: SPT-1, p65, IL-1β, and CD68 via qRT-PCR. Additionally, we measured racial differences in ectopic fat accumulation in skeletal muscle (IMCL) using oil Red O Sudan-type dye staining technique, a more direct method of assessment. Results . The principal findings of the study were that: (1) AAW had a lower expression of PPARγ (0.98 ± 0.06 vs. 1.20 ± 0.10) and PPARγ-regulated genes than CAW; (2) AAW had lower IMCL accumulation than CAW for Type I and II muscle fibers (p ≤ 0.05); and (3) there were no racial differences in the expression of inflammatory mediators between the two racial groups (p > 0.05). Conclusions . The findings from this study support a role for impaired adipocyte differentiation in subcutaneous fat as a potential risk factor in the development of T2D in AAW. Moreover, the data strongly suggest that there are important racial differences in lipid and glucose metabolism and that these differences must be further examined to improve disease diagnosis, treatment, and prevention for individuals of all ethnicities.
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