|Chung, Stephanie - National Institutes Of Health (NIH)|
|Matthan, Nirupa - Jean Mayer Human Nutrition Research Center On Aging At Tufts University|
|Galvan-de La Cruz, Mirella - National Institutes Of Health (NIH)|
|Onuzuruike, Anthony - National Institutes Of Health (NIH)|
|Kasturi, Kannan - National Institutes Of Health (NIH)|
|Mabundo, Lilian - National Institutes Of Health (NIH)|
|Gharib, Ahmed - National Institutes Of Health (NIH)|
|Lichtenstein, Alice - Jean Mayer Human Nutrition Research Center On Aging At Tufts University|
|Sumner, Anne - National Institutes Of Health (NIH)|
Submitted to: American Heart Association Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 8/8/2017
Publication Date: 11/14/2017
Citation: Chung, S.T., Matthan, N., Galvan-De La Cruz, M., Onuzuruike, A., Kasturi, K., Mabundo, L., Gharib, A., Lichtenstein, A.H., Sumner, A.E. 2017. RBC stearoyl-coA desaturase activity and the hepatic paradox in African descent women: the federal women's study [abstract]. American Heart Association's Scientific Sessions 2017. Abstract No. 16882.
Technical Abstract: In women of African descent, low hepatic fat is paradoxically related to insulin resistance and cardiovascular disease. The reasons for the race/ethnic difference in the relationship between hepatic fat and IR are unclear but could be related to lower hepatic de novo lipogenesis due to altered enzyme activity. Stearoyl-CoA desaturase (SCD-1) is a key regulator of hepatic lipogenesis. Red blood cell (RBC) phospholipid fatty acid profiles can be used to estimate SCD-1 activity, a surrogate marker of hepatic lipogenesis. To investigate the role of SCD-1 in mediating race/ethnic differences in hepatic fat accumulation and IR we estimated SCD-1 indices in 110 federally employed women without diabetes (15 African immigrant (AI), 59 African-American (AA) and 36 White: age 44+/-9 (mean +/- SD; range 24-62y); BMI 35 +/- 6 (range 21-46 kg/m^2). RBC fatty acid profiles were measured by gas chromatography (mol%) and those data were used to estimate SCD-116 (16:1n-7/to 16:0) and SCD-118 (18:1n-9/18:0) activities. Hepatic and visceral fat were measured with proton magnetic resonance spectroscopy, insulin sensitivity by the minimal model and habitual physical activity for 5-7 consecutive days with an accelerometer. Both estimates of SCD-1 activity were similar between AI and AA, and lower than in Whites, before and after adjusting for age and BMI (P<0.01, Table 1). The SCD-116 index and RBC 16:1n-7 correlated with hepatic fat (both r=0.34, P<0.01). In multivariate linear regression models, lower SCD-116 activity was independently associated with African ancestry, hepatic fat and insulin sensitivity (adjR^2=0.27 P<0.01). Lower SCD-116 desaturase activity in insulin resistant AI and AA women may be an important determinant of race/ethnic differences in hepatic fat content.