|Bell, Andrea - University Of Arkansas|
|Korourian, Soheila - University Of Arkansas|
|Phelps, Joshua - University Of Arkansas|
|Crook, Tina - University Of Arkansas|
|Gurley, Bill - University Of Arkansas|
|Feresin, Rafaela - University Of Arkansas|
|Hakka, Reza - University Of Arkansas|
Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/1/2017
Publication Date: 4/1/2017
Citation: Bell, A., Korourian, S., Zeng, H., Phelps, J., Crook, T., Gurley, B., Feresin, R.G., Hakka, R. 2017. Effects of a-high- and low-diadzein diet on liver steatosis and serum adipokines in female obese Zucker rats [abstract]. Journal of Federation of American Societies for Experimental Biology. 31:793.1.
Technical Abstract: Rates of obesity worldwide are increasing. Obesity is associated with adipokine dysregulation and insulin resistance, which are factors that increase the risk of developing chronic diseases. As such, the risk for non-alcoholic fatty liver disease (NAFLD) markedly increases in the presence of obesity. The ratio of serum adipokines, leptin/adiponectin (L/A), is associated with the severity of, and risk factors for, NAFLD in a limited number of human studies. We previously reported that a high-isoflavone soy protein isolate (HISPI) diet compared to a casein diet was associated with significantly reduced liver steatosis in obese Zucker rats (OZR). This study’s objective was to investigate whether daidzein, a soy isoflavone in HISPI, is responsible for reduced liver steatosis in OZR, and whether serum adipokine levels are associated with NAFLD severity in OZR. We hypothesized a casein diet containing high-daidzein (HD) compared to low-daidzein (LD) would mitigate hepatic steatosis in female OZR and affect serum adipokine levels. After one week of acclimation on an AIN-93G diet, 19 five-week-old, female OZR (fa/fa) were randomly assigned to a modified AIN-93G diet containing either HD (0.121g/kg feed) or LD (0.01g/kg feed) ad libitum for 8 weeks. Rats were weighed twice per week. At the end of the experiment, serum and livers were collected. Two 3-mm sections of liver lobe were fixed in 10% buffered formalin and evaluated for micro- and macrovesicular steatosis. Steatosis was semiquantitated as a score of 1 to 4 based upon the relative degree of steatosis within hepatocytes: 1) <25%, 2) 25-50%, 3) 50-75%, and 4) >75%. Serum leptin and adiponectin were measured by ELISA. Our results showed that mean body weights between groups were not significantly different (HD 475.8±24.2g vs. LD 486.4±30.4g; p=0.4). Mean liver steatosis scores for HD and LD groups were 3.9 and 3.8 respectively—this difference was not significant (p=0.7). Furthermore, serum leptin levels (HD 142.6±21.9ng/mL vs. LD 133.7±24.6ng/mL; p=0.4) and serum adiponectin levels (HD 6462.7±1050ng/mL vs. LD 6599.8±995ng/mL; p=0.7) were not significantly different between diet groups. Because liver steatosis was similar between HD and LD groups, no association could be drawn between the L/A ratio and severity of NAFLD. In conclusion, daidzein may not be the main component of HISPI responsible for reducing liver steatosis in OZR, but more research is needed to determine whether the significant reduction of steatosis associated with consumption of HISPI is also associated with serum leptin and adiponectin levels in OZR.