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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #334970
Title: A diet containing a high- versus low-daidzein level does not protect against liver steatosis in the obese Zucker rat model

Author
item BELL, ANDREA - University Of Arkansas
item KOROURIAN, SOHEILA - University Of Arkansas
item Zeng, Huawei
item PHELPS, JOSHUA - University Of Arkansas
item HAKKAK, REZA - University Of Arkansas

Submitted to: Food & Function
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/8/2017
Publication Date: 3/22/2017
Citation: Bell, A., Korourian, S., Zeng, H., Phelps, J., Hakkak, R. 2017. A diet containing a high- versus low-daidzein level does not protect against liver steatosis in the obese Zucker rat model. Food & Function. 8(3):1293-1298.

Interpretive Summary: Non-alcoholic fatty liver disease (NAFLD), the major cause of abnormal liver function, is often associated with obesity. It is also known that liver steatosis initiates the development of NAFLD. Lifestyle changes focusing on diet modification and increased physical activity are essential to reducing obesity, but certain dietary components, such as soy isoflavones, may offer specific protection against liver steatosis even in the presence of obesity. Daidzein, a major isoflavones in soy, has been reported to have a critical role in body weight, feed intake and liver steatosis. We hypothesize that a high-daidzein diet compared to a low-daidzein diet will affect body weight gain, energy intake, and decrease liver steatosis scores in obese rat model. However, our results demonstrated that diet containing a high- versus low-daidzein level does not protect against liver steatosis in a genetically obese-rat model lacking leptin-receptor signaling. The information will be useful for scientists, health-care and food-production professionals who are interested in soy consumption and obesity prevention.

Technical Abstract: The prevalence of obesity is increasing worldwide. Obesity increases the risk for non-alcoholic fatty liver disease through adipokine dysregulation and inflammation. Previously, we reported a high-isoflavone soy protein isolate (HISPI) diet was associated with significantly heavier body weights and reduced liver steatosis in obese Zucker rats (OZR) compared to a casein diet. The objective of this study was to investigate whether daidzein, a soy isoflavone in HISPI, is responsible for increased body weight gain or reduced liver steatosis. We hypothesized a casein diet containing high-daidzein (HD) compared to low-daidzein (LD) would mitigate hepatic steatosis in female OZR. Rats were randomly assigned to modified AIN-93G diet containing HD (0.12 g/kg feed) or LD (0.01 g/kg feed). Rats were weighed twice per week. Feed intake was measured once per week, and kcal/kg of body weight was calculated. After 8 weeks, rats were sacrificed. Serum and livers were collected. Sections of liver lobe were fixed in 10% buffered formalin and stained with hematoxylin and eosin. 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 did not show a significant difference in mean body weights, energy intake, liver steatosis scores, serum leptin or adiponectin between diet groups. In conclusion, daidzein may not be the main component of HISPI responsible for increasing body weight or reducing liver steatosis in OZR.