Reza Hakkak

Reza Hakkak

University of Arkansas for Medical Sciences, USA

Title: Obesity and fatty liver prevention by diet and weight loss


Reza Hakkak is working as a faculty member University of Arkansas for Medical Sciences, is a nutritionist, Professor and Chairman of the Department of Dietetics and Nutrition in the College of Health Related Professions, Professor of Pediatrics in the College of Medicine, and Professor of Maternal Child Health in the College of Public Health. His research is primarily in the areas of basic nutrition science research and nutrition education. His basic nutrition research interests include the influence of nutrition on cancer prevention, the influence of obesity on cancer promotion, and the effects of differing diets and nutrition on chemical carcinogenesis. For past 10 years, his research interests have focused on links between obesity, diet and breast cancer promotion.


Obesity has been an epidemic in the US and world for more than two decades, and the proportion of overweight and obese adults in the population continue to grow. Obesity is associated with serious health conditions, including type 2 diabetes, cardiovascular disease, certain types of cancers, hyperlipidemia, and liver steatosis. Weight Loss also has been associated with reducing these diseases. Fatty liver disease can range from fatty liver alone (liver steatosis) to fatty liver associated with inflammation (steatohepatitis). Non-alcoholic fatty liver disease (NAFLD) is one of the common causes of liver diseases with a prevalence of up to 34% in the US but this prevalence increases to more than 50% in the obese population. NAFLD is the major cause of abnormal liver function and often associated with obesity. Dehydroepiandrosterone (DHEA) is an over-the-counter dietary supplement used as an anti-cancer agent and anti-obesity supplement. We performed two different experiments. 1) To investigate long-term effects of obesity and DHEA treatment on body weight gain and liver steatosis. Rats were fed either chow or chow with the DHEA (6 g/kg diet) and were killed 155 days later. Obese rats fed the DHEA diet gained significantly less weight (P<0.001) and less liver steatosis (P<0.001) than control fed rats. These data suggest that there might be a link between liver damage and breast cancer development. 2) To determine the role of soy protein isolate (SPI) in reducing liver steatosis. Rats (6 weeks old) were assigned either casein (CAS) as control or a SPI diet with isoflavones (SPI) for 16 weeks. SPI gained more weight (P<0.05) than CAS rats. The SPI rats had lower liver steatosis scores (P<0.001) compared to CAS rats. SPI rats had lower serum alanine amino transferase (ALT) and aminotransferase (AST) levels (P<0.05) compared to CAS. Our results suggest that longer period of SPI feeding results in lower liver steatosis and serum ALT and AST levels.