Dietary Supplementation of Fructooligosaccharides Reduces Hepatic Steatosis Associated with Insulin Resistance in Obese Zucker Rats | Functional Foods in Health and Disease - Online ISSN: 2160-3855; Print ISSN: 2378-7007 Skip to main content Skip to main navigation menu Skip to site footer Open Menu Functional Foods in Health and Disease - Online ISSN: 2160-3855; Print ISSN: 2378-7007 Home Food Science Publisher Functional Food Center Current Archives About About the Journal Aims and Scope Contact Editing Services Editorial Team Express Peer Review Graphical Abstract Journal Insights Privacy Statement Submissions Announcements Search Search Register Login Home / Archives / Vol. 1 No. 5 (2011): May 2011 / Research Articles Dietary Supplementation of Fructooligosaccharides Reduces Hepatic Steatosis Associated with Insulin Resistance in Obese Zucker Rats Authors Lydia Kaume Food Science Department, University of Arkansas, 2650 N. Young Avenue, Fayetteville AR, 72704 William Gilbert Food Science Department, University of Arkansas, 2650 N. Young Avenue, Fayetteville AR, 72704 Vidya Gadang Food Science Department, University of Arkansas, 2650 N. Young Avenue, Fayetteville AR, 72704 Latha Devareddy Food Science Department, University of Arkansas, 2650 N. Young Avenue, Fayetteville AR, 72704 DOI: https://doi.org/10.31989/ffhd.v1i5.130 Abstract Background: One in five adults in the United States is obese as defined by a body mass index of 30 kg/m2. Obesity is associated with metabolic syndrome, a combination of medical conditions including cardiovascular disease, type 2 diabetes, hypertension, hypercholesterolemia, and hypertriglyceridemia. These conditions present challenges to the medical care system and require a multifaceted approach through a variety of interventions. This study investigated the effects of fructooligosaccharides (FOS) at the level of 5 % (w/w) in alleviating the complications associated with metabolic syndrome. Methods: The study was carried out using thirty-six, three-month old female lean and obese Zucker rats housed in an environmentally controlled laboratory. The Zucker rats were divided into three groups (N=12): Lean (L-CTRL) and obese controls (O-CTRL) and obese-FOS (O-FOS). The controls received AIN-93M purified rodent diet and the animals in the O-FOS group were fed AIN-93M diet modified to contain 5.0% FOS (w/w). After 100 days of treatment, the rats were fasted for 12 hours and sacrificed. Tissue and organs of interest, and blood were collected for analysis. Serum concentrations of the following were determined: glucose, glycosylated hemoglobin (HbA1c), total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), triglycerides (TG), and insulin. Gravimetric quantification of liver lipids was performed and peroxisome proliferator-activated receptor-γ (PPAR-γ) gene expression was determined in white adipose tissue by qRT-PCR. Results: No significant differences were observed in the serum lipids, fasting blood glucose, HbA1c and PPAR-γ gene expression in white adipose tissue of O-FOS group compared to O-CTRL group. FOS supplementation significantly lowered the percent total liver lipids by 12% with a subsequent reduction in the liver weights compared to O-CTRL rats. Serum insulin concentrations were lowered 3.6 fold in O-FOS group compared to O-CTRL (P < 0.05).  Conclusion: Based on these findings we conclude that dietary supplementation of 5% FOS (w/w) may reduce hepatic steatosis and the risk for non-alcoholic fatty liver disease (NAFLD) associated with insulin resistance without changes in blood lipids and glucose levels. Key words: Dietary fiber, Fructooligosaccharide, Hepatosteatosis, Liver lipids, Non-alcoholic fatty liver disease (NAFLD), Zucker. Downloads [Abstract] [Full Article] Published 2011-05-24 Issue Vol. 1 No. 5 (2011): May 2011 Section Research Articles License Authors retain the copyright of their articles and grant the Functional Food Center (FFC) and its journals the right of first publication under the terms of the Creative Commons Attribution 4.0 International License. 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