| Autor: |
Aboujassoum HM; Laboratory Animal Research Center, Qatar University, Doha P.O. Box 2713, Qatar., Mohamed-Ali V; Anti-Doping Laboratory Qatar, Sports City Road, Doha P.O. Box 2713, Qatar.; Centre of Metabolism and Inflammation, Division of Medicine, Royal Free Campus, University College London, Rowland Hill Street, London NW3 2PF, UK., Abraham D; Centre of Rheumatology and Connective Tissue Disorders, Division of Medicine, Royal Free Campus, University College London, Rowland Hill Street, London NW3 2PF, UK., Clapp LH; Institute of Cardiovascular Science, University College London, Rayne Building, 5 University Street, London WC1E 6JF, UK., Al-Naemi HA; Laboratory Animal Research Center, Qatar University, Doha P.O. Box 2713, Qatar.; Department of Biological and Environmental Sciences, Qatar University, Doha P.O. Box 2713, Qatar. |
| Abstrakt: |
Consumption of a high-carbohydrate diet has a critical role in the induction of weight gain and obesity-related pathologies. This study tested the hypothesis that a carbohydrate-rich diet induces weight gain, ectopic fat deposition, associated metabolic risks and development of non-alcoholic fatty liver disease (NAFLD), which are partially reversible following carbohydrate reduction. Sprague Dawley (SD) rats were fed a carbohydrate-enriched cafeteria diet (CAF) or normal chow (NC) ad libitum for 16-18 weeks. In the reversible group (REV), the CAF was replaced with NC for a further 3 weeks (18-21 weeks). Animals fed the CAF diet showed significantly increased body weight compared to those fed NC, accompanied by abnormal changes in their systemic insulin and triglycerides, elevation of hepatic triglyceride and hepatic steatosis. In the REV group, when the CAF diet was stopped, a modest, non-significant weight loss was associated with improvement in systemic insulin and appearance of the liver, with lower gross fatty deposits and hepatic triglyceride. In conclusion, a carbohydrate-enriched diet led to many features of metabolic syndrome, including hyperinsulinemia, while a dietary reduction in this macronutrient, even for a short period, was able to restore normoinsulinemia, and reversed some of the obesity-related hepatic abnormalities, without significant weight loss. |
