|
Rat model of metabolic syndrome induced by a high-carbohydrate, high-fat diet with fructose in drinking water |
|---|---|
| รหัสดีโอไอ | |
| Creator | Upa Kukongviriyapan |
| Title | Rat model of metabolic syndrome induced by a high-carbohydrate, high-fat diet with fructose in drinking water |
| Contributor | Ketmanee Senaphan,Poungrat Pakdeechote,Veerapol Kukongviriyapan,Patchareewan Pannangpetch |
| Publisher | Research and Technology Transfer Affairs Division.Khon Kaen University. |
| Publication Year | 2560 |
| Journal Title | Asia-Pacific Journal of Science and Technology (APST) |
| Journal Vol. | 22 |
| Journal No. | 2 |
| Page no. | 1-8 |
| Keyword | igh-carbohydrate, high-fatdiet,Hypertension, Insulin resistance, Dyslipidemia, Metabolic syndrome |
| URL Website | https://tci-thaijo.org/index.php/APST/index |
| Website title | https://tci-thaijo.org/index.php/APST/article/view/84862 |
| ISSN | 2539-6293 |
| Abstract | Metabolic syndrome (MS) is one of the most important challenges to public health and biomedical research. To control this disease, research in rodent models that closely mimic the MS in humans is essential. In this study, a rat model of MS has been developed in male Sprague-Dawley rats by feeding a high-carbohydrate, high-fat (HCHF) diet with 15% fructose solution added to the drinking water. Rats in control group were fed with standard chow diet. During 10 weeks on HCHF diet, rats had developed signs of MS, including hypertension, dyslipidemia, hyperglycemia and impaired glucose tolerance. These alterations were progressively increased throughout 16 weeks of the feeding period. The abdominal fat pads and organ wet weights (heart, liver and kidneys) were significantly increased. Moreover, a significant decrease in hepatic and renal functions was also observed in HCHF diet-fed rats. Overall results suggest that chronic consumption of a HCHF diet by normal rodents provides an adequate rodent model to mimic the human metabolic syndrome. This rat model of MS may be useful for studying the pathophysiological basis of MS in humans and for testing potential therapeutic interventions. |
