Panchal, Sunil K. and Poudyal, Hemant and Brown, Lindsay (2012) Quercetin ameliorates cardiovascular, hepatic, and metabolic changes in diet-induced metabolic syndrome in rats. The Journal of Nutrition, 142 (6). pp. 1026-1032. ISSN 0022-3166
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Official URL: http://jn.nutrition.org/content/142/6/1026
Identification Number or DOI: doi: 10.3945/jn.111.157263
Metabolic syndrome is a risk factor for cardiovascular disease and nonalcoholic fatty liver disease (NAFLD). We investigated the responses to the flavonol, quercetin, in male Wistar rats (8-9 wk old) divided into 4 groups. Two groups were given either a corn starch-rich (C) or high-carbohydrate, high-fat (H) diet for 16 wk; the remaining 2 groups were given either a C or H diet for 8 wk followed by supplementation with 0.8 g/kg quercetin in the food for the following 8 wk (CQ and HQ, respectively). The H diet contained ~68% carbohydrates, mainly as fructose and sucrose, and ~24% fat from beef tallow; the C diet contained ~68% carbohydrates as polysaccharides and ~0.7% fat. Compared with the C rats, the H rats had greater body weight and abdominal obesity, dyslipidemia, higher systolic blood pressure, impaired glucose tolerance, cardiovascular remodeling, and NAFLD. The H rats had lower protein expressions of nuclear factor (erythroid-derived 2)- related factor-2 (Nrf2), heme oxygenase-1 (HO-1), and carnitine palmitoyltransferase 1 (CPT1) with greater expression of NF-kB in both the heart and the liver and less expression of caspase-3 in the liver than in C rats. HQ rats had higher expression of Nrf2, HO-1, and CPT1 and lower expression of NF-kB than H rats in both the heart and the liver. HQ rats had less abdominal fat and lower systolic blood pressure along with attenuation of changes in structure and function of the heart and the liver compared with H rats, although body weight and dyslipidemia did not differ between the H and HQ rats. Thus, quercetin treatment attenuated most of the symptoms of metabolic syndrome, including abdominal obesity, cardiovascular remodeling, and NAFLD, with the most likely mechanisms being decreases in oxidative stress and inflammation.
|Item Type:||Article (Commonwealth Reporting Category C)|
|Additional Information:||Permanent restricted access to published version due to publisher copyright policy.|
|Uncontrolled Keywords:||body weight; carbohydrate diet; cardiovascular disease; cell metabolism; controlled study; dyslipidemia; glucose intolerance; hypertension; lipid diet; liver function; metabolic syndrome X; nonalcoholic fatty liver; obesity; oxidative stress; protein expression; systolic blood pressure; treatment response|
|Fields of Research (FOR2008):||06 Biological Sciences > 0601 Biochemistry and Cell Biology > 060104 Cell Metabolism|
11 Medical and Health Sciences > 1101 Medical Biochemistry and Metabolomics > 110107 Metabolic Medicine
11 Medical and Health Sciences > 1111 Nutrition and Dietetics > 111103 Nutritional Physiology
|Socio-Economic Objective (SEO2008):||E Expanding Knowledge > 97 Expanding Knowledge > 970111 Expanding Knowledge in the Medical and Health Sciences|
|Deposited On:||23 Sep 2012 22:39|
|Last Modified:||20 Feb 2013 08:31|
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