Abstract
The metabolic syndrome (MS) is characterized by insulin resistance, dyslipidemia and hypertension. It is associated with increased risk of cardiovascular diseases and type-2 diabetes. Consumption of fructose is linked to increased prevalence of MS. Ursodeoxycholic acid (UDCA) is a steroid bile acid with antioxidant, anti-inflammatory activities and has been shown to improve insulin resistance. The current study aims to investigate the effect of UDCA (150 mg/kg) on MS induced in rats by fructose administration (10%) in drinking water for 12 weeks. The effects of UDCA were compared to fenofibrate (100 mg/kg), an agonist of PPAR-α receptors. Treatment with UDCA or fenofibrate started from the 6th week after fructose administration once daily. Fructose administration resulted in significant increase in body weight, elevations of blood glucose, serum insulin, cholesterol, triglycerides, advanced glycation end products (AGEs), uric acid levels, insulin resistance index and blood pressure compared to control rats. Moreover, fructose increased oxidative stress in aortic tissues indicated by significant increases of malondialdehyde (MDA), expression of iNOS and reduction of reduced glutathione (GSH) content. These disturbances were associated with decreased eNOS expression, increased infiltration of leukocytes and loss of aortic vascular elasticity. Treatment with UDCA successfully ameliorated the deleterious effects of fructose. The protective effect of UDCA could be attributed to its ability to decrease uric acid level, improve insulin resistance and diminish oxidative stress in vascular tissues. These results might support possible clinical application of UDCA in MS patients especially those present with liver diseases, taking into account its tolerability and safety. However, further investigations on human subjects are needed before the clinical application of UDCA for this indication.
Highlights
The metabolic syndrome (MS) is a pathological condition characterized by obesity, insulin resistance, dyslipidemia, atherosclerosis and hypertension [1,2]
homeostasis model assessment index for insulin resistance (HOMA-IR) index, Systolic blood pressure (SBP), diastolic blood pressure (DBP) and Mean arterial pressure (MAP) were significantly reduced (P,0.001) by treatment with Ursodeoxycholic acid (UDCA) or fenofibrat compared to rats administered fructose alone (Table 1)
Metabolic syndrome (MS) comprises a constellation of disturbances such as abdominal obesity, insulin resistance and dyslipidemia, which eventually result in hypertension
Summary
The metabolic syndrome (MS) is a pathological condition characterized by obesity, insulin resistance, dyslipidemia, atherosclerosis and hypertension [1,2]. The metabolic disturbance associated with this syndrome has been shown to increase the risk of developing cardiovascular diseases and type-2 diabetes [3,4] These deleterious influences raised worldwide attention to the MS and to the possible strategies for its prevention [5]. Fructose overload in animals can result in insulin resistance, hyperinsulinemia, hypertriglyceridemia, impaired glucose tolerance and can raise blood pressure [7,8]. These metabolic disturbances bear a resemblance to the human MS [9,10]. The model of fructose-drinking rats is being widely used to induce the MS independent of obesity or genetic contributions and to study the possible interventions [11]
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