Abstract
BackgroundThe metabolic syndrome (MS) is characterized by variable coexistence of metabolic and pathophysiological alterations which are important risk factors for developing of type II diabetes and/or cardiovascular diseases. Increased of MS patients in worldwide has stimulated the development of experimental models. However, it is still challenging to find an dietetic model that most closely approximates human MS and, in addition, is not yet fully established the effect of different diets of MS in lipid metabolism in rats of different ages. The aim of this study was to evaluate the effect of different diets of MS in lipid metabolism and ectopic fat deposition and define the most appropriate diet for inducing the characteristic disturbances of the human MS in rats of different ages.MethodsYoung (4 weeks old) and adult rats (12 weeks old) were given a high-fat (FAT) or high-fructose diet (FRU) for 13 weeks and biochemical, physiological, histological and biometric parameters were evaluated.ResultsIn young rats, the FAT diet induced increased mean blood pressure (MAP) and heart rate (HR), body weight after 6 to 10 weeks, and in the 13th week, increased the liver, mesenteric, retroperitoneal and epididymal fat weights, fasting glucose, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and reduced HDL cholesterol; and also induced non-alcoholic fatty liver disease (NAFLD) and renal inflammatory infiltrates. In adult rats, the FRU diet induced transient elevations of MAP and HR in the 6th week, and, at 13 weeks, increased fasting glucose, triglycerides, total cholesterol, AST and ALT; increased liver, kidneys and retroperitoneal fat weights; and induced macrovesicular and microvesicular NAFLD, the presence of fat cells in the kidney, glomerular sclerosis, and liver and kidney inflammation. Additionally, the FAT and FRU diets induced, respectively, increases in liver glycogen in adults and young rats.ConclusionsOur data show that FRU diet in adult rats causes biggest change on metabolism of serum lipids and lipid accumulation in liver and kidney, while the FAT diet in young rats induces elevation of MAP and HR and higher increased visceral lipid stores, constituting the best nutritional interventions to induce MS in rats.
Highlights
The metabolic syndrome (MS) is characterized by variable coexistence of metabolic and pathophysiological alterations which are important risk factors for developing of type II diabetes and/or cardiovascular diseases
The increased number of MS patients worldwide has stimulated the development of experimental models that mimic the characteristics of human MS [12], in attempts to understand the biochemical, physiological and pathological alterations involved in the development and maintenance of excess body fat and MS [7]
In the tenth week of the diet, the values of mean blood pressure (MAP) and heart rate (HR) of the Young – FAT group remained higher than in the Young – control diet (CT), while the Young – fructose diet (FRU) group showed only increased HR compared to Young – CT (Figure 1A and C)
Summary
The metabolic syndrome (MS) is characterized by variable coexistence of metabolic and pathophysiological alterations which are important risk factors for developing of type II diabetes and/or cardiovascular diseases. The aim of this study was to evaluate the effect of different diets of MS in lipid metabolism and ectopic fat deposition and define the most appropriate diet for inducing the characteristic disturbances of the human MS in rats of different ages. Metabolic syndrome (MS) is a pathological condition in which three or more of the following risk factors are present: central obesity, high plasma triglyceride levels, low plasma HDL levels, high cholesterol, hyperglycemia, atherosclerosis, non-alcoholic fatty liver disease (NAFLD), The development and establishment of MS are mainly related to the consumption of high-fat diets and/or highcarbohydrate diets [7]. The increased number of MS patients worldwide has stimulated the development of experimental models that mimic the characteristics of human MS [12], in attempts to understand the biochemical, physiological and pathological alterations involved in the development and maintenance of excess body fat and MS [7]. Animal models that develop characteristics of MS without genetic manipulation, but only through consumption of specific nutritionally unbalanced diets are increasingly important [14] for use in simulating the most common cause of human MS
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