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High Fat/High Glucose Diet Induces Metabolic Syndrome in an Experimental Rat Model
- Moreno-Fernández, Silvia, Garcés-Rimón, Marta, Vera, Gema, Astier, Julien, Landrier, Jean François, Miguel, Marta
- Nutrients 2018 v.10 no.10
- ad libitum feeding, animal models, biomarkers, developed countries, energy expenditure, etiology, fructose, genes, glucose, glucose tolerance, high fat diet, hyperlipidemia, hypertension, insulin, laboratory animals, metabolic syndrome, mitochondria, obesity, oxidative stress, quantitative polymerase chain reaction, rats, reverse transcriptase polymerase chain reaction, triacylglycerols
- Metabolic syndrome (MetS) is defined as a constellation of many metabolic disorders such as hypertension, impaired glucose tolerance, dyslipidemia and obesity, being this last disorder a key factor in the etiology of the syndrome. The widespread of MetS in actual society, mainly in developed countries, is becoming an important health problem and is increasing the need to develop new treatments against this pathology is increasing fast. The main objective of the present study was to evaluate the MetS-associated alterations developed in a new glucose diet-induced-obesity (DIO) rodent model. These alterations were also compared to those alterations developed in a fructose-DIO rodent model. Wistar rats were divided into four groups: Control (C), High-fat (HF), High-fat/high-fructose (HFF) and High-fat/high-glucose (HFG). The animals were fed ad libitum for 20 weeks. At the end of the study, HFG animals showed lower expression of energy expenditure genes when compared to the other DIO groups. Oxidative stress biomarkers such as MDA and mitochondrial RT-qPCR analyses showed an increase of oxidative damage together with mitochondrial dysfunction in HFG group. This group also showed increased insulin and glucose plasma levels, though HFF animals showed the greatest increase on these parameters. All DIO groups showed increased plasma levels of triglycerides. Altogether, our results indicated a better impact of glucose than fructose, when combined with a high-fat diet, to induce most of the alterations associated with MetS in rats. In addition, our research facilitates a new animal model to evaluate future treatments for MetS.