Resumen de Efectes metabòlics, vasculars i cognitius del consum de sucres simples en rates femella
In the last decades increased consumption of added sugars, specially fructose, has been associated with the development of obesity and metabolic disorders such as diabetes, hypertension, and cardiovascular diseases. Recently, some studies also link high sugar intake with cognitive alterations. The rat is a good model for the study of the effects caused by fructose consumption, since it metabolizes fructose in a similar way to humans and also suffers comparable metabolic alterations.
In the present thesis, it is shown that subchronic (8 weeks) liquid sugar intake in female rats produces more deleterious metabolic and vascular effects than glucose intake.
Hypertriglyceridemia, as well as increased iNOS and reduced cAMP/PKA/VASP signaling in fructose-supplemented rats could be responsible for these alterations.
Hyperadiponectinemia could acts as a protective mechanism in glucose-supplemented rats.
Moreover, it is observed that chronic sugar consumption (28 weeks) produces hypertriglyceridemia, hyperinsulinemia, increased lipogenesis, reduced fatty acid oxidation and activates specific UPR branches but neither induces hepatic steatosis nor inflammation or oxidative stress. The higher activation of mTOR in fructose-consuming rats could be a plausible mechanism to explain the more severe effects elicited after fructose than glucose intake. In addition, long term fructose but not glucose intake impairs object recognition memory. Metabolic disorders such as impaired insulin signaling, oxidative stress and mitochondrial dysfunction in the cortex, promoted in part by high triglyceride plasma levels, could be the culprits.
Thus, under equicaloric conditions, fructose induces more deleterious effects than glucose consumption, showing that these alterations are produced not only by the amount of calories provided by fructose consumption, but also by its particular metabolism.
