Overview

The overactivation of the ECA/AT1r axis is closely related to Metabolic Syndrome and inflammation. Fructose administration has been used as a model for inducing hyperactivity of this axis and for studying AT1r-related inflammatory pathways. The aim of this study was to evaluate whether administration of a PPAR-beta/delta agonist could reduce ACE/AT1r axis hyperactivation and consequently reduce the damage caused by a high-fructose diet. For this purpose, male mice were fed a diet containing 47% fructose for eight weeks or a control diet. After eight weeks, the groups were redivided for the initiation of agonist administration for three weeks. The treated animals showed several improvements in the metabolic and inflammatory parameters evaluated in the liver, white adipose tissue, and kidneys. With these results, we can conclude that short-term administration of GW501516 could alleviate the deleterious effects caused by a fructose-rich diet and could be considered a new therapeutic tool in the treatment of ECA/AT1r axis overactivation.

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