Normotensive metabolic syndrome in mice deleted of the gene, Type 1 transient receptor potential canonical channel.

Metabolic syndrome has become a global epidemic, affecting all developed countries/communities with growing economies. Worldwide, increasing efforts have been directed at curbing this growing problem. Mice deleted of the gene encoding Type 1 Transient Receptor Potential Canonical Channel (Trpc1) were found to weigh heavier than controls. They had fasting hyperglycemia and impaired glucose tolerance vs. wild type controls. Beyond 1 year of age, plasma triglyceride level in null mice was elevated. Plasma cholesterol tended to be higher than controls. Livers in null mice were heavier, richer in triglyceride, and more echogenic vs. controls on ultrasound evaluation. Hematocrit was lower in null mice of both genders beginning at 2nd/3rd month of age in the absence of bleeding/ hemolysis. Measured by indirect tail-cuff method or by the direct arterial cannulation, blood pressures in null mice were lower than controls. We conclude that Trpc1 gene regulates body metabolism and that except for hypertension, phenotypes of mice after deletion of the Trpc1 gene resemble the metabolic syndrome, suggesting that this could be a good experimental model for future investigation on the pathogenesis and management of this disorder.