Normotensive metabolic syndrome in Transient Receptor Potential Canonical Channel type 1 Trpc1−/− mice.

Abstract

ABSTRACT Metabolic syndrome has become a global epidemic, affecting all developed countries and 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 compared with wild-type controls. Beyond 1 year of age, plasma triglyceride level in Trpc1−/− mice was elevated. Plasma cholesterol levels tended to be higher than in controls. The livers of Trpc1−/− mice were heavier, richer in triglyceride, and more echogenic than those of controls on ultrasound evaluation. Hematocrit was lower in Trpc1−/− mice of both genders beginning at the second to third months of age in the absence of bleeding or hemolysis. Measured by the 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 mice with metabolic syndrome, suggesting that this could be a good experimental model for future investigation of the pathogenesis and management of this disorder.