Murray State University

Enzymatic Activity of Renal H-K-ATPase in the Outer Medulla Collecting Duct (OMCD) Under Glucose Disease States

Institution

Murray State University

Abstract

It has been demonstrated that H-K-ATPase (HKA), a potassium dependent proton secretion transporter, plays an important role in acid-base homeostasis. Studies have shown that gastric isoform (gHKA) is dominant under normal conditions and colonic isoform (cHKA) is increased under low-k conditions. However, the enzymatic activity of HKA in the OMCD is incompletely understood. In order to understand the role that glucose plays in the activity of HKA, hyper and hypoglycemia were induced in animal models. Both wild type and transgenic mice were used, where the transgenic mice (HKAα2) have the cHKA isoform knocked out. Upon testing the enzymatic activity, wild type mice were found to produce a higher amount of ADP, which is produced through hydrolysis from ATP when activating H-KATPase. Transgenic HKAα2 production was significantly lower. Previous studies by S. Nakamura demonstrated the dependence of glucose on H-ATPase. Correlating data is expected with the H-K-ATPase glucose diseased states model. H-K-ATPase activity in hyperglycemic and hypoglycemic mice is yet to be tested.

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Enzymatic Activity of Renal H-K-ATPase in the Outer Medulla Collecting Duct (OMCD) Under Glucose Disease States

It has been demonstrated that H-K-ATPase (HKA), a potassium dependent proton secretion transporter, plays an important role in acid-base homeostasis. Studies have shown that gastric isoform (gHKA) is dominant under normal conditions and colonic isoform (cHKA) is increased under low-k conditions. However, the enzymatic activity of HKA in the OMCD is incompletely understood. In order to understand the role that glucose plays in the activity of HKA, hyper and hypoglycemia were induced in animal models. Both wild type and transgenic mice were used, where the transgenic mice (HKAα2) have the cHKA isoform knocked out. Upon testing the enzymatic activity, wild type mice were found to produce a higher amount of ADP, which is produced through hydrolysis from ATP when activating H-KATPase. Transgenic HKAα2 production was significantly lower. Previous studies by S. Nakamura demonstrated the dependence of glucose on H-ATPase. Correlating data is expected with the H-K-ATPase glucose diseased states model. H-K-ATPase activity in hyperglycemic and hypoglycemic mice is yet to be tested.