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Effect of Insulin on Transepithelial Na + Transport in Renal Principal Cells Grown Under Normo‐glycemic, Hyperinsulinemic Conditions
Author(s) -
Maue Ellen,
Brands Michael,
BlazerYost Bonnie
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.845.2
Subject(s) - hyperinsulinemia , medicine , endocrinology , insulin , reabsorption , chemistry , basal (medicine) , epithelial sodium channel , glucose transporter , kidney , insulin resistance , biology , sodium , organic chemistry
Metabolic Syndrome is associated with hyperinsulinemia, hyperglycemia and hypertension. It is our hypothesis that hyperinsulinemia contributes to hypertension by stimulating renal Na + reabsorption via the epithelial Na + channel (ENaC). A mouse cortical collecting duct cell line (mCCD) with the characteristics of the renal principal cells was used to study potential interactions between glucose and insulin in regulating ENaC activity. Electrophysiological studies were used to explore the natriferic (Na + retaining) response of the mCCD cells to insulin stimulation in cells grown with different insulin doses. In cells grown chronically (14 days) in high insulin (45 mU/ml) but normal (3.15 gr/L) glucose, the basal level of transepithelial Na + transport was significantly reduced compared to cells grown in normal glucose with no insulin. The basal level of transepithelial Na + flux was, however, not reduced by short‐term (24 hours) incubation with high insulin, normal glucose media after the cells were confluent. Despite the changes in basal transport, acute stimulation with insulin in cells mounted in an Ussing chamber exhibited statistically identical increases in Na + flux measured as an incremental change in transepithelial ion flux that was independent of the basal level of transport. These initial studies indicate the natriferic response to acute changes in insulin is unaltered by a previous hyperinsulinemic condition if the cells are grown in normal glucose. Extrapolating these studies to metabolic syndrome, we would predict that hyperinsulinemia per se is not sufficient to cause an increase in insulin‐stimulated Na + retention.