title: Renal Na-K-ATPase hyperactivity in diabetic Psammomys obesus is related to glomerular hyperfiltration but is insulin-independent.
abstract: Psammomys obesus, a desert rodent, develops diabetes when displaced from its natural environment and fed a high energy diet in the laboratory. This study was designed to examine variations in renal function in relation to the diabetic state with emphasis on changes in Na-K-ATPase activity. The following groups of Psammomys were studied: (1) Animals fed a saltbush diet; a low energy/high salt diet (natural). (2) Animals fed a low energy/low salt diet (laboratory). Both 1 and 2 were normoglycemic and normoinsulinemic and thus served as control. (3) Animals fed a high energy diet (group C) who were hyperglycemic and hyperinsulinemic; this group was divided into two subgroups: C1 presented with glomerular hyperfiltration rate and C2 with glomerular hypofiltration rate. (4) Animals fed a high energy diet presenting with hyperglycemia-hypoinsulinemia (group D). (5) Group D+I, similar to group D but treated with external insulin (2 U/24 h). Groups D and C1, whose glomerular filtration rose above normal by 30% and 70% respectively, exhibited metabolic similarity to Type I and Type II diabetes. In these groups, Na-K-ATPase activity in the cortex increased by 80-100% and in the medulla by 180% (P<0.001 vs control). In group C2 with reduced glomerular filtration rate (GFR), Na-K-ATPase activity did not differ from control. In group D+I, with normalized glomerular filtration rate, Na-K-ATPase activity was similar to control. There was a linear and significant correlation between GFR and Na-K-ATPase activity both in the cortex and in the medulla. These experiments present a well defined animal model of diabetes mellitus. Variations in glucose and in insulin did not correlate with Na-K-ATPase activity. These results clearly demonstrated that Na-K-ATPase activity in the diabetic Psammomys was determined by glomerular filtration but was independent of plasma glucose or insulin levels.
authors.affiliation: Nephrology and Hypertension Services, Hadassah University Hospital, Jerusalem, Israel.
authors.forename: P
authors.initials: P
authors.lastname: Scherzer
authors.forename: I
authors.initials: I
authors.lastname: Nachliel
authors.forename: H
authors.initials: H
authors.lastname: Bar-On
authors.forename: M M
authors.initials: MM
authors.lastname: Popovtzer
authors.forename: E
authors.initials: E
authors.lastname: Ziv
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000201:enzymology* / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000201:enzymology* / Q000503:physiopathology; D004032:Diet; D004195:Disease Models, Animal; D002149:Energy Intake; D005849:Gerbillinae; D005919:Glomerular Filtration Rate / Q000502:physiology*; D007328:Insulin / Q000097:blood; D007668:Kidney / Q000201:enzymology* / Q000503:physiopathology; D008297:Male; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D007328:Insulin; D000254:Sodium-Potassium-Exchanging ATPase