Literature DB >> 11054650

Renal Na-K-ATPase hyperactivity in diabetic Psammomys obesus is related to glomerular hyperfiltration but is insulin-independent.

P Scherzer1, I Nachliel, H Bar-On, M M Popovtzer, E Ziv.   

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.

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Year:  2000        PMID: 11054650     DOI: 10.1677/joe.0.1670347

Source DB:  PubMed          Journal:  J Endocrinol        ISSN: 0022-0795            Impact factor:   4.286


  4 in total

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2.  Proinsulin C-peptide reduces diabetes-induced glomerular hyperfiltration via efferent arteriole dilation and inhibition of tubular sodium reabsorption.

Authors:  Lina Nordquist; Russell Brown; Angelica Fasching; Patrik Persson; Fredrik Palm
Journal:  Am J Physiol Renal Physiol       Date:  2009-09-09

3.  C-Peptide: the missing link in diabetic nephropathy?

Authors:  Lina Nordquist; John Wahren
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4.  Psammomys obesus, a particularly important animal model for the study of the human diabetic nephropathy.

Authors:  Pnina Scherzer; Shachaf Katalan; Gay Got; Galina Pizov; Irene Londono; Anca Gal-Moscovici; Mordecai M Popovtzer; Ehud Ziv; Moise Bendayan
Journal:  Anat Cell Biol       Date:  2011-09-29
  4 in total

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