AJP - Renal Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Renal Physiol 246: F59-F66, 1984;
0363-6127/84 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wang, M. S.
Right arrow Articles by Kurokawa, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wang, M. S.
Right arrow Articles by Kurokawa, K.

AJP - Renal Physiology, Vol 246, Issue 1 59-F66, Copyright © 1984 by American Physiological Society


ARTICLES

Renal gluconeogenesis: axial and internephron heterogeneity and the effect of parathyroid hormone

M. S. Wang and K. Kurokawa

To better understand the regulation of renal gluconeogenesis that occurs in the proximal nephron, glucose production rates from various substrates were determined in defined proximal tubule segments of the rat. Tubule segments tested were the S1 and S2 segments of superficial (SF) nephrons, the S1 segments of juxtamedullary (JM) nephrons, and the S3 segments. Glucose production (in decreasing order) was: from alpha-ketoglutarate, JM S1, SF S1, SF S2; from pyruvate, SF S2, JM S1, and SF S1; from glutamine, SF S1, JM S1; and from glutamate, SF S1 = JM S1. Little glucose was produced in the S3 segments. Glucose production from glutamate was lower than that from the other three substrates in JM S1, and glutamine was the best gluconeogenic substrate in SF S1. The effects of parathyroid hormone (PTH), a known stimulator of renal gluconeogenesis, and cAMP were examined using alpha-ketoglutarate as the substrate. Both stimulated glucose production in the S1 and S2 segments of the SF nephron. Although PTH stimulated adenylate cyclase in the S1 segments of the SF and JM nephrons, it had no effect on glucose production in the JM S1. Glucose production rose in the SF S1 and JM S1 in response to increasing concentrations of hydrogen or calcium ions, indicating that gluconeogenesis can be increased in these nephron segments. Differences may therefore be present in the cellular responses to PTH distal to cAMP formation in the nephron segments of the SF and JM nephrons. These findings show the presence of both axial and internephron heterogeneity of renal gluconeogenesis and suggest the difference in the effects of PTH on the function of SF and JM nephrons.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online