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Studies of the regulation of renal gluconeogenesis in normal and P i depleted proximal tubule cells
Author(s) -
Nakagawa Takeshi,
Butterworth Peter J.
Publication year - 1990
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.290080106
Subject(s) - gluconeogenesis , pyruvate carboxylase , cytosol , fructose , endocrinology , medicine , biology , biochemistry , glycolysis , pyruvate kinase , chemistry , metabolism , enzyme
P i depletion of proximal tubule cells isolated from mouse kidney results in a decrease in the cell content of fructose‐2,6‐bisphosphate and an increase in the rate of gluconeogenesis from pyruvate, malate and succinate. Gluconeogenesis from glycerol is unaffected by P i depletion. Introduction of fructose‐2,6‐bisphosphate into the cytosol of ATP‐permeabilized cells is accompanied by a fall in gluconeogenesis. The presence of external Ca 2+ stimulates gluconeogenesis. When cytosolic Ca 2+ is raised to 1·8 μM by permeabilization, the resealed cells still require 2·5 mM Ca 2+ in the bathing medium in order to perform gluconeogenesis at the maximum rate. Cells permeabilized in the presence of cAMP show a decreased rate of glucose production. Phorbol ester stimulates gluconeogenesis provided that the phorbol treatment is performed in the absence of Ca 2+ ions. It is suggested that P i depletion may stimulate pyruvate carboxylase activity and facilitate the entry of certain gluconeogenic substrates into mitochondria. It is also proposed that important aspects of the control of renal gluconeogenesis by parathyroid hormone are mediated by protein kinase C.