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Research Article Free access | 10.1172/JCI107754

Phospholipid Metabolism in the Initiation of Renal Compensatory Growth after Acute Reduction of Renal Mass

F. Gary Toback, Patricia D. Smith, and Leah M. Lowenstein

Department of Medicine, Boston University School of Medicine, Boston University Medical Center, Boston, Massachusetts 02118

Boston City Hospital, Boston, Massachusetts 02118

Find articles by Toback, F. in: PubMed | Google Scholar

Department of Medicine, Boston University School of Medicine, Boston University Medical Center, Boston, Massachusetts 02118

Boston City Hospital, Boston, Massachusetts 02118

Find articles by Smith, P. in: PubMed | Google Scholar

Department of Medicine, Boston University School of Medicine, Boston University Medical Center, Boston, Massachusetts 02118

Boston City Hospital, Boston, Massachusetts 02118

Find articles by Lowenstein, L. in: PubMed | Google Scholar

Published July 1, 1974 - More info

Published in Volume 54, Issue 1 on July 1, 1974
J Clin Invest. 1974;54(1):91–97. https://doi.org/10.1172/JCI107754.
© 1974 The American Society for Clinical Investigation
Published July 1, 1974 - Version history
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Abstract

Membrane metabolism was studied during the initiation of compensatory growth after acute reduction in renal mass. The rate of [14C]choline incorporation into phospholipid in renal cortical slices was increased by 37% at 5 min of compensatory growth in mice. The rate increased to the maximal value of 68% by 20 min and remained there for 3 h. The rate then remained increased at 28-34% above normal for 2 days and returned to normal by the 6th day.

The increase in rate of choline incorporation into renal phospholipid was independent of choline uptake. [14C]Choline was found to be a specific precursor of the three renal phospholipids, phosphatidylcholine, lysophosphatidylcholine, and sphingomyelin, which comprise over half the amount of the phospholipids. The relative distribution of the label in each of the three phospholipid classes did not change with compensatory growth. An increased rate of choline incorporation was also observed in kidneys of rats during compensatory growth and in the compensating kidneys of mice treated with indomethacin before uninephrectomy. The rate was increased 24% at 3 h after uninephrectomy in vivo. The increase appeared to be specific for the kidney, since it did not occur in the livers of these mice.

The results indicate that the onset of renal compensatory growth is associated with a specific enhancement of the synthesis of renal choline-containing phospholipids. Since the phospholipids largely occur in the cell membrane, early alterations in cell membrane metabolism may thus play a role in the initiation of cell growth.

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