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Endocrinology, doi:10.1210/endo-120-2-595
Endocrinology Vol. 120, No. 2 595-601
Copyright © 1987 by the Endocrine Society.
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Stimulation of Phosphatidylcholine Biosynthesis in Diabetic Hypertrophic Kidneys*

YASUO SUZUKI, AURORA FAUSTO, KEITH A. HRUSKA and LOUIS V. AVIOLI

Division of Bone and Mineral Metabolism, Washington University Medical Center, and Renal Division, Jewish Hospital of St. Louis St. Louis, Missouri 63110

Address reprint requests to: Louis V. Avioli, M.D., The Jewish Hospital of St Louis, 216 South Kingshighway, St. Louis, Missouri 63110.

Abstract

Choline metabolism and phosphatidylcholine biosynthesis were studied in renocortical slices of rats rendered diabetic with streptozotocin. The rates of [14C]choline incorporation into both acid-soluble and acid-insoluble fractions were increased in diabetic relative to control kidneys. While choline uptake into the control kidneys reached a plateau after 30 min of incubation, the tissue uptake of choline by the diabetic kidneys showed a time-dependent increase over 120 min, rising to a level exceeding that of control kidneys. In the control kidney, the oxidation of choline to betaine was similar to the level of phosphocholine accumulation during the first 30 min, while the formation of phosphocholine in the diabetic kidney was 1.9-fold higher than that in the control kidney (P < 0.02) and 1.4-fold higher than the formation of betaine in diabetics (P < 0.05). These data suggest that most of the choline transported into cells enters the Kennedy pathway by phosphorylation to phosphocholine in diabetic kidneys. The diabetic kidney also demonstrated a marked increase in the formation of three cholinecontaining phospholipids; phosphatidylcholine, lysophosphatidylcholine, and sphingomyelin. The treatment of diabetes with insulin restored these abnormalities toward normal. The absolute content of phosphatidylcholine significantly increased in diabetic kidneys (P < 0.05) while contents of other major phospholipids and total lipid phosphorus in diabetic kidneys were not different from those in control kidneys.

Our results indicate that renal hypertrophy in experimental diabetes is associated with a stimulation of the biosynthesis of renal phosphatidylcholine, presumably caused by an enhanced tissue uptake of choline and a stimulation of choline kinase. Since an enhancement of the membrane phosphatidylcholine biosynthesis is one of the early responses to growth signals, an alteration in phosphatidylcholine biosynthesis may contribute to the development of renal hypertrophy in experimental diabetes. (Endocrinology 120: 595–601,1987)

Footnotes

* Supported by NIH Program Project Grant AM-32087.

Received February 21, 1986.






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Endocrinology Endocrine Reviews J. Clin. End. & Metab.
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Copyright © 1987 by The Endocrine Society