Glycogen deposition in distal tubular cells during HgCl2 induced acute renal failure.
An unusual cytoplasmic accumulation of glycogen within the distal tubular epithelium of the kidney was produced by subcutaneouse administration of a single dose of HgCl2 (4 mg/kg body weight), used to induce acute renal failure. Since the plasma immune-reactive insulin was increased while plasma and urine glucose levels remained normal, it was concluded that activation of glycogen synthase might have lead to this effect. Furthermore, the accumulated glycogen was considered to contribute to the protection of distal tubular cells against HgCl2-induced injury, since oxidative energy metabolism was severely depressed after HgCl2 administration.
D058186:Acute Kidney Injury / Q000139:chemically induced / Q000473:pathology*; D000818:Animals; D006003:Glycogen / Q000378:metabolism*; D007684:Kidney Tubules / Q000648:ultrastructure*; D007686:Kidney Tubules, Distal / Q000378:metabolism / Q000648:ultrastructure*; D008297:Male; D008630:Mercury Poisoning / Q000378:metabolism / Q000473:pathology*; D008854:Microscopy, Electron; D051381:Rats
D006003:Glycogen