[Studies of trichloroethylene-induced glycosuria: blood glucose and renal glucose reabsorption in rats exposed to trichloroethylene].
In our previous experiments, a remarkable increase in urinary excretion of glucose was found in rats exposed to 821 ppm trichloroethylene for 12 wk. This was not accompanied with proteinuria, aminoaciduria, phosphaturia and definite histological changes in renal tubular structure. In order to ascertain the mechanism of the increase in urinary glucose excretion, blood glucose level and renal glucose reabsorption were studied in 10 male rats exposed to 783 ppm trichloroethylene for more than 3 wk. Another 10 male rats were studied as control. The following results were obtained: 1. Urine glucose of the trichloroethylene group increased after exposure for 2 wk. All the rats showed glycosuria (above 250 mg/dl) by the 4th week of exposure. 2. Plasma glucose levels were depressed by trichloroethylene to as low as 77% of that of the control group. Glycohemoglobin was similarly decreased. 3. Intravenous glucose tolerance tests (0.5 g/kg load) revealed that decreasing constant of plasma glucose (K value) was elevated by trichloroethylene, suggesting that induced hyperglycemia in the exposed rats improved more rapidly than in the controls. Trichloroethylene did not modify the secretion of insulin after glucose load, regardless of the depression in plasma insulin level before load. 4. Glucose titration tests revealed that tubular transport maximum for glucose (TmG) was decreased by trichloroethylene to as low as 46% of that of the control group. The ratio of TmG to glomerular filtration rate (the theoretical renal threshold for glucose) was also depressed to as low as 55% of that of the control group. The foregoing results indicate that trichloroethylene-induced glycosuria is attributable to deteriorated tubular reabsorption of glucose, and not to hyperglycemia. However, the mechanism for the selective disturbance of renal reabsorption of glucose is yet unknown.
Department of Environmental Health, Jichi Medical School.
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Arai
D000818:Animals; D001786:Blood Glucose / Q000032:analysis*; D003864:Depression, Chemical; D005947:Glucose / Q000378:metabolism*; D006029:Glycosuria / Q000139:chemically induced*; D007684:Kidney Tubules / Q000378:metabolism*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D014241:Trichloroethylene / Q000633:toxicity*
D001786:Blood Glucose; D014241:Trichloroethylene; D005947:Glucose