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.