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1 Department of Medicine, University of Cincinnati School of Medicine, Cincinnati MSB 5502; and 2 Veterans Affairs Medical Center at Cincinnati, Ohio
Starvation causes impairment in the urinary concentrating
ability. The mechanism of this defect, however, remains unknown. We
tested the possibility that food deprivation might affect the expression and activity of aquaporins (AQP1, 2), thereby impairing renal water reabsorption in the kidney. Rats fasted for 24 h
exhibited severe polyuria (urine volume increased from 11 before
fasting to 29 ml/24 h after fasting, P < 0.0001) along
with failure to concentrate their urine (urine osmolality decreased
from 1,485 before fasting to 495 mosmol/kgH2O after
fasting, P < 0.0001). Refeeding for 24 h returned
the urinary concentrating ability back to normal. Northern
hybridization and immunoblot analysis demonstrated that fasting was
associated with a decrease in AQP2 protein (
80%, P 
0.002) and mRNA levels (69%, P 0.003) in the outer
medulla. In the cortex, fasting decreased AQP2 protein abundance by
60% (P 0.004) but did not alter its mRNA expression. During the recovery phase, AQP2 expression returned to normal level in
both tissues. In the inner medulla, the expression of AQP2 was not
altered in fasting, but was increased significantly at both protein ( ± 92%) and mRNA ( ± 43%) levels during the recovery from fasting.
The proximal nephron water channel (AQP1) was not affected in response
to fasting or recovery from fasting. We conclude that 1)
fasting impairs the urinary concentrating ability in rats, and
2) the renal water-handling defect in fasting results
specifically from the downregulation of AQP2 in the cortical and outer
medullary collecting duct.
urinary concentrating mechanism; aquaporin 2; hypoglycemia
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