Phosphate (Pi) deprivation and IGFs stimulate renal Pi reabsorption. We studied the involvement of IGFs in the adaptation of Pi transport to Pi deprivation in MDCK cells.
Deprivation of Pi for 15 h increased the steady-state content of IGF-II mRNA (77 ± 12% whereas IGF-I mRNA was not detectable in MDCK cells in either control or Pi-deprived cells. IGF-II (10 −7 m) and IGF-I 10−8m) stimulated the Na-dependent Pi uptake (1·23and 1·3-fold increase at 15 h respectively). The effect of IGF-I appeared after 15 h and increased up to 40 h of treatment (2·15-fold increase). In contrast, Pi uptake was increased by Pi deprivation as early as 8 h (1·5-fold) and up to 40 h of Pi deprivation (1·9-fold increase). IGF-II mRNA was not increased before 15 h of Pi deprivation and returned to control at 40 h. The combination of IGF-I and Pi deprivation had a more than additive effect on Pi transport (fivefold increase) (P<0·001).
At variance with Pi deprivation, high concentrations of insulin stimulated Na-coupled alanine transport (6 ± 2% and 16 ± 4% in Pi-treated and Pi-depleted cells respectively). Pi deprivation and high concentrations of insulin decreased Na,K-ATPase activity (−48 and −64% respectively) and these effects were not additive.
We concluded that: (1) long-term Pi deprivation increased the content of IGF-II mRNA in MDCK cells but that the paracrine/autocrine effects of IGFs could not account for the effects of Pi deprivation on Pi transport in MDCK cells and (2) IGFs could be involved in other changes occurring during Pi deprivation such as the decrease in Na,K-ATPase activity.
Journal of Endocrinology (1995) 145, 325–331
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