Brush Border Vesicle Transport Effects of 1,25-Dihydroxy Vitamin D₃

Abstract

Evidence has accumulated from investigations performed in this laboratory and in others that the renal tubular effect of 1,25-dihydroxy vitamin D₃ (1,25 D₃), the active form of the vitamin, is to increase phosphate reabsorption by the kidney (1–3). We recently reported that the infusion of 2.5 ng of 1,25 D₃ per hour along with 0.2 U of PTH/hr. for six hours resulted in an antiphosphaturia in thyroparathyroidectomized (TPTX), vitamin D-deficient (−D) rats (3). This dose of the metabolite has been considered to be in the physiological range, and was not effective unless given with the non-phosphaturic “permissive” dose of PTH. The development of the brush border vesicle (BBV) transport technique (4) provided us with an opportunity to study the locus of this antiphosphaturic action of the metabolite. Furthermore, glucose metabolism has been reported to be linked to phosphate (Pi) transport events; Rasmussen and his coworkers have reported (5) that parathyroid hormone (PTH), a substance which diminishes phosphate uptake by brush border vesicles (4), increases gluconeogenesis (GNG). Accordingly, we examined the effect of the antiphosphaturic agent 1,25 D₃, on BBV Pi uptake and on GNG.