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Effects of somatostatin on phosphate transport: Evidence for the role of basal insulin

1983; Elsevier BV; Volume: 24; Issue: 1 Linguagem: Inglês

10.1038/ki.1983.120

1523-1755

Kai Lau, J. Guntupalli, Bonnie Eby,

Neuroendocrine Tumor Research Advances

Abstract Effects of somatostatin on phosphate transport: Evidence for the role of basal insulin. Previous studies suggest that normoglycemic hyperinsulinemia is associated with enhanced proximal tubule and overall renal phosphate (PO 4 ) reabsorption. It is unclear whether the basal level of insulin also regulates PO 4 transport. Furthermore, the role of parathyroid hormone, the associated antinatriuresis, and the distal nephron is uncertain. To examine these issues, clearance and recollection micro-puncture studies were performed in volume-expanded parathyroidectomized rats. Infusion of des-Asn 5 -D-Trp 8 -D-Ser 13 , a somatostatin analogue highly selective for insulin at 10 µg/kg/hr, decreased plasma insulin (12.6 to 2.8 µU/ml), and increased plasma glucose (93 to 140 mg%) and fractional excretion (FE) of sodium (Δ = 2.5%). The clearance of PO 4 (118 to 297 µl/min) and FE PO 4 (2.4 to 6.8%) was increased. Continued somatostatin infusion produced a sustained phosphaturia whereas the addition of insulin (0.10 U/kg/hr) abolished the phosphaturic effects. Separate loading with saline and glucose to achieve comparable ΔFE Na (2.9%) and Δplasma glucose (52 mg%) did not increase PO 4 excretion. Between basal and experimental phases, there was no difference in plasma ultrafiltrable PO 4 , GFR, or segmental fluid reabsorption. While fractional delivery of PO 4 (FD PO 4 ) was unchanged in the control, somatostatin increased FD PO 4 to late proximal (50 vs. 32%), early distal (28.2 vs. 13.4%), late distal tubules (11.8 vs. 6.4%), and to the urine (8.5 vs. 4.9%). These data indicate that (1) insulin deficiency, as produced by somatostatin infusion, impairs tubular PO 4 reabsorption, suggesting an important role for the basal level of insulin in renal PO 4 homeostasis; (2) the phosphaturia of somatostatin is independent of the concomitant natriuresis, hyperglycemia, PTH, and changes in plasma PO 4 ; and (3) insulinopenia reduces PO 4 transport in the proximal convoluted tubule and the distal nephron. Effets de la somatostatine sur le transport du PO 4 : Preuve d'un role de l'insuline basale. Des etudes anterieures suggerent que l'hyperinsulinemie normoglycemique est associee a une augmentation de la reabsorption renale de phosphate (PO 4 ) globale et dans le tubule proximal. On ne sait pas bien si le niveau basal d'insuline regule egalement le transport de PO 4 . En outre, le role de l'hormone parathyroidienne, de l'antinatriurese associee et du nephron distal est incertain. Afin d'examiner ces possibilites, des etudes de clearance et de microponction avec recollection ont ete effectuees chez des rats parathyroidectomises en expansion volemique. La perfusion de des-Asn 5 -D-Trp 8 -D-Ser 13 , un analogue de la somatostatine hautement selectif pour l'insuline a 10 µg/kg/hr, a diminue l'insuline plasmatique (12.6 a 2.8 µU/ml), augmente la glycemie (de 93 a 140 mg%) et l'excretion fractionnelle (FE) de sodium (Δ = 2.5%). La clearance de PO 4 (118 a 297 µl/min) et FE PO 4 (2.4 a 6.8%) se sont elevees. Une perfusion prolongee de somatostatine a entraine une phosphaturie persistante tandis que l'addition d'insuline (0.10 U/kg/hr) a aboli les effets phosphaturiants. Une charge separee avec du solute sale et du glucose pour obtenir un Δ FE Na (2.9%) et un Δ glycemie (52 mg%) comparables n'a pas augmente l'excretion de PO 4 . Entre les phases basale et experimentale il n'y avait pas de difference dans le PO 4 ultrafiltrable, le GFR ni la reabsorption segmentaire de fluide. Tandis que la fraction delivree de PO 4 (FD PO 4 ) etait inchangee pendant le controle, la somatostatine a augmente FD PO 4 aux tubules proximal tardif (50 contre 32%), distal precoce (28.2 contre 13.4%) et tardif (11.8 contre 6.4%), et a l'urine (8.5 contre 4.9%). Ces donnees indiquent que (1) la carence en insuline resultant d'une perfusion de somatostatine altere la reabsorption tubulaire de PO 4 , suggerant un role important de la concentration de l'insuline de base dans l'homeostasie du PO 4 ; (2) la phosphaturie due a la somatostatine est independante de la natriurese concomitante, de l'hyperglycemie, de la PTH, et des modifications du PO 4 plasmatique; (3) l'insulinopenie reduit le transport de PO 4 dans le tubule contourne proximal et le nephron distal.