当前位置： SCI文献检索 > EXPERIMENTAL PHYSIOLOGY期刊下所有文献 > Postprandial adjustments in renal phosphate excretion do not involve a gut-derived phosphaturic factor.

Postprandial adjustments in renal phosphate excretion do not involve a gut-derived phosphaturic factor.

Abstract：

NEW FINDINGS:What is the central question of this study? Does a previously hypothesized signalling mechanism, believed to detect postprandial increases in intestinal phosphate and that can stimulate the kidneys to rapidly excrete phosphate, operate under physiological conditions? What is the main finding and its importance? Contrary to earlier reports, rapid signalling between the small intestine and kidney mediated by a gut-derived phosphaturic factor in response to a physiological intestinal phosphate load is not supported by the present findings; moreover, hyperphosphataemia and increased parathyroid hormone concentrations are likely to be the underlying factors responsible for the phosphaturia following a supraphysiological intestinal phosphate load. To date, the role of the small intestine in the regulation of postprandial phosphate homeostasis has remained unclear and controversial. Previous studies have proposed the presence of a gut-derived phosphaturic factor that acts independently of changes in plasma phosphate concentration or parathyroid hormone (PTH) concentration; however, these early studies used duodenal luminal phosphate concentrations in the molar range, and therefore, the physiological relevance of this is uncertain. In the present study, we used both in vivo and in vitro approaches to investigate the presence of this putative 'intestinal phosphatonin'. Instillation of 1.3 m phosphate into the duodenum rapidly induced phosphaturia, but in contrast to previous reports, this was associated with significant hyperphosphataemia and elevated PTH concentration; however, there was not the expected decrease in abundance of the renal sodium-phosphate cotransporter NaPi-IIa. Instillation of a physiological (10 mm) phosphate load had no effect on plasma phosphate concentration, PTH concentration or phosphate excretion. Moreover, phosphate uptake by opossum kidney cells was unaffected after incubation with serosal fluid collected from intestinal segments perfused with different concentrations of phosphate. Taken together, these findings do not support the concept of a gut-derived phosphaturic factor that can mediate rapid signalling between the gut and kidney, leading to increased urinary phosphate excretion, as part of normal phosphate homeostasis.

journal_name

Exp Physiol

journal_title

Experimental physiology

authors

Lee GJ,Mossa-Al Hashimi L,Debnam ES,Unwin RJ,Marks J

doi

10.1113/EP086062

subject

Has Abstract

pub_date

2017-04-01 00:00:00

pages

462-474

issue

eissn

0958-0670

issn

1469-445X

journal_volume

102

pub_type

杂志文章

在线工具

Postprandial adjustments in renal phosphate excretion do not involve a gut-derived phosphaturic factor.