Abstract
BackgroundProton-pump inhibitor-induced hypomagnesemia (PPIH) is the most recognized side effect of proton-pump inhibitors (PPIs). Additionally, PPIH is associated with hypocalcemia and hypokalemia. It is hypothesized that PPIs reduce epithelial proton secretion and thereby increase the pH in the colon, which may explain the reduced absorption of and Mg2+ and Ca2+. Fermentation of dietary oligofructose-enriched inulin fibers by the microflora leads to acidification of the intestinal lumen and by this enhances mineral uptake. This study aimed, therefore, to improve mineral absorption by application of dietary inulin to counteract PPIH.MethodsHere, C57BL/J6 mice were supplemented with omeprazole and/or inulin. Subsequently, Mg2+ and Ca2+ homeostasis was assessed by means of serum, urine and fecal electrolyte measurements. Moreover, the mRNA levels of magnesiotropic and calciotropic genes were examined in the large intestine and kidney by real-time PCR.ResultsTreatment with omeprazole significantly reduced serum Mg2+ and Ca2+ levels. However, concomitant addition of dietary inulin fibers normalized serum Ca2+ but not serum Mg2+ concentrations. Inulin abolished enhanced expression of Trpv6 and S100g in the colon by omeprazole. Additionally, intestinal and renal mRNA levels of the Trpm6 gene were reduced after inulin intake.ConclusionsThis study suggests that dietary inulin counteracts reduced intestinal Ca2+ absorption upon PPI treatment. In contrast, inulin did not increase intestinal absorption of Mg2+ sufficiently to recover serum Mg2+. The clinical potential of dietary inulin treatment should be the subject of future studies.
Highlights
Since their introduction two decades ago, proton pump inhibitors (PPIs) became the mainstay in gastro esophageal reflux (GERD), peptic ulcer disease (PUD), persistent non-steroidal antiinflammatory drug (NSAID) treatment and generalized dyspepsia [1,2,3]
Intestinal and renal mRNA levels of the Trpm6 gene were reduced after inulin intake
This study suggests that dietary inulin counteracts reduced intestinal Ca2+ absorption upon PPI treatment
Summary
Since their introduction two decades ago, proton pump inhibitors (PPIs) became the mainstay in gastro esophageal reflux (GERD), peptic ulcer disease (PUD), persistent non-steroidal antiinflammatory drug (NSAID) treatment and generalized dyspepsia (heartburn) [1,2,3]. PPIs form a class of drugs that is widely prescribed, with millions of chronic users worldwide. The most recognized side effect of all marketed PPIs is proton-pump inhibitor-induced hypomagnesemia (PPIH) [5, 6]. It is widely anticipated that PPIH is the consequence of intestinal Mg2+ malabsorption, since a renal leak was never detected [6, 11]. The clinical significance of reduced calcium (Ca2+) levels was emphasized by several dozens of studies showing increased risk of bone fractures after chronic PPI use [14]
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