Publications by authors named "Lisanne M M Gommers"

Article Synopsis
  • * Researchers used intestine-specific TRPM6 knockout mice to examine magnesium absorption after a 4-day omeprazole treatment, finding that these knockout mice had lower Mg absorption and serum levels compared to control mice.
  • * Ultimately, the results suggest that TRPM6 isn't impacted by short-term PPI use for magnesium absorption in the intestines, as no significant changes in magnesium homeostasis were observed.
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Article Synopsis
  • This study investigates how short-chain fatty acids (SCFAs), specifically butyrate, affect magnesium (Mg) absorption in the intestines and its relationship with gut bacteria.
  • Researchers found that higher butyrate levels in the colon correlate with lower serum magnesium levels in mice.
  • The study reveals that butyrate inhibits Mg absorption by directly affecting a specific channel in gut cells, indicating that butyrate's influence on mineral absorption is independent of metabolic changes.
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Proton pump inhibitors (PPIs) reliably suppress gastric acid secretion and are therefore the first-line treatment for gastric acid-related disorders. Hypomagnesemia (serum magnesium [Mg ] <0.7 mmol/L) is a commonly reported side effect of PPIs.

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Dietary fibers have been shown to increase the intestinal absorption of calcium (Ca) and magnesium (Mg). However, the mechanisms that explain the enhanced electrolyte absorption remain unknown. Therefore, this study aims to investigate the short-term and long-term effects of 5% (w/w) sodium butyrate (Na-butyrate), an important end-metabolite of bacterial fermentation of dietary fibers, on Ca and Mg homeostasis in mice.

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Intestinal enterocytes are key players in the absorption of magnesium (Mg) and calcium (Ca). Understanding the exact molecular mechanisms by which their absorption behavior is regulated could greatly improve treatment strategies for stimulating intestinal absorption in diseases with Mg and/or Ca deficiency. However, such studies are hampered by the lack of in vitro intestinal cell models mimicking the mechanical and physiological properties of the gut.

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Proton pump inhibitors (PPIs) are used by millions of patients for the treatment of stomach acid-reflux diseases. Although PPIs are generally considered safe, about 13% of the users develop hypomagnesemia. Despite rising attention for this issue, the underlying mechanism is still unknown.

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There is an increasing amount of clinical evidence that hypomagnesemia (serum Mg2+ levels < 0.7 mmol/l) contributes to type 2 diabetes mellitus pathogenesis. Amongst other hypotheses, it has been suggested that Mg2+ deficiency affects insulin secretion.

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Over the past decades, hypomagnesemia (serum Mg(2+) <0.7 mmol/L) has been strongly associated with type 2 diabetes mellitus (T2DM). Patients with hypomagnesemia show a more rapid disease progression and have an increased risk for diabetes complications.

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Background: Proton-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+.

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