Low gut microbiota diversity and dietary magnesium intake are associated with the development of PPI-induced hypomagnesemia.

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.

Renal phospholipidosis and impaired magnesium handling in high-fat-diet-fed mice.

Hypomagnesemia (blood Mg concentration <0.7 mM) is a common electrolyte disorder in patients with type 2 diabetes (T2D), but the etiology remains largely unknown. In patients with T2D, reduced blood Mg levels are associated with an increased decline in renal function, independent of glycemic control and hypertension.

Diabetes-induced hypomagnesemia is not modulated by metformin treatment in mice.

Approximately 30% of patients with type 2 diabetes mellitus (T2D) have hypomagnesemia (blood magnesium (Mg) concentration <0.7 mmol/L). In T2D patients, treatment with metformin is associated with reduced blood Mg levels.

Increased NEFA levels reduce blood Mg in hypertriacylglycerolaemic states via direct binding of NEFA to Mg.

Aims/hypothesis: The blood triacylglycerol level is one of the main determinants of blood Mg concentration in individuals with type 2 diabetes. Hypomagnesaemia (blood Mg concentration <0.7 mmol/l) has serious consequences as it increases the risk of developing type 2 diabetes and accelerates progression of the disease.

Magnesium deficiency prevents high-fat-diet-induced obesity in mice.

Aims/hypothesis: Hypomagnesaemia (blood Mg <0.7 mmol/l) is a common phenomenon in individuals with type 2 diabetes. However, it remains unknown how a low blood Mg concentration affects lipid and energy metabolism.

Polycystin-1 dysfunction impairs electrolyte and water handling in a renal precystic mouse model for ADPKD.

The PKD1 gene encodes polycystin-1 (PC1), a mechanosensor triggering intracellular responses upon urinary flow sensing in kidney tubular cells. Mutations in PKD1 lead to autosomal dominant polycystic kidney disease (ADPKD). The involvement of PC1 in renal electrolyte handling remains unknown since renal electrolyte physiology in ADPKD patients has only been characterized in cystic ADPKD.