Fluctuations in metabolite content in the liver of magnesium-deficient rats

Abstract

Mg deficiency induces various metabolic disturbances including glucose metabolism in the liver. However, no comprehensive information is currently available on the metabolic pathways affected by Mg deficiency. The present study examined metabolite content in the liver of Mg-deficient rats using a metabolomic analysis. In this study, 4-week-old, male Sprague-Dawley rats were fed a control diet or a Mg-deficient diet for 8 weeks. The metabolomic analysis identified 105 metabolites in the liver, and significant differences were observed in the hepatic contents for thirty-three metabolites between the two groups. An analysis by MetaboAnalyst, a web-based metabolome data analysis tool, indicated that the Mg deficiency affected taurine/hypotaurine metabolism, methionine metabolism and glycine/serine/threonine metabolism; taurine, hypotaurine, glycine, serine and threonine contents were increased by Mg deficiency, whereas the amounts of 2-ketobutyric acid (a metabolite produced by the catabolism of cystathionine or threonine) and 5'-methylthioadenosine (a metabolite involved in spermidine synthesis) were decreased. The amount of glucose 6-phosphate, a hub metabolite of glycolysis/gluconeogenesis and the pentose phosphate pathway, was significantly decreased in Mg-deficient rats. Mg deficiency also decreased metabolite contents from the citric acid cycle, including citric acid, fumaric acid and malic acid. Aberrant metabolism may be related to the allosteric regulation of enzymes; the mRNA levels of enzymes were generally similar between the two groups. The present study suggests that the Mg deficiency-mediated modulation of hepatic metabolism is as yet uncharacterised.

The magnesium transporter NIPAL1 is a pancreatic islet–expressed protein that conditionally impacts insulin secretion

“…Given this, NIPAL1 could play a role in facilitating magnesium entry into the Golgi in a manner that directly impacts the ionic flux governing the trafficking of insulin vesicles within the organelle. A potential driving force may be magnesium's role as a primary ATP-binding co-factor (Mg-ATP) involved in facilitating phosphate transfer reactions (5,6) that are critical for fueling secretory granule movements (45,46) and both glycolysis and the citric acid cycle (47,48). Both Golgi and mitochondrial functions are highly dependent on the availability of ATP delivered by bound magnesium.…”

Rosiglitazone-induced changes in the oxidative stress metabolism and fatty acid composition in relation with trace element status in the primary adipocytes

“…Our data showed that 0.1 µmol/L RSG treatment induced increased Ca and K levels in the cells that may show inducing the insulin secretion ( Figure 2 ). On the other hand, Mg is essential for glycolysis, citric acid cycle, increasing insulin sensitivity and improving lipid profile [34] [35] [36] [37] [38] . We showed that 0.1 µmol/L RSG treatment caused an increase in magnesium concentrations that may be explained by the necessity of Mg in the cells to improve insulin sensitivity and the lipid profile ( Figure 2 ).…”

Effect of long‐distance transportation on serum metabolic profiles of steer calves

“…Then the solution was treated as described previously (Shigematsu et al . ). Briefly, the samples were lyophilized, and then 40 μL of 20 mg/mL methoxyamine hydrochloride (Sigma‐Aldrich) was added, dissolved in pyridine for oximation.…”

“…A sample of 50 lL of serum was mixed with 5 lL of 1 mg/mL 2-isopropylmalic acid (Sigma-Aldrich, Tokyo, Japan) in distilled water as an internal standard, and 250 lL of methanol/chloroform/water (2.5/1/1). Then the solution was treated as described previously (Shigematsu et al 2016). Briefly, the samples were lyophilized, and then 40 lL of 20 mg/mL methoxyamine hydrochloride (Sigma-Aldrich) was added, dissolved in pyridine for oximation.…”