scholarly journals Effect of Dapagliflozin and Magnesium Supplementation on Renal Magnesium Handling and Magnesium Homeostasis in Metabolic Syndrome

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4088
Author(s):  
Hwee-Yeong Ng ◽  
Wei-Hung Kuo ◽  
You-Lin Tain ◽  
Foong-Fah Leung ◽  
Wen-Chin Lee ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Magnesium Sulfate ◽  
Serum Magnesium ◽  
Sglt2 Inhibitors ◽  
Magnesium Concentration ◽  
Magnesium Supplementation ◽  
Intracellular Magnesium ◽  
Glucose Transporter 2 ◽  
Magnesium Excretion

The prevalence of metabolic syndrome (MetS) is increasing, and patients with MetS are at an increased risk of cardiovascular disease and diabetes. There is a close link between hypomagnesemia and MetS. Administration of sodium-glucose transporter 2 (SGLT2) inhibitors has been reported to increase serum magnesium levels in patients with diabetes. We investigated the alterations in renal magnesium handling in an animal model of MetS and analyzed the effects of SGLT2 inhibitors. Adult rats were fed a fructose-rich diet to induce MetS in the first 3 months and were then treated with either dapagliflozin or magnesium sulfate-containing drinking water for another 3 months. Fructose-fed animals had increased insulin resistance, hypomagnesemia, and decreased urinary magnesium excretion. Dapagliflozin treatment improved insulin resistance by decreasing glucose and insulin levels, increased serum magnesium levels, and reduced urinary magnesium excretion. Serum vitamin D and parathyroid hormone levels were decreased in fructose-fed animals, and the levels remained low despite dapagliflozin and magnesium supplementation. In the kidney, claudin-16, TRPM6/7, and FXDY expression was increased in fructose-fed animals. Dapagliflozin increased intracellular magnesium concentration, and this effect was inhibited by TRPM6 blockade and the EGFR antagonist. We concluded that high fructose intake combined with a low-magnesium diet induced MetS and hypomagnesemia. Both dapagliflozin and magnesium sulfate supplementation improved the features of MetS and increased serum magnesium levels. Expression levels of magnesium transporters such as claudin-16, TRPM6/7, and FXYD2 were increased in fructose-fed animals and in those administered dapagliflozin and magnesium sulfate. Dapagliflozin enhances TRPM6-mediated trans-epithelial magnesium transport in renal tubule cells.

Disorders of tubular electrolyte handling

2020 ◽  
pp. 5112-5123
Author(s):  
Nine V.A.M. Knoers ◽  
Elena N. Levtchenko
Keyword(s):  
Serum Magnesium ◽  
Serum Phosphate ◽  
Magnesium Concentration ◽  
Main Site ◽  
Fanconi’S Syndrome ◽  
Tubular Transport ◽  
Bone Changes ◽  
Proximal Tubular ◽  
Magnesium Excretion ◽  
Fanconi's Syndrome

Glycosuria—glucose reabsorption in the proximal tubule is carried out by two different pairs of apical Na+-dependent (SGLT1 and -2) and basolateral Na+-independent (GLUT1 and -2) glucose transporters. Abnormalities in renal glucose transport can be seen in association with other defects of proximal tubular transport. Familial renal glycosuria is a rare autosomal recessive condition caused by mutations in the SGLT2-encoding gene, SLC5A2. Phosphate-handling disorders—the plasma concentration of inorganic phosphate depends on the balance between intestinal absorption, renal excretion, and the internal contribution from bone. Changes of serum phosphate levels can be caused by numerous inherited and acquired conditions. Disorders associated with increased urinary phosphate excretion and low serum phosphate levels produce symptoms that mainly affect the bones: rickets in children and osteomalacia in adults. Magnesium-handling disorders—normal plasma magnesium concentration is achieved by variation of urinary magnesium excretion in response to altered uptake by the intestine. The main site of magnesium absorption is the small bowel, via paracellular simple diffusion at high intraluminal concentrations, and via active transcellular uptake through the magnesium channel TRPM6 at low concentrations. Regulation and fine-tuning of serum magnesium concentration occurs primarily in the kidney. Genetic disorders of magnesium handling include Gitelman’s syndrome. Aminoaciduria and renal Fanconi’s syndrome—most amino acids (except for tryptophan, which is protein bound) are freely filtered by the glomerulus, after which 95 to 99.9% are reabsorbed in the proximal tubules by apical Na+-dependent cotransporters and Na+-independent cotransporters. Aminoaciduria is defined as urinary excretion of more than 5% of the filtered load of an amino acid. Renal Fanconi’s syndrome is characterized by a generalized defect of both Na+-coupled and receptor-mediated proximal tubular transport.

Magnesium Sulfate Does Not Reduce Postoperative Analgesic Requirements

2001 ◽  
Vol 95 (3) ◽  
pp. 640-646 ◽  
Author(s):  
Seong-Hoon Ko ◽  
Hye-Rin Lim ◽  
Dong-Chan Kim ◽  
Young-Jin Han ◽  
Huhn Choe ◽  
...  
Keyword(s):  
Postoperative Pain ◽  
Magnesium Sulfate ◽  
Serum Magnesium ◽  
Magnesium Concentration ◽  
Saline Control ◽  
Control Group ◽  
Forced Expiration ◽  
Inverse Relation ◽  
Analgesic Consumption ◽  
Intravenous Magnesium

Background Because magnesium blocks the N-methyl-D-aspartate receptor and its associated ion channels, it can prevent central sensitization caused by peripheral nociceptive stimulation. However, transport of magnesium from blood to cerebrospinal fluid (CSF) across the blood-brain barrier is limited in normal humans. The current study was designed to evaluate whether perioperative intravenous magnesium sulfate infusion affects postoperative pain. Methods Sixty patients undergoing abdominal hysterectomy received 50 mg/kg intravenous magnesium sulfate as a bolus dose followed by a continuous infusion of 15 mg x kg(-1) x h(-1) for 6 h (magnesium group) or the same volume of isotonic saline (control group). At the end of surgery, serum and CSF magnesium concentration were measured in both groups. The cumulative postoperative analgesic consumption was measured to assess the analgesic effect using a patient-controlled epidural analgesia device. Pain intensities at rest and during forced expiration were evaluated at 6, 24, 48, and 72 h postoperatively. Results At the end of surgery, patients in the magnesium group had significantly greater postoperative serum magnesium concentrations compared with both preoperative and control group values (P < 0.001). Despite significantly higher serum magnesium concentrations in the magnesium group, there was no significant difference in magnesium concentration measured in postoperative CSF. Cumulative postoperative analgesic doses were similar in both groups. However, there was observed an inverse relation between cumulative postoperative analgesic consumption and the CSF magnesium concentration in both groups. Visual analog pain scores at rest and during forced expiration were similar and less than 4 in both groups. Conclusions Perioperative intravenous administration of magnesium sulfate did not increase CSF magnesium concentration and had no effects on postoperative pain. However, an inverse relation between cumulative postoperative analgesic consumption and the CSF magnesium concentration was observed. These results suggest that perioperative intravenous magnesium infusion may not be useful for preventing postoperative pain.

scholarly journals Small for Gestational Age and Magnesium in Cord Blood Platelets: Intrauterine Magnesium Deficiency May Induce Metabolic Syndrome in Later Life

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Junji Takaya ◽  
Kazunari Kaneko
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Cord Blood ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Magnesium Deficiency ◽  
Blood Platelets ◽  
Later Life ◽  
Intracellular Magnesium ◽  
Increased Risk

Magnesium deficiency in pregnancy frequently occurs because of inadequate or low intake of magnesium. Magnesium deficiency during pregnancy can induce not only maternal and fetal nutritional problems, but also consequences that might last in offspring throughout life. Many epidemiological studies have disclosed that small for gestational age (SGA) is associated with an increased risk of insulin resistance in adult life. We reported that intracellular magnesium of cord blood platelets is lower in SGA groups than that in appropriate for gestational age groups, suggesting that intrauterine magnesium deficiency may result in SGA. Taken together, intrauterine magnesium deficiency in the fetus may lead to or at least program insulin resistance after birth. In this review, we propose that intrauterine magnesium deficiency may induce metabolic syndrome in later life. We discuss the potential contribution of aberrant magnesium regulation to SGA and to the pathogenesis of metabolic syndrome.

The Role of Distubances of Phosphate Metabolism in Metabolic Syndrome

2013 ◽  
Vol 20 (3) ◽  
pp. 307-313 ◽  
Author(s):  
Marilena Stoian ◽  
Victor Stoica ◽  
Gabriela Radulian
Keyword(s):  
Metabolic Syndrome ◽  
Serum Magnesium ◽  
Healthy Population ◽  
Phosphate Metabolism ◽  
The Metabolic Syndrome ◽  
Study Population ◽  
Excretion Rates ◽  
Magnesium Excretion ◽  
The Relationship

Abstract Background and Aims: Metabolic syndrome represents a cluster of cardiovascular risk factors and reached epidemic proportions. It was hypothesized that disturbances in phosphate metabolism may represent a feature of the metabolic syndrome. The aim of the study was to investigate the relationship between phosphate levels and the presence of metabolic syndrome components, as well as the putative mechanism for reduced phosphate level in metabolic syndrome. Materials and Methods: We enrolled 155 subjects: 64 with metabolic syndrome and 91 controls. Biochemical parameters of the metabolic syndrome study population were compared with the healthy population. Results: Patients with metabolic syndrome showed significantly lower phosphate (46%) and magnesium levels compared with controls (22.7%) (p<0.001). Women showed significantly greater serum phosphate levels than men (3.32 mg/dl versus 3.18 mg/dl) (p<0.03). Serum magnesium levels did no differ significantly between men and women. Fractional phosphate excretion rates in patients with metabolic syndrome were similar with controls (10.1±10.2% vs 13.1±9.9%), as well as fractional magnesium excretion (3.1±1.6% vs 2.8±1.3%). Conclusions: Patients with metabolic syndrome show significantly lower phosphate and magnesium concentrations compared to controls. This reduction is likely to be attributed to internal redistribution of phosphate and is more pronounced as the number of components of metabolic syndrome increases

Effect of Magnesium Loading Dose on Insulin Resistance in Patients With Stress-Induced Hyperglycemia: A Randomized Clinical Trial

2018 ◽  
Vol 35 (7) ◽  
pp. 687-693 ◽  
Author(s):  
Zinat Heidary ◽  
Hossein Khalili ◽  
Mostafa Mohammadi ◽  
Mohammad-Taghi Beigmohammadi ◽  
Alireza Abdollahi
Keyword(s):  
Insulin Resistance ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Model Assessment ◽  
Loading Dose ◽  
Homeostasis Model Assessment ◽  
Magnesium Supplementation ◽  
Intracellular Magnesium ◽  
The Mean ◽  
To Receive

Objectives: There is currently no evidence that whether magnesium supplementation would improve stress-induced hyperglycemia (SIH) in critically ill patients. In this study, effects of magnesium loading dose on insulin resistance (IR) indices were evaluated in critically ill patients without diabetes having SIH. Methods: Seventy critically ill patients with SIH were assigned to receive a loading dose of magnesium (7.5 g of magnesium sulfate in 500 mL normal saline as intravenous infusion over an 8-hour period) or placebo. Changes in baseline of serum and intracellular magnesium and serum adiponectin (AD) levels, homeostasis model assessment of IR (HOMA-IR), and HOMA-AD ratio were assessed in this study. Results: Serum and intracellular magnesium levels increased significantly in patients in the magnesium group ( P < .001). At day 3, there were significant differences between the magnesium group and the placebo group in the mean changes from baseline in the HOMA (between-group difference: −0.11; 95% confidence interval [CI]: −0.19 to −0.01; P = .02), the AD (between-group difference: 0.94; 95% CI: 0.41-1.48; P = .04), and the HOMA-AD ratio (between-group difference: −0.03; 95% CI: −0.04 to −0.01; P < .001). Conclusion: In the present study, a single-loading dose of intravenous magnesium improved IR indices in critically ill patients with SIH.

scholarly journals Magnesium Sulfate for Severe Acute Asthma in Children

2003 ◽  
Vol 8 (1) ◽  
pp. 40-45 ◽  
Author(s):  
H. William Kelly
Keyword(s):  
Magnesium Sulfate ◽  
Acute Asthma ◽  
Muscle Relaxation ◽  
Serum Magnesium ◽  
Bronchial Hyperresponsiveness ◽  
The Body ◽  
Smooth Muscle Relaxation ◽  
Severe Toxicity ◽  
Intracellular Magnesium ◽  
Β2 Agonists

Magnesium is an abundant intracellular cation that has been used for years in the treatment of hyper-tension and seizures associated with eclampsia of pregnancy as well as used as a tocolytic agent.1 Over sixty years ago, Haury showed that magnesium sulfate (MgSO4) could produce bronchodilation in asthmatics.2 However, interest in magnesium sulfate as a potential therapy for acute asthma surfaced in the late 1980s following a series of studies demonstrating that magnesium produced dose-dependent bronchodilation. The precise mechanism by which magnesium produces smooth muscle relaxation is not known, but it is thought to act by enhancing calcium uptake in the sarcoplasmic reticulum3 and/or as a calcium antagonist.4 In addition, magnesium is a cofactor regulating a number of enzymatic and cellular activities in the body, including adenyl cyclase and sodium-potassium ATP-ase, potentially enhancing the effects of β2-agonists.5 Other potential beneficial mechanisms in asthma include inhibition of acetylcholine release from cholinergic nerves6 and reduction of histamine release from mast cells.7 It is not clear whether magnesium acts as a functional antagonist to bronchoconstriction like the β2-agonists and theophylline or a specific antagonist like anticholinergics and antihistamines. Studies showing attenuation of the bronchoconstriction from histamine and methacholine would suggest functional antagonism.8,9 Some suggest that the response to intravenous magnesium sulfate is dependent upon achieving serum magnesium concentrations of 4–6 mg/dL (1.6–2.4 mmol/L).10 These values are similar to those that are employed to achieve tocolysis (4–8 mg/dL) and about one half those associated with severe toxicity of respiratory failure, cardiac arrhythmias and death (12–15 mg/ dL).1 It should be pointed out that studies have not reported lower magnesium concentrations in asthmatics than controls although one study reported correlation with bronchial hyperresponsiveness and intracellular magnesium concentrations in asthmatics. 11–13 Thus, it is unlikely that the bronchodilator response to magnesium is a result of restoring normal homeostasis but most likely a function of its direct antagonistic effects on intracellular calcium activity.

Management of an i.v. fluid shortage through use of electronic medical record alerts

2020 ◽  
Vol 77 (7) ◽  
pp. 546-551
Author(s):  
Melissa Sandler ◽  
Jared Cavanaugh ◽  
Ted Walton ◽  
Laurie Cavendish ◽  
Kruti Shah
Keyword(s):  
Oral Dose ◽  
Magnesium Sulfate ◽  
Medical Record ◽  
Magnesium Oxide ◽  
Electronic Medical Record ◽  
Primary Outcome ◽  
Serum Magnesium ◽  
Magnesium Concentration ◽  
Drug Shortage ◽  
Oral Magnesium

Abstract Purpose Evaluation of mechanisms used to cope with an i.v. fluid shortage to determine if prescribing habits were changed and if substitution of an i.v. dose of magnesium with an oral dose impacted patient outcomes. Methods A single-center, retrospective analysis of electronic medical record (EMR) alerts and medical records covering 6-month periods before and during an i.v. fluid shortage was conducted. Records of adult medical and surgical inpatients admitted during these periods who had an order for i.v. or oral magnesium were screened for inclusion. The primary outcome of part 1 of the study was the percent acceptance of drug shortage–related EMR alert recommendations associated with i.v. magnesium. The primary outcome of part 2 of the study was the change in serum magnesium concentration (SMC) after an i.v. or oral dose of magnesium was administered. Results Of the 7,476 EMR alerts generated during provider ordering of i.v. magnesium products, 4.8% resulted in the provider accepting the recommendation to switch to an oral alternative, 89% resulted in continuation of an i.v. magnesium order, and 6.2% resulted in order cancellation. Among patients who received magnesium doses, SMC values increased by a mean (SD) of 0.135 (0.08) mg/dL per gram of i.v. magnesium sulfate administered (n = 251), compared to an increase of 0.058 (0.08) mg/dL per 400-mg tablet of magnesium oxide administered (n = 42). Conclusion Acceptance of the EMR alert recommendations was low. Both i.v. magnesium sulfate and oral magnesium oxide are viable options for increasing SMC.

scholarly journals Lower serum magnesium concentration is associated with diabetes, insulin resistance, and obesity in South Asian and white Canadian women but not men

2015 ◽  
Vol 59 (1) ◽  
pp. 25974 ◽  
Author(s):  
Jesse Bertinato ◽  
Chao Wu Xiao ◽  
W. M. Nimal Ratnayake ◽  
Lois Fernandez ◽  
Christopher Lavergne ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
South Asian ◽  
Serum Magnesium ◽  
Magnesium Concentration ◽  
Lower Serum ◽  
Serum Magnesium Concentration

scholarly journals Association between serum magnesium concentration and metabolic syndrome, diabetes, hypertension and hyperuricaemia in knee osteoarthritis: a cross-sectional study in Hunan Province, China

BMJ Open ◽  
2018 ◽  
Vol 8 (9) ◽  
pp. e019159 ◽  
Author(s):  
Yilun Wang ◽  
Jie Wei ◽  
Chao Zeng ◽  
Tuo Yang ◽  
Hui Li ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Knee Osteoarthritis ◽  
Serum Magnesium ◽  
Cross Sectional Study ◽  
Hunan Province ◽  
Magnesium Concentration ◽  
Inverse Association ◽  
Sectional Study ◽  
Cross Sectional ◽  
Knee Oa

ObjectivesTo examine the associations between serum magnesium (Mg) concentration with the prevalence of metabolic syndrome (MetS), diabetes mellitus (DM), hypertension (HP) and hyperuricaemia (HU) in patients with radiographic knee osteoarthritis (OA).MethodsThe present study was conducted at the Health Management Center of Xiangya Hospital. Radiographic OA was evaluated for patients aged over 40 years with basic characteristics and blood biochemical assessment. Serum Mg concentration was measured using the chemiluminescence method. MetS, DM, HP and HU were diagnosed based on standard protocols. The associations between serum Mg concentration with MetS, DM, HP and HU were evaluated by conducting multivariable adjusted logistic regression.ResultsA total of 962 patients with radiographic knee OA were included. Compared with the lowest quintile, the multivariable adjusted ORs and related 95% CIs of DM were 0.40 (95% CI 0.23 to 0.70, p=0.001), 0.33 (95% CI 0.18 to 0.60, p<0.001), 0.27 (95% CI 0.14 to 0.52, p<0.001) and 0.22 (95% CI 0.11 to 0.44, p<0.001) in the second, third, fourth and highest quintiles of serum Mg, respectively (p for trend <0.001); the multivariable adjusted ORs of HU were 0.33 (95% CI 0.19 to 0.59, p<0.001), 0.52 (95% CI 0.30 to 0.91, p=0.022) and 0.39 (95% CI 0.22 to 0.70, p=0.001) in the third, fourth and highest quintiles of serum Mg, respectively (p for trend <0.001); and the multivariable adjusted ORs of MetS were 0.59 (95% CI 0.36 to 0.94, p=0.027) in the second and 0.56 (95% CI 0.34 to 0.93, p=0.024) in the highest quintiles of serum Mg. However, the inverse association between serum Mg and the prevalence of MetS was non-linear (p for trend=0.067). There was no significant association between serum Mg and HP in patients with OA.ConclusionsThe serum Mg concentration was inversely associated with the prevalence of MetS, DM and HU in patients with radiographic knee OA.Level of evidenceLevel III, cross-sectional study.

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