"Magnesium gluconate studies" by Al222 (19776 pt) | 2021-Sep-02 11:05 |
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Compendium of the most significant studies with reference to properties, intake, effects.
Zhang Q, Zhou PH, Zhou XL, Zhang DL, Gu Q, Zhang SJ, Zhang J, Zhang JS, Qian ZY. Effect of magnesium gluconate administration on lipid metabolism, antioxidative status, and related gene expression in rats fed a high-fat diet. Magnes Res. 2018 Nov 1;31(4):117-130. doi: 10.1684/mrh.2019.0445.
Abstract
To explore the effect of magnesium gluconate (MgG) on lipid metabolism and its regulation mechanism through animal experiments, and to provide basis for MgG dietary intervention in hyperlipidemia. The first four weeks was hyperlipidemia-inducing period through high-fat diet and the following eight weeks was the MgG supplementation. At the end of the experiment, blood and liver samples were collected for the measurements of lipid profile, antioxidative indexes, pathological examination, and cholesterol metabolism-related gene expression. Oral administration of MgG notably decreased the blood levels of TC, TG, LDL-C and liver function index ALT and AST of hyperlipidemic rats. The rats supplemented with magnesium showed a huge increase in the GSH-Px and SOD activities, and reduced the heart weight and liver lipid accumulation of high-fat diet fed rats. MgG remarkably up-regulated the mRNA expression levels of LDLR and CYP7A1 of liver enzymes related to cholesterol metabolism. Oral magnesium supplementation inhibited an increase in lipid profile and liver function index by a high-fat diet, and enhanced the activity of the antioxidant enzymes. Magnesium has lipid-lowering and antioxidative effects that protect the liver against hyperlipidemia.
Li S, Tian H. Oral low-dose magnesium gluconate preventing pregnancy induced hypertension. Zhonghua Fu Chan Ke Za Zhi. 1997 Oct;32(10):613-5. Chinese.
Abstract
Objective: To study the effects of oral low-dose magnesium gluconate in prevention of pregnancy induced hypertension (PIH) and its mechanism.
Methods: A prospective randomized double-blind study was carried out in 51 pregnant women as treatment group (including 22 cases as treatment group 1 and 29 cases as treatment group 2) and 51 pregnant women as controls (including 28 cases as controls group 1 and 23 cases as control group 2). Low-dose magnesium gluconate (3 g/day) or placebo was given from the 28th week of gestation to delivery consecutively.
Results: 4% of the pregnant women developed PIH after magnesium gluconate treatment, which was substantially lower than that in the control group (16%) (P < 0.05). In the treatment group 2, women showed higher concentration of 6-keto-prostaglandin F1 alpha (PGF1a) and 6-keto-/thromboxane B2(TXB2) (P/T) ratio than that of the control group 2. Moreover, TXB2 level was lower than that in the control group 2. In the treatment group 1 women showed higher ratio of P/T than that of the control group 1. There were no significant differences of serum magnesium concentration among all groups.
Conclusion: Low-dose magnesium gluconate may efficiently prevent PIH in high risk women. The mechanism of action of magnesium gluconate probably involves to keep the balance of PGI2 and TXA2, but not associates with serum magnesium level.
Martin RW, Martin JN Jr, Pryor JA, Gaddy DK, Wiser WL, Morrison JC. Comparison of oral ritodrine and magnesium gluconate for ambulatory tocolysis. Am J Obstet Gynecol. 1988 Jun;158(6 Pt 1):1440-5. doi: 10.1016/0002-9378(88)90379-1.
Abstract
Magnesium sulfate has been administered intravenously to arrest preterm labor but the oral form of this drug cannot be used for continual tocolysis. This trial involved the administration of oral magnesium gluconate to determine its effectiveness compared with that of ritodrine hydrochloride in 50 patients whose labor had been arrested by parenteral therapy. Group A (n = 25) received 1 gm of oral magnesium gluconate every 2 to 4 hours for tocolysis and group B (n = 25) received 10 mg of ritodrine every 2 to 4 hours. The number of patients who progressed to 37 weeks' gestation was similar (group A, 21 versus group B, 19) and the time gained in utero was not different (group A, 6.4 weeks versus group B, 5.9 weeks). There was a trend toward more side effects with the use of ritodrine (40%) compared with magnesium gluconate (16%), but the numbers were too small to reveal a significant difference. These data suggest that magnesium gluconate used as an oral tocolytic is as effective as a beta-agonist in patients whose labor is arrested initially with intravenous therapy.
Kaufman SS, Loseke CA, Anderson JB, Murray ND, Vanderhoof JA, Young RJ. Magnesium acetate vs. magnesium gluconate supplementation in short bowel syndrome. J Pediatr Gastroenterol Nutr. 1993 Jan;16(1):104-5. doi: 10.1097/00005176-199301000-00025.
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