Magnesium Deficiency and Carbohydrate Metabolism

Kahil, Michel E.; Parrish, John E.; Simons, E. L.; Brown, Harold

doi:10.2337/diab.15.10.734

Cited by 22 publications

(13 citation statements)

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“…On the other hand, irrespective of the presence of insulin, glucose uptake by the diaphragm obtained from Mg-deficient rats was enhanced in Mg-free medium when compared to the uptake by the control diaphragm. The addition of Mg to the Mg-free medium reduced glucose uptake by the diaphragm of Mg-deficient rats, while uptake by control diaphragm was not affected by the presence of Mg in medium (28). These results suggest that the decrease of extracellular Mg stimulates the uptake of glucose by tissue in a Mg-deficient state, which may explain the lower blood glucose level.…”

Section: Glut4 In Adipocytesmentioning

confidence: 44%

Change in Glucose Homeostasis in Rats by Long-Term Magnesium-Deficient Diet.

Kimura

Murase

Nagata

1996

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryIt is widely known that hypomagnesemia is one of the symptoms observed in diabetic patients. This study was performed to assess the effect of chronic magnesium (Mg) deficiency on glucose metab olism in rats. Male Sprague-Dawley rats (at the age of four weeks) were given a Mg-deficient diet or a control diet for two to eight weeks. The rats were orally administered sucrose solution (2g/kg BW) every two weeks, and blood was drawn from a tail vein before and 15min after sucrose loading to determine the concentrations of blood glucose and plasma insulin. At the same time, other rats in a non-fasted condition were sacrificed by decapitation (rats sacrificed at eight weeks were rats used for sucrose loading). The epididymal fat pads were immediately removed and adipocytes were isolated. The amount of glucose transporter 4 (GLUT4) in the plasma membranes and low-density microsomal mem branes prepared from the adipocytes was measured by immunoblotting to estimate the influence of chronic Mg deficiency on glucose metabolism at the cellular level. In addition, plasma biochemical parameters and muscle mineral contents were also evaluated. The glucose concentration in fasted blood was significantly lower in Mg-deficient rats than in control rats throughout the experiment period. The feeding of a Mg-deficient diet also attenuated the response of blood glucose and plasma insulin: the glucose level in blood tended to be lower in Mg-deficient rats at 15min after oral sucrose administration, and the difference was significant at two and eight weeks. The plasma insulin level in Mg-deficient rats was also lower, reaching a significant difference at two weeks. When animals were sacrificed in a non-fasted condition at 2-week intervals, the plasma glucose level was also significantly decreased in Mg-deficient rats as compared to control rats throughout the experiment period. The plasma insulin level in non-fasted Mg-deficient rats was also significantly decreased at two and six weeks. The Mg-deficient diet increased plasma triglyceride, but the difference was significant only at four weeks, and plasma cholesterol remained unchanged. The plasma Mg level was markedly lower in Mg-deficient rats throughout the experiment period. In Mg-deficient rats, 407

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Section: Glut4 In Adipocytesmentioning

confidence: 44%

Change in Glucose Homeostasis in Rats by Long-Term Magnesium-Deficient Diet.

Kimura

Murase

Nagata

1996

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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“…An earlier disappearance of hyperglycaemia has been previously reported during magnesium deficiency (Kahil, Parrish, Simons and Brown l966;Lentz, Madsen, Miller and Hansard 1976) but the means by which magnesium depletion enhances glucose utilization is not clear. This increased glucose uptake did not seem to be related to insulin, but rather to modification of cell permeability to glucose in a manner not dependent on insulin (Kahil et al 1966). Whether this is linked to a perturbation of the structural integrity of membrane or a depressed affinity of the glucose transport system is unknown.…”

Section: Discussionmentioning

confidence: 66%

The Effect of Magnesium Deficiency on Glucose Stimulated Insulin Secretion in Rats

Gueux¹,

Rayssiguier²

1983

Horm Metab Res

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Weanling Sherman rats were pair-fed for 8 days on a control or a magnesium deficient diet containing 70.5% sucrose. After a 12-hour fast, the rats were injected intraperitoneally with glucose (250 mg/100 g body weight) and arterial blood was drawn at 0, 15, 30, 60, 90 minutes after injection. Before glucose loading, in magnesium deficient rats, plasma magnesium levels were significantly increased. The plasma triglyceride concentration was significantly higher in magnesium deficient rats compared to controls. After glucose loading, in the control group, the plasma insulin concentrations increased to 67.9 +/- 5.8 microU/ml at 15 minutes and returned to pretreatment levels by 30 minutes; in the magnesium-deficient rats, the plasma insulin levels were significantly lower at 15 minutes 32.9 +/- 5.6 microU/ml (P less than 0.01) and returned more slowly to the pre-challenge level. No significant differences were observed in plasma glucose levels between the two groups of rats.

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“…All these variables make the interpretation of the data difficult. Finally (43,44), magnesium (48), or potassium (49) may affect insulin secretion. The difference in the insulin response to hyperglycemia in our NPX and NPX-PTX dogs could not be attributed to differences in the plasma concentrations of these electrolytes because the levels of the latter were similar in both groups.…”

Section: Discussionmentioning

confidence: 99%

Role of parathyroid hormone in the glucose intolerance of chronic renal failure.

et al. 1985

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Evidence has accumulated suggesting that the state of secondary hyperparathyroidism and the elevated blood levels of parathyroid hormone (PTH) in uremia participate in the genesis of many uremic manifestations. The present study examined the role of PIH in glucose intolerance of chronic renal failure (CRF). Intravenous glucose tolerance tests (IVGTI) and euglycemic and hyperglycemic clamp studies were performed in dogs with CRF with (NPX) and without parathyroid glands (NPX-PTX). There were no significant differences among the plasma concentrations of electrolytes, degree of CRF, and its duration. The serum levels of PTH were elevated in NPX and undetectable in NPX-PTX.The NPX dogs displayed glucose intolerance after CRF and blood glucose concentrations during IVGTT were significantly (P < 0.01) higher than corresponding values before CRF. In contrast, blood glucose levels after IVGTT in NPX-PTX before and after CRF were not different. K-g rate fell after CRF from 2.86±0.48 to 1.23±0.18%/min (P < 0.01) in NPX but remained unchanged in NPX-PTX (from 2.41±0.43 to 2.86±0.86%/min) dogs. Blood insulin levels after IVGTT in NPX-PTX were more than twice higher than in NPX animals (P < 0.01) and for any given level of blood glucose concentration, the insulin levels were higher in NPX-PTX than NPX dogs.Clamp studies showed that the total amount of glucose utilized was significantly lower (P < 0.025) in NPX (6.64±1.13 mg/kg *min) than in NPX-PTX (10.74±1.1 mg/kg *min) dogs.The early, late, and total insulin responses were significantly (P < 0.025) greater in the NPX-PTX than NPX animals. The values for the total response were 143±28 vs. 71±10 ;&U/ml, P < 0.01. There was no significant difference in the ratio of glucose metabolized to the total insulin response, a measure of tissue sensitivity to insulin, between the-two groups. The glucose metabolized to total insulin response ratio in NPX (5.12±0.76 mg/kg min per ttU/ml) and NPX-PTX (5.18±0.57 mg/kg. min per pU/ml) dogs was not different but significantly (P < 0.01) lower than in normal animals (9.98±1.26 mg/ kg.in per pU/ml). The metabolic clearance rate of insulin was significantly (P < 0.02) reduced in both NPX (12.1±0.7 ml/kg min) and NPX-PTX (12.1±0.9 ml/kg min) dogs, as compared with normal animals (17.4±1.8 ml/kg min). The basal hepatic glucose production was similar in both groups of animals and not different from normal dogs; both the time Address correspondence to Dr. Massry, Division of Nephrology.

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Magnesium Deficiency and Carbohydrate Metabolism

Cited by 22 publications

References 0 publications

Change in Glucose Homeostasis in Rats by Long-Term Magnesium-Deficient Diet.

Change in Glucose Homeostasis in Rats by Long-Term Magnesium-Deficient Diet.

The Effect of Magnesium Deficiency on Glucose Stimulated Insulin Secretion in Rats

Role of parathyroid hormone in the glucose intolerance of chronic renal failure.

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