OBJECTIVE—To determine whether oral magnesium supplementation (as magnesium chloride [MgCl2] solution) improves both insulin sensitivity and metabolic control in type 2 diabetic subjects with decreased serum magnesium levels.

RESEARCH DESIGN AND METHODS—This study was a clinical randomized double-blind placebo-controlled trial. A total of 63 subjects with type 2 diabetes and decreased serum magnesium (serum magnesium levels ≤0.74 mmol/l) treated by glibenclamide received either 50 ml MgCl2 solution (containing 50 g MgCl2 per 1,000 ml solution) or placebo daily for 16 weeks. Chronic diarrhea, alcoholism, use of diuretic and/or calcium antagonist drugs, and reduced renal function were exclusion criteria. Homeostasis model assessment for insulin resistance (HOMA-IR) was used as the parameter of insulin sensitivity and glucose and HbA1c as parameters of metabolic control.

RESULTS—At the end of the study, subjects who received magnesium supplementation showed significant higher serum magnesium concentration (0.74 ± 0.10 vs. 0.65 ± 0.07 mmol/l, P = 0.02) and lower HOMA-IR index (3.8 ± 1.1 vs. 5.0 ± 1.3, P = 0.005), fasting glucose levels (8.0 ± 2.4 vs. 10.3 ± 2.1 mmol/l, P = 0.01), and HbA1c (8.0 ± 2.4 vs. 10.1 ± 3.3%, P = 0.04) than control subjects.

CONCLUSIONS—Oral supplementation with MgCl2 solution restores serum magnesium levels, improving insulin sensitivity and metabolic control in type 2 diabetic patients with decreased serum magnesium levels.

Hypomagnesemia, a frequent condition in patients with diabetes (1,2), could be involved in the development of poor metabolic control and chronic complications (3,4). A large body of evidence that shows a link between hypomagnesemia and reduction of tyrosine-kinase activity at the insulin receptor level, which may result in the impairment of insulin action and development of insulin resistance, has been progressively accumulated in previous years (510). Although evidence suggests that magnesium supplementation could be useful in the treatment of diabetes and to prevent the development of its chronic complications (1113), the possible benefits of magnesium administration as an adjuvant factor for the treatment of type 2 diabetes, based in a randomized controlled trial, are scarce (1419) and controversial (19).

So, the aim of this study was to determine whether oral magnesium supplementation, as magnesium chloride (MgCl2) solution, 2.5 g daily, improves insulin sensitivity and metabolic control in type 2 diabetic subjects with decreased serum magnesium levels.

With approval of the protocol by the Mexican Social Security Institute (MSSI) Research Committee and after obtaining informed consent from subjects, a randomized double-blind placebo-controlled trial was carried out.

Type 2 diabetic subjects recruited from an outpatient Primary Level Medical Care Office in Durango, a city in Northern Mexico, were eligible to participate in the study if they had decreased serum magnesium levels. Based on previous results of healthy subjects from our population, in whom normal values ranged from 0.75 to 0.99 mmol/l, decreased serum magnesium levels were defined by magnesium concentration ≤0.74 mmol/l (20).

Before their inclusion at the study, all of the subjects were clinically evaluated and laboratory tested in order to determine the presence of chronic diarrhea, alcohol intake (≥30 g per day), use of diuretic and/or calcium antagonist drugs, and reduced renal function (exclusion criteria). In addition, subjects receiving magnesium supplementation were not included.

The primary trial end point was the change in insulin sensitivity and metabolic control. Sample size was estimated based on a statistical power of 80%, α value 0.05, and allowing for nonimprovement in the serum insulin level of 35 and 75% for the subjects receiving magnesium supplementation and placebo, respectively. The required sample size to detect a treatment effect was 24 subjects per group (21).

A total of 65 eligible subjects were enrolled and randomly allocated to receive either magnesium supplementation or placebo daily for 16 weeks. We used the MgCl2 solution (50 g MgCl2 per 1,000 ml solution [5% solution]) because MgCl2 solution shows a higher bioavailability than other commercial magnesium preparations (22). In fasting conditions, subjects in the MgCl2 group drank 50 ml of the 5% solution (2.5 g MgCl2 daily).

Computer-generated random numbers were used to assign participants to oral magnesium supplementation or placebo groups. The final distribution was as follows: 32 subjects in the MgCl2 group (group A) and 31 subjects in the placebo group (group B) (Fig. 1).

All of the subjects withdrew pharmacological treatment and were advised to consume a diet with >50% of daily calories from carbohydrates, <10% from saturated fat, 20% from mono- and polyunsaturated fat, and ∼1 g protein per kg ideal body wt per day for the 3 months before the beginning of the trial (23). In addition, and according to age and physical condition of each participant, all of the subjects were advised to perform physical activity. The goal was achieved when the subjects performed 30 min of physical activity at least three times per week. After 3 months of lifestyle intervention, glibenclamide was started and individually adjusted to achieve glucose control. Subjects who reached serum glucose levels ≥16.7 mmol/l during the lifestyle intervention period began pharmacological treatment and were not included in the study (Fig. 1).

At baseline and after 16 weeks of treatment, anthropometric measurements, HbA1c, lipid profile, serum glucose, and serum insulin and magnesium levels were measured. Furthermore, serum glucose and magnesium levels were measured every 4 weeks. The type 2 diabetic patients and the personnel assessing outcomes were blinded to group assignment. Subjects in the group A received 2.5 g MgCl2 daily, and those in group B received placebo.

Adherence to pharmacological treatment and lifestyle intervention was assessed every month by personal interview, tablet count and remnant solution measurement, and independent interview with the individual in charge of preparing meals for the family.

Measurements.

Height and weight were taken using standard protocols with the subjects in light clothing and without shoes. BMI was calculated as weight (in kilograms) divided by height (in meters squared). Waist circumference was taken as the minimum circumference at umbilicus level.

Serum glucose was measured by the glucose-oxidase method with the intra- and interassay variations of 2.5 and 4.0%, respectively. Insulin levels were measured by radioimmunoassay with intra- and interassay variation coefficients of 4.5 and 6.9%, respectively. Serum magnesium concentrations were measured by colorimetric method, with intra- and interassay variations of 1.0 and 2.5%, respectively.

The homeostasis model assessment for insulin resistance (HOMA-IR) (fasting glucose [mmol/l] × fasting insulin [μUI/ml]/22.5) was used for estimating insulin sensitivity (24).

Statistical analysis.

The preplanned intent-to-treat analysis of the primary study end point was done for all the randomly allocated participants who satisfactorily completed the follow-up (Fig. 1).

To establish the differences between the groups, we used two-tailed unpaired Student’s t test for comparison of normally distributed variables (Mann Whitney U test for skewed data) or the χ2 test for categoric variables. Two-tailed paired t test (or Wilcoxon’s test) was performed before and after treatment comparisons. A 95% CI was considered, and a P value <0.05 defined the level of statistical significance. Data analysis was performed using the SPSS version 10.0 statistical package.

A total of 210 patients were screened (Fig. 1). Of these, 130 subjects did not satisfactorily complete the phase of lifestyle intervention and 80 that fulfilled the inclusion criteria were randomized to receive either MgCl2 solution or placebo. Eight subjects withdrew consent and were not included in the intent-to-treat period; finally, 35 subjects were included in the MgCl2 group and 37 in the placebo group. Nine subjects dropped-out (three in MgCl2 group and six in placebo group) (Fig. 1). Magnesium supplement was well tolerated, and there were no serious adverse events or side effects due to MgCl2 or placebo. Slight abdominal and unspecific bone pain in the first month, which did not require treatment or discontinuation of magnesium administration, was the most frequent side effect in the magnesium-supplemented subjects (37.5%). In addition, slight diarrhea with duration <2 days that did not require interruption of the treatment was present in two magnesium-supplemented (6.25%) and one control (3.2%) patient.

Altogether, 63 subjects who satisfactorily completed the follow-up were included in the analysis of data. Adherence to treatment was achieved for 32 (91.4%) subjects in the MgCl2 group and 31 (88.6%) subjects in the placebo group.

From the beginning of the study, the oral hypoglycemic drug used was glibenclamide (5 mg t.i.d.), in doses that remained without change for all participants during the study. In addition, there were no significant differences for treatment with other drugs, such as ACE inhibitors, statins, etc., between both groups. In the same way, other complications, such as cardiovascular disease, were also similarly distributed (68 vs. 71% for the magnesium-supplemented and control patients, respectively).

Table 1 shows the characteristics of the evaluated participants, which at the beginning of the study did not differ between the groups. On the other hand, at the end of the study the serum magnesium levels showed a significant increase in the subjects who received MgCl2 and remained without significant change in the control subjects. In addition, subjects in both groups had reduced fasting glucose and HbA1c, which were significantly lower in the magnesium-supplemented than in the control subjects. Finally, fasting insulin levels increased in the subjects of both groups, but only subjects who received MgCl2 significantly reduced their HOMA-IR index.

Magnesium levels in the MgCl2 group decreased by the first 4 weeks of treatment, showing a gradual and sustained increase in the following weeks, whereas serum magnesium in the control subjects did not show significant variations (Fig. 2).

This study shows the benefits of oral magnesium supplementation as an adjuvant therapy for reducing fasting glucose, HbA1c, and HOMA-IR index in subjects with type 2 diabetes and decreased serum magnesium levels treated with glibenclamide.

In the early 1980s, the importance of magnesium on insulin sensitivity was suggested (25,26) and in following years was supported by clinical evidence showing the essential role of magnesium on insulin-mediated glucose uptake (17,27,28). However, the benefits of chronic administration of magnesium salts given to subjects with type 2 diabetes is controversial (4,29,30) and remains to be adequately evaluated.

In this study, subjects who received magnesium supplementation showed an important increase in serum magnesium concentration (15.5%) and reductions of fasting glucose (−37.5%), HbA1c (−30.4%), and HOMA-IR index (−9.5%) that were more significant than those observed in control subjects, despite the fact that time since diagnosis of diabetes, doses and type of hypoglycemic drugs used, and lifestyle intervention were similar. In this regard, although serum glucose (−27.5%) and HbA1c (−14.4%) levels were reduced in control subjects, HOMA-IR index (6.4%) increased and there were no significant variations in serum magnesium levels (−1.3%). This could be explained by taking into account the fact that control subjects remained with impaired metabolic control (average serum glucose and HbA1c 10.3 mmol/l and 10.1%, respectively), one of the most important sources for magnesium reduction. These findings support the necessity of oral magnesium supplementation to achieve an increase in serum magnesium concentration and to improve insulin sensitivity in type 2 diabetic subjects with decreased serum magnesium levels.

On the other hand, although time since diagnosis of diabetes and doses of glibenclamide in the subjects of both groups were similar, at the end of the study insulin levels in the magnesium-supplemented group were lower than those in the control group. This is a controversial finding because there are previous reports showing a high insulin response in subjects with low serum magnesium levels (26,30), and yet other reports (2,7) show an impairment of insulin secretion in magnesium deficiency subjects. In this regard, it is necessary to take into account the fact that the participants in our study were treated with sulfonylureas, which exert secretory stimuli on pancreatic β-cells (31). However, whether the lower insulin levels that we documented in the magnesium-supplemented subjects were a direct effect of magnesium on β-cell or a consequence of improvement in the insulin-mediated glucose disposal cannot be adequately elucidated in this study; as such, further research is needed to address this issue.

In addition, magnesium-supplemented subjects showed a significant reduction in HOMA-IR index values. The decrease of magnesium concentration results in both defective tyrosine-kinase activity and reduction of autophosphorylation on the β-subunit at the insulin-receptor level (5,32), exerting deleterious effects on glucose metabolism due to insulin sensitivity reduction (2,79,3134), which contributes to poor metabolic control in diabetic subjects (1,3,35,36). Thus, the main question is not related to the benefits of magnesium supplementation in the treatment of diabetic subjects, but rather to the type, dose, and time of administration of magnesium salts. Based on improvement of metabolic control and minimal side effects, it seems to be recommendable to add MgCl2 solution as an adjuvant therapy for patients with type 2 diabetes and decreased serum magnesium levels, at least by 4 months. In addition, for adequate surveillance of magnesium levels in patients with type 2 diabetes, determination of serum magnesium must be done twice a year because magnesium levels have a propensity to decline (4).

Interestingly, in the magnesium-supplemented subjects, serum magnesium concentration showed a significant decrease by the first month, followed by a gradual and sustained increase in the following months. This early change in serum magnesium could be related to a shift of magnesium into intracellular stores, thus causing magnesium compartment redistribution; however, because we did not measure intracellular magnesium, we cannot be sure that this is actually the case. This finding is in contrast with that reported by Lima et al. (16), showing that diabetic subjects who received magnesium oxide (41.4 mmol/l) for 1 month achieved serum magnesium levels similar to those of healthy control subjects. Differences in magnesium salt and doses used could explain the divergence between both studies. In addition, and most importantly, neither Lima et al. (16) nor us measured the duration of hypomagnesemic status or magnesium pool distribution, which are powerful confounding variables that must be controlled for in order to demonstrate the nature of early serum magnesium variations in magnesium-supplemented subjects.

Several limitations of this study deserve mentioning. First, we did not measure erythrocyte or lymphocyte magnesium content. As magnesium is a predominantly intracellular ion, its serum measurements are not representative of magnesium status or intracellular pool. In this regard, significant intracellular magnesium depletion could be seen with normal serum concentrations (37); however, because we only included diabetic subjects with decreased serum magnesium levels, this potential limitation did not influence (or minimally influenced) our objective and conclusions. Second, we did not measure pancreatic store or β-cell function, which influence pancreatic insulin secretion; in this regard, because diabetic subjects in both groups had similar time since diagnosis of diabetes and received the same type and doses of sulfonylureas, this potential limitation is also slight. In addition, because diabetic patients usually require pharmacological treatment to achieve metabolic control, all of the subjects received glibenclamide, which does not influence insulin sensitivity, in order to minimize the influence of antidiabetic agents on our results. Finally, it was not possible to calculate baseline or daily food and water intake in terms of magnesium. However, because there are not variations in the source of water in Durango, the subjects received similar foods and were randomly allocated, again only minimally influencing the results.

In conclusion, oral magnesium supplementation with 2.5 g MgCl2 restores serum magnesium and improves insulin sensitivity in subjects with type 2 diabetes and decreased serum magnesium levels, thus contributing to metabolic control.

Figure 1—

Study participant flow diagram.

Figure 1—

Study participant flow diagram.

Close modal
Figure 2—

Mean and SD of serum magnesium in all participants evaluated (•, 32 MgCl2 recipients; ○, 31 placebo recipients). Magnesium levels in the subjects who received MgCl2 showed a significant reduction for the first month, followed by a sustained and significant increase. Until the end of the study, subjects who received MgCl2 achieved a significant increase of serum magnesium levels. *P < 0.001; †P < 0.05.

Figure 2—

Mean and SD of serum magnesium in all participants evaluated (•, 32 MgCl2 recipients; ○, 31 placebo recipients). Magnesium levels in the subjects who received MgCl2 showed a significant reduction for the first month, followed by a sustained and significant increase. Until the end of the study, subjects who received MgCl2 achieved a significant increase of serum magnesium levels. *P < 0.001; †P < 0.05.

Close modal
Table 1—

Baseline characteristics of subjects randomly allocated to receive either magnesium chloride 2.5 g daily (MgCl2 group) or placebo (control group) for 16 weeks

MgCl2 group (n = 32)
Control group (n = 31)
Baseline*EndBaseline*End
Age (years) 59.7 ± 8.3 — 54.1 ± 9.6 — 
Time since diagnosis of diabetes (years) 8.8 ± 4.9 — 9.4 ± 5.5 — 
BMI (kg/m227.6 ± 9.1 27.7 ± 9.6 28.6 ± 4.2 28.9 ± 4.7 
Weight (kg) 72.9 ± 10.7 73.1 ± 10.4 69.3 ± 10.1 69.6 ± 9.9 
Waist-to-hip ratio 0.98 ± 0.06 0.98 ± 0.07 0.96 ± 0.04 0.96 ± 0.06 
Systolic blood pressure (mmHg) 148.3 ± 32.3 140.2 ± 28.1 138.1 ± 25.6 135 ± 19.6 
Diastolic blood pressure (mmHg) 86.3 ± 17.0 82.7 ± 16.4 80.5 ± 14.6 79.1 ± 13.5 
Fasting glucose (mmol/l) 12.8 ± 5.6 8.0 ± 2.4 14.2 ± 3.9 10.3 ± 2.1§ 
HbA1c (%) 11.5 ± 4.1 8.0 ± 2.4 11.8 ± 4.4 10.1 ± 3.3§ 
Fasting insulin (mmol/l) 47.4 ± 30.0 67.8 ± 39 48.6 ± 34.8 75.6 ± 33.0§ 
HOMA-IR index 4.3 ± 1.2 3.8 ± 1.1 4.7 ± 1.5 5.0 ± 1.3 
Total cholesterol (mmol/l) 6.8 ± 1.7 6.4 ± 1.9 7.1 ± 1.4 7.0 ± 1.7 
HDL cholesterol (mmol/l) 0.9 ± 0.2 0.9 ± 0.1 0.8 ± 0.1 0.8 ± 0.1 
LDL cholesterol (mmol/l) 4.8 ± 1.6 4.7 ± 1.8 4.9 ± 2.0 4.8 ± 2.2 
Triglycerides (mmol/l) 2.4 ± 1.4 2.3 ± 1.5 2.5 ± 1.1 2.5 ± 1.6 
Magnesium (mmol/l) 0.64 ± 0.12 0.74 ± 0.10 0.65 ± 0.09 0.65 ± 0.07§ 
Calcium (mmol/l) 2.5 ± 0.4 2.5 ± 0.5 2.4 ± 0.4 2.4 ± 0.4 
Calcium-to-magnesium ratio 3.9 ± 3.3 3.4 ± 3.2 3.7 ± 3.4 3.7 ± 3.5 
MgCl2 group (n = 32)
Control group (n = 31)
Baseline*EndBaseline*End
Age (years) 59.7 ± 8.3 — 54.1 ± 9.6 — 
Time since diagnosis of diabetes (years) 8.8 ± 4.9 — 9.4 ± 5.5 — 
BMI (kg/m227.6 ± 9.1 27.7 ± 9.6 28.6 ± 4.2 28.9 ± 4.7 
Weight (kg) 72.9 ± 10.7 73.1 ± 10.4 69.3 ± 10.1 69.6 ± 9.9 
Waist-to-hip ratio 0.98 ± 0.06 0.98 ± 0.07 0.96 ± 0.04 0.96 ± 0.06 
Systolic blood pressure (mmHg) 148.3 ± 32.3 140.2 ± 28.1 138.1 ± 25.6 135 ± 19.6 
Diastolic blood pressure (mmHg) 86.3 ± 17.0 82.7 ± 16.4 80.5 ± 14.6 79.1 ± 13.5 
Fasting glucose (mmol/l) 12.8 ± 5.6 8.0 ± 2.4 14.2 ± 3.9 10.3 ± 2.1§ 
HbA1c (%) 11.5 ± 4.1 8.0 ± 2.4 11.8 ± 4.4 10.1 ± 3.3§ 
Fasting insulin (mmol/l) 47.4 ± 30.0 67.8 ± 39 48.6 ± 34.8 75.6 ± 33.0§ 
HOMA-IR index 4.3 ± 1.2 3.8 ± 1.1 4.7 ± 1.5 5.0 ± 1.3 
Total cholesterol (mmol/l) 6.8 ± 1.7 6.4 ± 1.9 7.1 ± 1.4 7.0 ± 1.7 
HDL cholesterol (mmol/l) 0.9 ± 0.2 0.9 ± 0.1 0.8 ± 0.1 0.8 ± 0.1 
LDL cholesterol (mmol/l) 4.8 ± 1.6 4.7 ± 1.8 4.9 ± 2.0 4.8 ± 2.2 
Triglycerides (mmol/l) 2.4 ± 1.4 2.3 ± 1.5 2.5 ± 1.1 2.5 ± 1.6 
Magnesium (mmol/l) 0.64 ± 0.12 0.74 ± 0.10 0.65 ± 0.09 0.65 ± 0.07§ 
Calcium (mmol/l) 2.5 ± 0.4 2.5 ± 0.5 2.4 ± 0.4 2.4 ± 0.4 
Calcium-to-magnesium ratio 3.9 ± 3.3 3.4 ± 3.2 3.7 ± 3.4 3.7 ± 3.5 

Data are means ± SD.

*

At baseline, there were no significant differences for any parameters between both groups;

P < 0.05 from beginning to end for magnesium-supplemented subjects;

P < 0.05 from beginning to end for control subjects;

§

P < 0.05 at end of the study between magnesium-supplemented and control subjects.

This work was supported by grants from the Consejo Nacional de Ciencia y Tecnología de México (FOSIVILLA 20000402008) and the Fondo de Fomento a la Investigación of the Mexican Social Security Institute (FP 2001/354).

1
Tosiello L: Hypomagnesemia and diabetes mellitus: a review of clinical implications.
Arch Intern Med
156
:
1143
–1148,
1996
2
Sheehan JP: Magnesium deficiency and diabetes mellitus.
Magnes Trace Elem
10
:
215
–219,
1991
3
Resnick L, Altura BT, Gupta R, Laragh J, Alderman M, Altura BM: Intracellular and extracellular magnesium depletion in type 2 (non-insulin-dependent) diabetes mellitus.
Diabetologia
36
:
767
–770,
1993
4
Eibl N, Schnack C, Schernthaner G: Magnesium supplementation in type 2 diabetes (Letter).
Diabetes Care
21
:
2031
–2032,
1998
5
Paolisso G, Barbagallo M: Hypertension, diabetes mellitus, and insulin resistance: the role of intracellular magnesium.
Am J Hypertens
10
:
346
–355,
1997
6
Paolisso G, Ravussin E: Intracellular magnesium and insulin resistance: results in Pima Indians and Caucasians.
J Clin Endocrinol Metab
80
:
1382
–1385,
1995
7
Lefebvre PJ, Paolisso G, Scheen AJ: Magnesium and glucose metabolism.
Therapie
49
:
1
–7,
1994
8
Nadler JL, Buchanan T, Natarajan R, Antonipillai I, Bergman R, Rude R: Magnesium deficiency produces insulin resistance and increased thromboxane synthesis.
Hypertension
21
:
1024
–1029,
1993
9
Paolisso G, Scheen A, D’Onofrio F, Lefebvre P: Magnesium and glucose homeostasis.
Diabetologia
33
:
511
–514,
1990
10
Resnick LM: Cellular calcium and magnesium metabolism in the pathophysiology and treatment of hypertension and related metabolic disorders.
Am J Med
93
:
11S
–20S,
1992
11
Schnack C, Bauer I, Pregant P, Hopmeier P, Schernthaner G: Hypomagnesemia in type 2 (non-insulin-dependent) diabetes mellitus is not corrected by improvement of long-term metabolic control.
Diabetologia
35
:
77
–79,
1992
12
Isbir T, Tamer L, Taylor A, Isbir M: Zinc, cooper and magnesium status in insulin-dependent diabetes.
Diabetes Res
26
:
41
–45,
1994
13
Fox C, Ramsoomair D, Carter C: Magnesium: it’s proven and potential clinical significance.
South Med J
94
:
1195
–1201,
2001
14
Eibl NL, Kopp HP, Nowak HR, Schnack CJ, Hopmeier PG, Schernthaner G: Hypomagnesemia in type II diabetes: effect of 3-month replacement therapy.
Diabetes Care
18
:
188
–192,
1995
15
Walti MK, Zimmermann MB, Spinas GA, Jacob S, Hurrerl RF: Dietary magnesium intake in type 2 diabetes.
Eur J Clin Nutr
56
:
409
–414,
2002
16
Lima M de L, Cruz T, Pousada JC, Rodrigues LE, Barbosa K, Cangucu V: The effect of magnesium supplementation in increasing doses on the control of type 2 diabetes.
Diabetes Care
21
:
682
–686,
1998
17
Paolisso G, Scheen A, Cozzolino D, Di Mario G, Varricchio M, D’Onofrio F, Lefebvre P: Changes in glucose turnover parameters and improvement of glucose oxidation after 4-week magnesium administration in elderly noninsulin-dependent (type II) diabetic patients.
J Clin Endocrinol Metab
78
:
1510
–1514,
1994
18
Corica F, Allegra A, Di Benedetto A, Giacobbe MS, Romano G, Cucinotta D, Buemi M, Ceruso D: Effects of oral magnesium supplementation on plasma lipid concentrations in patients with non-insulin-dependent diabetes mellitus.
Magnes Res
7
:
43
–47,
1994
19
De Valk HW, Verkaaik R, van Rijn HJ, Geerdink RA, Struyvenberg A: Oral magnesium supplementation in insulin-requiring type-2 diabetic patients.
Diabet Med
15
:
503
–507,
1998
20
Guerrero-Romero F, Rodríguez-Morán M: Relationship between serum magnesium levels and C-reactive protein concentration, in non-diabetic, non-hypertensive obese subjects.
Int J Obes Relat Metab Disord
26
:
469
–474,
2002
21
Mejía-Aranguré JM, Fajardo-Gutierrez A, Gómez-delgado A, Cuevas-Uriostegui ML, Hernández Hernández DM, Garduño-Espinoza J, Navarrete-Navarro S, Veláquez-Pérez L, Martínez-García MC: El tamaño de la muestra. Un enfoque práctico en la investigación clínica pediátrica.
Bol Med Hosp Infant Mex
52
:
381
–391,
1995
22
Firoz M, Graber M: Bioavailability of US comercial magnesium preparations.
Magnes Res
14
:
257
–262,
2001
23
Eriksson J, Lindström J, Valle T, Aunola S, Hämaäläinen H, Ilanne-Parikka P, Keinänen-Kiukaanniemi S, Laakso M, Lauhkonen M, Lehto P, Lehtonen A, Louheranta A, Mannelin M, Martikkala V, Rastas M, Sundvall J, Turpeinen A, Viljnanen T, Uusitupa M, Tuomilehto J: Finnish Diabetes Prevention Group: prevention of type II diabetes in subjects with impaired glucose tolerance: the Diabetes Prevention Study (DPS) in Finland.
Diabetologia
42
:
793
–801,
1999
24
Matthews D, Hosker J, Rudenski A, Naylor B, Treacher D, Turner R: Homeostasis model assessment: insulin resistance and B-cell function from fasting plasma glucose and insulin concentrations in man.
Diabetologia
28
:
412
–419,
1985
25
Bergman RN, Philips LS, Cobelli C: Physiologic evaluation of factors controlling glucose disposition in man: measurement of insulin sensitivity and B-cell glucose sensitivity from the response to intravenous glucose.
J Clin Invest
68
:
1456
–1467,
1981
26
Yajnik CS, Smith RF, Hockaday TDR, Ward NI: Fasting plasma magnesium concentrations and glucose disposal in diabetes.
BMJ
288
:
1032
–1034,
1984
27
Paolisso G, Sgambato S, Giuglinao D, Torella R, Varicchio M, Scheen AJ, D’Onofrio F, Lefebvre PJ: Impaired insulin mediated erythrocyte magnesium accumulation is correlated to impaired insulin-mediated glucose disposal in type 2 (non-insulin-dependent) diabetic patients.
Diabetologia
31
:
910
–915,
1988
28
Dzurik R, Stefikova K, Spustova V, Fetkovska N: The role of magnesium deficiency in insulin resistance: an in vitro study.
J Hypertens
9 (Suppl. 6)
:
S312
–S313,
1991
29
Paolisso G, Sgambato S, Pizza G, Passariello N, Varricchio M, D’Onofrio F: Improved insulin response and action by chronic magnesium administration in aged NIDDM subjects.
Diabetes Care
12
:
265
–269,
1989
30
Rosolova H, Mayer O Jr, Reaven G: Effect of variations in plasma magnesium concentration on resistance to insulin-mediated glucose disposal in nondiabetic subjects.
J Endocrinol Metab
82
:
3783
–3785,
1997
31
Göke B: Type 2 diabetes. Are current oral treatment options sufficient?
Exp Clin Endocrinol Diabetes
108 (Suppl. 2)
:
S243
–S249,
2000
32
Suárez A, Pulido N, Casla A, Casanova B, Arrieta FJ, Rovira A: Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats.
Diabetologia
38
:
1262
–1270,
1995
33
Curry DL, Joy RM, Holley DC, Bennett L: Magnesium modulation of glucose-induced insulin secretion by the perfused rat pancreas.
Endocrinology
101
:
203
–208,
1997
34
Balon TW, Jasman A, Scott S, Meehan WP, Rude RK, Nadler JL: Dietary magnesium prevents fructose-induced insulin sensitivity in rats.
Hypertension
23
:
1036
–1039,
1994
35
Vanroelen L, Gaal L, Van Rooy P, De Leeuw I: Serum and erythrocyte magnesium level in type I and type II diabetics.
Acta Diabetol
22
:
185
–190,
1985
36
Crook M, Couchman S, Tutt P, Amiel S, Swamenathan R: Erythrocyte, plasma total, ultrafiltrable and platelet magnesium in type 2 (non-insulin-dependent) diabetes mellitus.
Diabetes Res
27
:
73
–79,
1994
37
Reinhart R, Marx J, Haas R, Desbiens N: Intracellular magnesium of mononuclear cells from venous blood of clinical healthy subjects.
Clin Chim Acta
48
:
2415
–2420,
1988

Address correspondence and reprint requests to Martha Rodríguez-Morán, Siqueiros 225 esq./Castañeda, 34000 Durango, Dgo., Mexico. E-mail: rodriguez_moran@hotmail.com.

Received for publication 28 November 2002 and accepted in revised form 3 January 2003.

A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.