Magnesium Abstracts 4 - Diabetes

© 2012

Serum ionized magnesium levels in relation to metabolic syndrome in type 2 diabetic patients

            (Corica, Corsonello et al. 2006) Download

OBJECTIVE: To evaluate circulating serum ionized magnesium (i-Mg) concentrations in patients with type 2 diabetes mellitus, and to investigate its relationship with the components of the metabolic syndrome. DESIGN: cross-sectional study. SETTING: Outpatients' service for diabetic patients at the University Hospital of Messina, Italy. SUBJECTS: 290 patients with type 2 diabetes mellitus. Measures of Outcome: Serum i-Mg was measured by ion selective electrode. Age, gender, body mass index (BMI), waist circumference, blood pressure, fasting glucose, HbA1c, HDL cholesterol, triglycerides, and urinary albumin excretion rate (UAER) were considered in the analyses. Patients with hypomagnesemia, defined as serum i-Mg <0.46 mmol/l, were compared with those having normal serum i-Mg levels, and variables proven to be associated with low i-Mg levels in the univariate analysis were entered in a multivariable logistic regression model to obtain a deconfounded estimate of the association between metabolic parameters and hypomagnesemia. RESULTS: In univariate analysis, serum i-Mg levels were significantly reduced in patients with low HDL cholesterol, high triglycerides values, high waist circumference, high blood pressure, microalbuminuria and clinical proteinuria. Hypomagnesemia was highly prevalent in our study population (N = 143, 49.3%). After adjusting for potential confounders, plasma triglycerides (OR = 4.71; 95% CI = 2.56-8.67), waist circumference (OR = 2.21; 95% CI = 1.21-4.04), microalbuminuria (OR = 2.43; 95% CI = 1.16-5.08) and clinical proteinuria (OR = 2.04; 95% CI = 1.02-5.68) were independently associated with hypomagnesemia. CONCLUSIONS: Hypomagnesemia is highly prevalent in diabetic outpatients. High plasma triglycerides, waist circumference and albuminuria are independent correlates of hypomagnesemia.


The effect of lowering blood pressure by magnesium supplementation in diabetic hypertensive adults with low serum magnesium levels: a randomized, double-blind, placebo-controlled clinical trial

            (Guerrero-Romero and Rodriguez-Moran 2009) Download

To test the blood pressure (BP)-lowering effect of oral magnesium supplementation (that is, magnesium chloride (MgCl(2)) solution) in diabetic hypertensive adults with hypomagnesaemia not on diuretic treatment but receiving concurrent captopril, we conducted a double-blind, placebo-controlled trial. Eighty-two subjects between 40 and 75 years of age were randomly enrolled. Over 4 months, subjects in the intervention group received 2.5 g of MgCl(2) (50 ml of a solution containing 50 g of MgCl(2) per 1000 ml of solution) equivalent to 450 mg of elemental magnesium, and control subjects inert placebo. The primary trial end point was a reduction in systolic (SBP) and diastolic (DBP) blood pressure. Complete follow-up was achieved for 79 of the 82 randomized subjects. SBP (-20.4+/-15.9 versus -4.7 +/- 12.7 mm Hg, P=0.03) and DBP (-8.7+/-16.3 versus -1.2+/-12.6 mm Hg, P=0.02) showed significant decreases, and high-density lipoprotein-cholesterol (0.1+/-0.6 versus -0.1+/-0.7 mmol l(-1), P=0.04) a significant increase in the magnesium group compared to the placebo group. The adjusted odds ratio between serum magnesium and BP was 2.8 (95%CI: 1.4-6.9). Oral magnesium supplementation with MgCl(2) significantly reduces SBP and DBP in diabetic hypertensive adults with hypomagnesaemia.

Magnesium improves the beta-cell function to compensate variation of insulin sensitivity: double-blind, randomized clinical trial

            (Guerrero-Romero and Rodriguez-Moran 2011) Download

BACKGROUND: Given that role of magnesium in insulin secretion is uncertain, our objective was to determine whether oral supplementation with magnesium chloride (MgCl(2)) improves the ability of beta-cells to compensate for variations in insulin sensitivity in non-diabetic individuals with significant hypomagnesaemia. MATERIALS AND METHODS: Eligible individuals were non-diabetic, normo-tensive men and non-diabetic, normo-tensive, non-pregnant women with serum magnesium levels </=0.70 mM/L; they were enrolled in a randomized double-blind clinical trial to receive either 50 mL of 5% MgCl(2) solution or 50 mL of inactive solution daily for 3 months. The primary trial end point was a change in the AUC of the hyperbolic model of beta-cell function (HMbCF) derived from the fasting state. Individuals, caregivers and personnel who assessed the outcomes were all blinded to the group assignments. RESULTS: A total of 54 and 52 individuals were assigned to the MgCl(2) and placebo groups, respectively; five individuals in the MgCl(2) group and four in the placebo group dropped out. There were no serious adverse events or side effects because of MgCl(2) or placebo. At the beginning of the study, the AUC of the HMbCF was similar in both groups (AUC = 7.591 and 7.895 cm(2)); at the end of follow-up, the curve of the MgCl(2) group showed a hyperbolic distribution (AUC = 18.855 cm(2)), whereas in the placebo group, there were no changes (AUC = 7.631 cm(2)). CONCLUSIONS: MgCl(2) 2.5 g daily improves the ability of beta-cells to compensate for variations in insulin sensitivity in non-diabetic individuals with significant hypomagnesaemia.

Serum and dietary magnesium and the risk for type 2 diabetes mellitus: the Atherosclerosis Risk in Communities Study

            (Kao, Folsom et al. 1999) Download

BACKGROUND: Experimental studies in animals and cross-sectional studies in humans have suggested that low serum magnesium levels might lead to type 2 diabetes; however, this association has not been examined prospectively. METHODS: We assessed the risk for type 2 diabetes associated with low serum magnesium level and low dietary magnesium intake in a cohort of nondiabetic middle-aged adults (N = 12,128) from the Atherosclerosis Risk in Communities Study during 6 years of follow-up. Fasting serum magnesium level, categorized into 6 levels, and dietary magnesium intake, categorized into quartiles, were measured at the baseline examination. Incident type 2 diabetes was defined by self-report of physician diagnosis, use of diabetic medication, fasting glucose level of at least 7.0 mmol/L (126 mg/dL), or nonfasting glucose level of at least 11.1 mmol/L (200 mg/dL). RESULTS: Among white participants, a graded inverse relationship between serum magnesium levels and incident type 2 diabetes was observed. From the highest to the lowest serum magnesium levels, there was an approximate 2-fold increase in incidence rate (11.1, 12.2, 13.6, 12.8, 15.8, and 22.8 per 1000 person-years; P = .001). This graded association remained significant after simultaneous adjustment for potential confounders, including diuretic use. Compared with individuals with serum magnesium levels of 0.95 mmol/L (1.90 mEq/L) or greater, the adjusted relative odds of incident type 2 diabetes rose progressively across the following lower magnesium categories: 1.13 (95% CI, 0.79-1.61), 1.20 (95% CI, 0.86-1.68), 1.11 (95% CI, 0.80-1.56), 1.24 (95% CI, 0.86-1.78), and 1.76 (95% CI, 1.18-2.61) (for trend, P = .01). In contrast, little or no association was observed in black participants. No association was detected between dietary magnesium intake and the risk for incident type 2 diabetes in black or white participants. CONCLUSIONS: Among white participants, low serum magnesium level is a strong, independent predictor of incident type 2 diabetes. That low dietary magnesium intake does not confer risk for type 2 diabetes implies that compartmentalization and renal handling of magnesium may be important in the relationship between low serum magnesium levels and the risk for type 2 diabetes.


Magnesium intake in relation to systemic inflammation, insulin resistance, and the incidence of diabetes

         (Kao, Folsom et al. 1999) Download

BACKGROUND: Experimental studies in animals and cross-sectional studies in humans have suggested that low serum magnesium levels might lead to type 2 diabetes; however, this association has not been examined prospectively. METHODS: We assessed the risk for type 2 diabetes associated with low serum magnesium level and low dietary magnesium intake in a cohort of nondiabetic middle-aged adults (N = 12,128) from the Atherosclerosis Risk in Communities Study during 6 years of follow-up. Fasting serum magnesium level, categorized into 6 levels, and dietary magnesium intake, categorized into quartiles, were measured at the baseline examination. Incident type 2 diabetes was defined by self-report of physician diagnosis, use of diabetic medication, fasting glucose level of at least 7.0 mmol/L (126 mg/dL), or nonfasting glucose level of at least 11.1 mmol/L (200 mg/dL). RESULTS: Among white participants, a graded inverse relationship between serum magnesium levels and incident type 2 diabetes was observed. From the highest to the lowest serum magnesium levels, there was an approximate 2-fold increase in incidence rate (11.1, 12.2, 13.6, 12.8, 15.8, and 22.8 per 1000 person-years; P = .001). This graded association remained significant after simultaneous adjustment for potential confounders, including diuretic use. Compared with individuals with serum magnesium levels of 0.95 mmol/L (1.90 mEq/L) or greater, the adjusted relative odds of incident type 2 diabetes rose progressively across the following lower magnesium categories: 1.13 (95% CI, 0.79-1.61), 1.20 (95% CI, 0.86-1.68), 1.11 (95% CI, 0.80-1.56), 1.24 (95% CI, 0.86-1.78), and 1.76 (95% CI, 1.18-2.61) (for trend, P = .01). In contrast, little or no association was observed in black participants. No association was detected between dietary magnesium intake and the risk for incident type 2 diabetes in black or white participants. CONCLUSIONS: Among white participants, low serum magnesium level is a strong, independent predictor of incident type 2 diabetes. That low dietary magnesium intake does not confer risk for type 2 diabetes implies that compartmentalization and renal handling of magnesium may be important in the relationship between low serum magnesium levels and the risk for type 2 diabetes.


Magnesium intake in relation to systemic inflammation, insulin resistance, and the incidence of diabetes

            (Kim, Xun et al. 2010) Download

OBJECTIVE: To investigate the long-term associations of magnesium intake with incidence of diabetes, systemic inflammation, and insulin resistance among young American adults. RESEARCH DESIGN AND METHODS: A total of 4,497 Americans, aged 18-30 years, who had no diabetes at baseline, were prospectively examined for incident diabetes based on quintiles of magnesium intake. We also investigated the associations between magnesium intake and inflammatory markers, i.e., high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and fibrinogen, and the homeostasis model assessment of insulin resistance (HOMA-IR). RESULTS: During the 20-year follow-up, 330 incident cases of diabetes were identified. Magnesium intake was inversely associated with incidence of diabetes after adjustment for potential confounders. The multivariable-adjusted hazard ratio of diabetes for participants in the highest quintile of magnesium intake was 0.53 (95% CI, 0.32-0.86; P(trend) < 0.01) compared with those in the lowest quintile. Consistently, magnesium intake was significantly inversely associated with hs-CRP, IL-6, fibrinogen, and HOMA-IR, and serum magnesium levels were inversely correlated with hs-CRP and HOMA-IR. CONCLUSIONS: Magnesium intake was inversely longitudinally associated with incidence of diabetes in young American adults. This inverse association may be explained, at least in part, by the inverse correlations of magnesium intake with systemic inflammation and insulin resistance.

Magnesium intake and risk of type 2 diabetes: a meta-analysis

            (Larsson and Wolk 2007) Download

OBJECTIVE: To assess the association between magnesium intake and risk of type 2 diabetes. DESIGN: Meta-analysis of prospective cohort studies. DATA SOURCES: We retrieved studies published in any language by systematically searching MEDLINE from 1966 to February 2007 and by manually examining the references of the original articles. STUDY SELECTION: We included prospective cohort studies reporting relative risks with 95% confidence intervals for the association between magnesium intake and incidence of type 2 diabetes. RESULTS: The seven identified cohort studies of magnesium intake [from foods only (n = 4) or from foods and supplements combined (n = 3)] and incidence of type 2 diabetes included 286,668 participants and 10,912 cases. All but one study found an inverse relation between magnesium intake and risk of type 2 diabetes, and in four studies the association was statistically significant. The overall relative risk for a 100 mg day(-1) increase in magnesium intake was 0.85 (95% CI, 0.79-0.92). Results were similar for intake of dietary magnesium (RR, 0.86; 95% CI, 0.77-0.95) and total magnesium (RR, 0.83; 95% CI, 0.77-0.89). There was no evidence of publication bias (P = 0.99). CONCLUSIONS: Magnesium intake was inversely associated with incidence of type 2 diabetes. This finding suggests that increased consumption of magnesium-rich foods such as whole grains, beans, nuts, and green leafy vegetables may reduce the risk of type 2 diabetes.

Diabetes is the main factor accounting for hypomagnesemia in obese subjects

            (Lecube, Baena-Fustegueras et al. 2012) Download

OBJECTIVE: Type 2 diabetes (T2DM) and obesity are associated with magnesium deficiency. We aimed to determine whether the presence of type 2 diabetes and the degree of metabolic control are related to low serum magnesium levels in obese individuals. METHODS: A) Case-control study: 200 obese subjects [50 with T2DM (cases) and 150 without diabetes (controls)] prospectively recruited. B) Interventional study: the effect of bariatric surgery on serum magnesium levels was examined in a subset of 120 obese subjects (40 with type 2 diabetes and 80 without diabetes). RESULTS: Type 2 diabetic patients showed lower serum magnesium levels [0.75+/-0.07 vs. 0.81+/-0.06 mmol/L; mean difference -0.06 (95% CI -0.09 to -0.04); p<0.001] than non-diabetic patients. Forty-eight percent of diabetic subjects, but only 15% of non-diabetic subjects showed a serum magnesium concentration lower than 0.75 mmol/L. Significant negative correlations between magnesium and fasting plasma glucose, HbA1c, HOMA-IR, and BMI were detected. Multiple linear regression analysis showed that fasting plasma glucose and HbA1c independently predicted serum magnesium. After bariatric surgery serum magnesium increased only in those patients in whom diabetes was resolved, but remain unchanged in those who not, without difference in loss weight between groups. Changes in serum magnesium negatively correlated with changes in fasting plasma glucose and HbA1c. Absolute changes in HbA1c independently predicted magnesium changes in the multiple linear regression analysis. CONCLUSIONS: Our results provide evidence that the presence of diabetes and the degree of metabolic control are essential in accounting for the lower levels of magnesium that exist in obese subjects.

Magnesium intake and risk of type 2 diabetes in men and women

            (Lopez-Ridaura, Willett et al. 2004) Download

OBJECTIVE: To examine the association between magnesium intake and risk of type 2 diabetes. RESEARCH DESIGN AND METHODS: We followed 85,060 women and 42,872 men who had no history of diabetes, cardiovascular disease, or cancer at baseline. Magnesium intake was evaluated using a validated food frequency questionnaire every 2-4 years. After 18 years of follow-up in women and 12 years in men, we documented 4,085 and 1,333 incident cases of type 2 diabetes, respectively. RESULTS: After adjusting for age, BMI, physical activity, family history of diabetes, smoking, alcohol consumption, and history of hypertension and hypercholesterolemia at baseline, the relative risk (RR) of type 2 diabetes was 0.66 (95% CI 0.60-0.73; P for trend <0.001) in women and 0.67 (0.56-0.80; P for trend <0.001) in men, comparing the highest with the lowest quintile of total magnesium intake. The RRs remained significant after additional adjustment for dietary variables, including glycemic load, polyunsaturated fat, trans fat, cereal fiber, and processed meat in the multivariate models. The inverse association persisted in subgroup analyses according to BMI, physical activity, and family history of diabetes. CONCLUSIONS: Our findings suggest a significant inverse association between magnesium intake and diabetes risk. This study supports the dietary recommendation to increase consumption of major food sources of magnesium, such as whole grains, nuts, and green leafy vegetables.

Oral magnesium supplementation reduces insulin resistance in non-diabetic subjects

            (Mooren, Kruger et al. 2011) Download

The incidence of insulin resistance and metabolic syndrome correlates with the availability of magnesium (Mg). We studied the effect of oral Mg supplementation on insulin sensitivity and other characteristics of the metabolic syndrome in normomagnesemic, overweight, insulin resistant, non-diabetic subjects. Subjects were tested for eligibility using oral glucose tolerance test (OGTT) and subsequently randomized to receive either Mg-aspartate-hydrochloride (n = 27) or placebo (n = 25) for 6 months. As trial endpoints, several indices of insulin sensitivity, plasma glucose, serum insulin, blood pressure and lipid profile were determined. Mg supplementation resulted in a significant improvement of fasting plasma glucose and some insulin sensitivity indices (ISIs) compared to placebo. Blood pressure and lipid profile did not show significant changes. The results provide significant evidence that oral Mg supplementation improves insulin sensitivity even in normomagnesemic, overweight, non-diabetic subjects emphasizing the need for an early optimization of Mg status to prevent insulin resistance and subsequently type 2 diabetes.

Daily magnesium supplements improve glucose handling in elderly subjects

            (Paolisso, Sgambato et al. 1992) Download

We demonstrated similar plasma concentrations and urinary losses but lower erythrocyte magnesium concentrations (2.18 +/- 0.04 vs 1.86 +/- 0.03 mmol/L, P less than 0.01) in twelve aged (77.8 +/- 2.1 y) vs 25 young (36.1 +/- 0.4 y), nonobese subjects. Subsequently, aged subjects were enrolled in a double-blind, randomized, crossover study in which placebo (for 4 wk) and chronic magnesium administration (CMA) (4.5 g/d for 4 wk) were provided. At the end of each treatment period an intravenous glucose tolerance test (0.33 g/kg body wt) and a euglycemic glucose clamp with simultaneous [D-3H]glucose infusion and indirect calorimetry were performed. CMA vs placebo significantly increased erythrocyte magnesium concentration and improved insulin response and action. Net increase in erythrocyte magnesium significantly and positively correlated with the decrease in erythrocyte membrane microviscosity and with the net increase in both insulin secretion and action. In aged patients, correction of a low erythrocyte magnesium concentration may allow an improvement of glucose handling.

Oral magnesium supplementation improves insulin sensitivity and metabolic control in type 2 diabetic subjects: a randomized double-blind controlled trial

            (Rodriguez-Moran and Guerrero-Romero 2003) Download

OBJECTIVE: To determine whether oral magnesium supplementation (as magnesium chloride [MgCl(2)] 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 MgCl(2) solution (containing 50 g MgCl(2) 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 HbA(1c) 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 HbA(1c) (8.0 +/- 2.4 vs. 10.1 +/- 3.3%, P = 0.04) than control subjects. CONCLUSIONS: Oral supplementation with MgCl(2) solution restores serum magnesium levels, improving insulin sensitivity and metabolic control in type 2 diabetic patients with decreased serum magnesium levels.

Dietary magnesium intake in relation to plasma insulin levels and risk of type 2 diabetes in women

            (Song, Manson et al. 2004) Download

OBJECTIVE: Higher intake of magnesium appears to improve glucose and insulin homeostasis; however, there are sparse prospective data on the association between magnesium intake and incidence of type 2 diabetes. RESEARCH DESIGN AND METHODS: In the Women's Health Study, a cohort of 39,345 U.S. women aged >/=45 years with no previous history of cardiovascular disease, cancer, or type 2 diabetes completed validated semiquantitative food frequency questionnaires in 1993 and were followed for an average of 6 years. We used Cox proportional hazard models to estimate multivariate relative risks (RRs) of type 2 diabetes across quintiles of magnesium intake compared with the lowest quintile. In a sample of 349 apparently healthy women from this study, we measured plasma fasting insulin levels to examine their relation to magnesium intake. RESULTS: During 222,523 person-years of follow-up, we documented 918 confirmed incident cases of type 2 diabetes. There was a significant inverse association between magnesium intake and risk of type 2 diabetes, independent of age and BMI (P = 0.007 for trend). After further adjustment for physical activity, alcohol intake, smoking, family history of diabetes, and total calorie intake, the multivariate-adjusted RRs of diabetes from the lowest to highest quintiles of magnesium intake were attenuated at 1.0, 1.06, 0.81, 0.86, and 0.89 (P = 0.05 for trend). Among women with BMI >/=25 kg/m2, the inverse trend was significant; multivariate-adjusted RRs were 1.0, 0.96, 0.76, 0.84, and 0.78 (P = 0.02 for trend). Multivariate-adjusted geometric mean insulin levels for overweight women in the lowest quartile of magnesium intake was 53.5 compared with 41.5 pmol/l among those at the highest quartile (P = 0.03 for trend). CONCLUSIONS: These findings support a protective role of higher intake of magnesium in reducing the risk of developing type 2 diabetes, especially in overweight women.

Effects of oral magnesium supplementation on glycaemic control in Type 2 diabetes: a meta-analysis of randomized double-blind controlled trials

            (Song, He et al. 2006) Download

AIMS: The aim of this study was to assess the evidence on the effect of oral magnesium supplementation on glycaemic control in patients with Type 2 diabetes. METHODS: We searched the electronic databases of medline, embase and the Cochrane Controlled Trials Register up to January 2005. We identified nine randomized double-blind controlled trials with a total of 370 patients with Type 2 diabetes and of duration 4-16 weeks. The median dose of oral magnesium supplementation was 15 mmol/day (360 mg/day) in the treatment groups. The primary outcome was glycaemic control, as measured by glycated haemoglobin (HbA(1c)) or fasting blood glucose levels; the secondary outcomes included body mass index, blood pressure (BP) and lipids. Using a random-effects model, we calculated the weighted mean differences (WMD) and 95% confidence interval (CI). RESULTS: After a median duration of 12 weeks, the weighted mean post-intervention fasting glucose was significantly lower in the treatment groups compared with the placebo groups [-0.56 mmol/l (95% CI, -1.10 to -0.01); P for heterogeneity = 0.02]. The difference in post-intervention HbA(1c) between magnesium supplementation groups and control groups was not significant [-0.31% (95% CI, -0.81 to 0.19); P for heterogeneity = 0.10]. Neither systolic nor diastolic BP was significantly changed. Magnesium supplementation increased on high-density lipoprotein (HDL) cholesterol levels [0.08 mmol/l (95% CI, 0.03 to 0.14); P for heterogeneity = 0.36] but had no effect on total cholesterol, low-density lipoprotein (LDL) cholesterol and triglyceride. CONCLUSIONS: Oral magnesium supplementation for 4-16 weeks may be effective in reducing plasma fasting glucose levels and raising HDL cholesterol in patients with Type 2 diabetes, although the long-term benefits and safety of magnesium treatment on glycaemic control remain to be determined.


References

Corica, F., A. Corsonello, et al. (2006). "Serum ionized magnesium levels in relation to metabolic syndrome in type 2 diabetic patients." J Am Coll Nutr 25(3): 210-5.

Guerrero-Romero, F. and M. Rodriguez-Moran (2009). "The effect of lowering blood pressure by magnesium supplementation in diabetic hypertensive adults with low serum magnesium levels: a randomized, double-blind, placebo-controlled clinical trial." J Hum Hypertens 23(4): 245-51.

Guerrero-Romero, F. and M. Rodriguez-Moran (2011). "Magnesium improves the beta-cell function to compensate variation of insulin sensitivity: double-blind, randomized clinical trial." Eur J Clin Invest 41(4): 405-10.

Kao, W. H., A. R. Folsom, et al. (1999). "Serum and dietary magnesium and the risk for type 2 diabetes mellitus: the Atherosclerosis Risk in Communities Study." Arch Intern Med 159(18): 2151-9.

Kim, D. J., P. Xun, et al. (2010). "Magnesium intake in relation to systemic inflammation, insulin resistance, and the incidence of diabetes." Diabetes Care 33(12): 2604-10.

Larsson, S. C. and A. Wolk (2007). "Magnesium intake and risk of type 2 diabetes: a meta-analysis." J Intern Med 262(2): 208-14.

Lecube, A., J. A. Baena-Fustegueras, et al. (2012). "Diabetes is the main factor accounting for hypomagnesemia in obese subjects." PLoS One 7(1): e30599.

Lopez-Ridaura, R., W. C. Willett, et al. (2004). "Magnesium intake and risk of type 2 diabetes in men and women." Diabetes Care 27(1): 134-40.

Mooren, F. C., K. Kruger, et al. (2011). "Oral magnesium supplementation reduces insulin resistance in non-diabetic subjects - a double-blind, placebo-controlled, randomized trial." Diabetes Obes Metab 13(3): 281-4.

Paolisso, G., S. Sgambato, et al. (1992). "Daily magnesium supplements improve glucose handling in elderly subjects." Am J Clin Nutr 55(6): 1161-7.

Rodriguez-Moran, M. and F. Guerrero-Romero (2003). "Oral magnesium supplementation improves insulin sensitivity and metabolic control in type 2 diabetic subjects: a randomized double-blind controlled trial." Diabetes Care 26(4): 1147-52.

Song, Y., K. He, et al. (2006). "Effects of oral magnesium supplementation on glycaemic control in Type 2 diabetes: a meta-analysis of randomized double-blind controlled trials." Diabet Med 23(10): 1050-6.

Song, Y., J. E. Manson, et al. (2004). "Dietary magnesium intake in relation to plasma insulin levels and risk of type 2 diabetes in women." Diabetes Care 27(1): 59-65.