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Journal of the American College of Nutrition, Vol. 25, No. 3, 210-215 (2006)
Published by the American College of Nutrition

Serum Ionized Magnesium Levels in Relation to Metabolic Syndrome in Type 2 Diabetic Patients

Francesco Corica, MD, Andrea Corsonello, MD, Riccardo Ientile, ChD, Domenico Cucinotta, MD, Antonino Di Benedetto, MD, Francesco Perticone, MD, Ligia J. Dominguez, MD and Mario Barbagallo, MD

Department of Internal Medicine (F.C., D.C., A.D.B.)
Department of Biochemical, Physiological and Nutritional Sciences (R.I.)
University of Messina, Messina, Italian National Research Center on Aging (INRCA), Cosenza (A.C.)
Department of Clinical and Experimental Medicine, University of "Magna Graecia", Catanzaro (F.P.)
Institute of Internal Medicine and Geriatrics, University of Palermo, Palermo (L.J.D., M.B.), ITALY

Address reprint requests to: Andrea Corsonello, MD, Via della Resistenza Pal. Alfa Scala H, I-87036 Rende (CS), ITALY. E-mail: andrea_corsonello{at}tin.it


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
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.

Key words: serum ionized magnesium, diabetes mellitus, metabolic syndrome, plasma triglycerides, waist circumference, albuminuria


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
People with the metabolic syndrome are at increased risk for developing diabetes mellitus and cardiovascular disease as well as increased mortality from cardiovascular disease and all causes [1,2]. Thus, the knowledge of the underlying mechanisms involved in the metabolic syndrome may help to produce tailored interventions aimed to slow the growing epidemic of this dangerous condition.

Several evidences suggest that magnesium (Mg) depletion may play a key role in the pathophysiology of insulin-resistance, diabetes mellitus, hypertension, and dyslipidemia [3–7]. The Atherosclerosis Risk in the Community (ARIC) study found a significant association between hypomagnesemia and the incidence of type 2 diabetes mellitus (DM) [8]. Mg depletion is frequently observed in diabetic patients [9,10], and it is believed that an impairment of Mg homeostasis may favor the onset and progression of diabetic complications [11,12]. Furthermore, it has recently been suggested that a reduced intracellular Mg concentration might be the missing link helping to explain the epidemiological association between DM and hypertension [13]. Although several studies investigated the relationship between Mg status and metabolic or cardiovascular risk factors [14,15], we could find only one study considering a wide spectrum of metabolic syndrome variables in relation to total Mg (t-Mg) levels in non-diabetic patients [16]. Serum ionized Mg (i-Mg) levels have not been previously studied in relation to metabolic syndrome in patients with type 2 DM. Therefore, we performed this cross-sectional study to evaluate circulating i-Mg concentrations in patients with type 2 DM, and to investigate its relationship with the components of the metabolic syndrome.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects
Our series consisted of 290 informed consent type 2 diabetic patients. All diabetic patients were recruited from the population attending the Outpatient’s Service for Diabetic Patients at the University Hospital of Messina, Italy. Exclusion criteria included renal failure (serum creatinine >1.4 mg/dl), smoking habit, malignancies, alcoholism and psychiatric problems. Subjects who were receiving treatment with drugs known to modify magnesium metabolism (such as diuretics) were also excluded from the study.

Diagnostic criteria used for metabolic syndrome where those suggested by the U.S. National Cholesterol Education Program—Adult Treatment Panel III (NCEP ATP-III): waist circumference >102 cm for men or >88 cm for women; plasma triglycerides ≥150 mg/dl; high density lipoprotein (HDL) cholesterol <40 mg/dl for men and <50 mg/dl for women; blood pressure ≥130/85 mmHg; fasting plasma glucose ≥6.1 mmol/l [17].

The study protocol was approved by the local ethical committee.

Measurements
Body height was measured without shoes to the nearest 0.5 cm; body weight was measured without clothes to the nearest 0.1 kg; body mass index (BMI) was calculated as weight/height2 (kg/m2). Waist circumference was measured midway between the lower rib margin and the iliac crest. Arterial blood pressure was measured with a Riva-Rocci sphygmomanometer (Zenith, Rome, Italy). Blood pressure values were taken with patient at rest in supine position from at least 5 minutes. The first measurement was excluded and the average of the following three measurements, taken at 3-min. intervals was considered. Mean blood pressure was calculated by the sum of diastolic blood pressure plus one third of pulse pressure (i.e. systolic-diastolic blood pressure). On each subject, in the morning after a 12-hour fasting, a venous blood sample with EDTA was collected to assay fasting glucose (AutoAnalyzer, Beckman, Milan, Italy), HbA1c (HPLC, Diaman DM Bio Rad, Segrate, Milan, Italy), HDL cholesterol and triglycerides (CHOP-PAP procedure, Boehringer Biochemia, Milan, Italy). A heparinized venous blood sample was separately collected, and the serum obtained by centrifugation was used for the determination of ionized magnesium (NOVA 8 Ion Selective Analyzer, NOVA Biomedical, Waltham, MA, USA).

The 24h urinary albumin excretion rate (UAER) was determined by nephelometric method (Behring Nephelometer Analyzer, Istituto Behring, Scoppito, L’Aquila, Italy), and patients were categorized as having normal albuminuria (UAER < 20 µg/min), microalbuminuria (20 < UAER < 200 µg/min), or clinical proteinuria (UAER > 200 µg/min).

Analytic Approach
The main outcome or our study was to investigate the impact of metabolic syndrome criteria on serum levels of i-Mg. Firstly, we evaluated the distribution of serum i-Mg, and we found that it was normally distributed in the population studied (Kolmogorov-Smirnov Z = 0.809, two-tailed p = 0.529). Second, we investigated serum i-Mg levels in patients divided according to the presence or absence of each diagnostic criteria for metabolic syndrome described above. Since UAER and HbA1c are known to be inversely associated with i-Mg levels [18], we also considered these variables as potential correlates of i-Mg values. We then compared patients with hypomagnesemia with those having normal serum i-Mg levels. The cut-off for hypomagnesemia was 0.46 mmol/l as previously reported by Ising et al [19]. Statistical analysis was performed using ANOVA one-way test for continuous variables, and chi-square test for categorical variables. Scheffè post-hoc test for multiple comparisons was used in preliminary analyses when appropriate. Finally, 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 low i-Mg levels. All statistical procedures were performed using SPSS statistical software package release 10.0 (SPSS Inc, Chicago, IL, USA). Data are presented as mean ± SD for continuous variables or number of cases (percentage) for categorical variables.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
General characteristics of the population studied are shown in Table 1. The mean age was 63.1 ± 10.4 years, with an almost equal number of men and women. The mean serum i-Mg was 0.44 ± 0.08 mmol/l (range: 0.24–0.73).


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  		Table 1. Demographic and Clinical Characteristic of the Subjects Studied (N = 290)

 
Serum i-Mg was significantly lower in patients with low HDL cholesterol (0.40 ± 0.07 vs 0.44 ± 0.09 mmol/l, p < 0.001), high triglycerides values (0.37 ± 0.08 vs 0.45 ± 0.08 mmol/l, p < 0.001), high waist circumference (0.39 ± 0.06 vs 0.46 ± 0.09 mmol/l, p < 0.001), and high blood pressure (0.40 ± 0.08 vs 0.43 ± 0.09 mmol/l, p < 0.01). Patients having either hyperglycemia (0.42 ± 0.08 mmol/l) or normal plasma glucose (0.43 ± 0.09 mmol/l) had similar i-Mg values (p = 0.314).

When patients were divided according to their UAER values, the groups with microalbuminuria and clinical proteinuria had lower serum i-Mg concentrations with respect to normoalbuminuric patients (0.39 ± 0.08, p < 0.05, and 0.39 ± 0.09, p < 0.01 vs 0.43 ± 0.08 mmol/l, respectively), while no significant difference was observed between microalbuminuria and clinical proteinuria subgroups. Furthermore, patients with HbA1c levels greater than 7% had lower serum i-Mg concentrations with respect to patients having normal HbA1c values (0.41 ± 0.08 vs 0.44 ± 0.08 mmol/l, respectively; p < 0.01).

When patients were divided according to their i-Mg levels, we found that hypomagnesemia was highly prevalent in our study population, since it was present in 143 (49.3%) out of the 290 patients studied. Diabetic patients with hypomagnesemia were slightly older than those with Mg levels greater or equal to 0.46 mmol/l. Furthermore, the prevalence of hypertension, abdominal adiposity, lipid abnormalities, poor glycometabolic control, microalbuminuria and clinical proteinuria was higher in patients with hypomagnesemia (Table 2). Multivariable logistic regression analysis showed that plasma triglycerides concentrations were strongly associated with the outcome, and waist circumference, microalbuminuria and clinical proteinuria were also significant predictors of hypomagnesemia, while the association between hypertension, HbA1c, and HDL cholesterol with the outcome was no longer statistically significant (Table 3).


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  		Table 2. Demographic and Clinical Characteristic of Patients Divided according to their i-Mg Levels

 

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  		Table 3. Summary Logistic Regression Model of Selected Risk Factors to Having i-Mg Levels Lower than 0.46 mmol/l

 

   DISCUSSION
 
The present study show that metabolic syndrome is associated with low serum i-Mg in diabetic patients. To the best of our knowledge, there is only one study investigating Mg status in relation to such a wide spectrum of metabolic syndrome parameters. It shows that in non-diabetic patients the metabolic syndrome is independently associated with low serum total (t-Mg) levels, and among the components of metabolic syndrome, dyslipidemia and hypertension are strongly related to hypomagnesemia [16]. Our results add to the present knowledge by demonstrating that type 2 diabetic patients having a high risk lipid profile, high blood pressure or abdominal adiposity had lower circulating i-Mg levels with respect to patients without metabolic risk factors. Furthermore, plasma triglycerides, waist circumference, and UAER are independently associated with hypomagnesemia.

Our results are quitely different from those reported in the study by Guerrero-Romero et al [16], in which high blood pressure and dyslipidemia were the strongest correlates of hypomagnesemia among the metabolic syndrome parameters. However, our study population of type 2 diabetic patients is not comparable with the population of non-diabetic subjects enrolled in the former study. Furthermore, Guerrero-Romero et al investigated Mg status by measuring serum t-Mg [16], which is not a sensitive indicator of total body content of the cation [19]. Indeed, serum i-Mg can be significantly reduced in frankly type 2 diabetic subjects compared with non-diabetic control subjects, while serum t-Mg levels remain normal [10]. Finally, the close relationship between serum i-Mg (but not total) and intracellular free Mg concentrations measured by the gold standard method 31P-NMR spectroscopy [10], makes our results more comparable with those obtained with the complex and not easily available determination of free intracellular Mg [4,7].

Hypomagnesemia is known to contribute to the pathophysiology of cardiovascular diseases. Indeed, an altered steady-state ionic content, i.e. suppressed intracellular free magnesium and elevated cytosolic free calcium levels, have been suggested to concomitantly alter the function of many tissues. In blood vessels to cause vasoconstriction, arterial stiffness, and hypertension; in the heart, cardiac hypertrophy; in platelets, increased aggregation and thrombosis; in fat and skeletal muscle, insulin resistance; in pancreatic beta cells and sympathetic neurons, potentiated stimulus-secretion coupling resulting in hyperinsulinemia, and increased sympathetic nerve activity [3–7]. Our results seem to be in agreement with this "ionic hypothesis", and furtherly confirm that an alteration in Mg metabolism may play a key pathophysiological role in the metabolic syndrome [5,13].

The strong association between plasma triglycerides and hypomagnesemia was not unexpected, as well as the lower i-Mg levels observed in patients with low HDL cholesterol. Indeed, an increase in serum lipid concentrations has been found to be associated with Mg depletion in experimental models [20]. Additionally, an inverse correlation between plasma triglycerides and serum i-Mg has been observed in older people with impaired glucose tolerance [15], and similar findings have been obtained with t-Mg determination in patients with diabetes mellitus, irrespective of plasma glucose levels [16]. Thus, hypomagnesemia may contribute to the pathophysiology of cardiovascular diabetes complications by altering blood lipid profile in a way that predispose to atherosclerosis [21]. Finally, oral magnesium supplementation to patients with type 2 diabetes resulted in a significant decrease in total and LDL cholesterol, and an increase in HDL cholesterol [22].

The relationship between body fat distribution and Mg status has received little attention until now. Obesity per se was not associated with hypomagnesemia [16], and our results confirm that a BMI greater than 30 kg/m2 is not associated with decreased i-Mg. De Leeuw et al [23] reported that women with upper body fat distribution had increased erythrocyte t-Mg concentrations as compared to those with gynoid fat distribution, while Laires et al [24] found that erythrocyte t-Mg concentrations were significantly related to insulin resistance and fat free mass, but not to abdominal fat, in obese and non-obese postmenopausal women. However, increased visceral adiposity is known to predispose to a reduced insulin sensitivity [25], which in turn may worsen Mg status [13]. Thus, a greater resistance to insulin action could explain the strong association between waist circumference and hypomagnesemia.

Patients with hypertension or high HbA1c had lower circulating i-Mg concentrations with respect to those with normal blood pressure or HbA1c values, but these associations were no longer significant in multivariable analysis. Nevertheless, the fact that Mg depletion may contribute to increase blood pressure merits to be mentioned. Indeed, decreased availability of Mg is known to enhance calcium-mediated vasoconstriction, to blunt cardiac and smooth muscle relaxation, and to decrease cellular glucose utilization, thus contributing to elevated blood pressure and peripheral insulin resistance [13]. Additionally, a poor glycometabolic control is a well-known risk factor for magnesium depletion in diabetic patients [9,18]. Hyperglycemia and glycosuria may interfere with renal magnesium handling, mainly by reducing the tubular reabsorption of the cation [26]. Thus, although Mg excretion was not measured in the present study, an increased urinary Mg loss could be invoked to explain the low concentration of serum i-Mg observed in patients with HbA1c values greater than 7%. In this case, it is worth noting that HbA1c, but not fasting plasma glucose, qualified as a significant correlate of hypomagnesemia in our study. While fasting plasma glucose measurement reflects the actual glucose concentration at the time of the test, the HbA1c values reflect the glycometabolic control that a patient had in the last 2–3 months [27], and is a strong correlate of mean daily glucose, but not of single value fasting plasma glucose concentrations [28]. This difference is likely to explain the lack of correlation between fasting plasma glucose and magnesium status in our and previous studies [15,29,30], and suggests that the putative role of increased urinary Mg loss may be linked to a prolonged, more than actual, hyperglycemic state.

In our study, both microalbuminuria and clinical proteinuria qualified as independent correlates of i-Mg. A recent study shows that diabetic patients with chronic renal failure (CRF) have low serum i-Mg levels with respect to non-diabetic CRF patients, and declining creatinine clearance is not accompanied by increases in serum i-Mg concentrations in diabetic CRF patients, thus suggesting that the progression of renal dysfunction may exacerbate the risk of hypomagnesemia in diabetic patients [31]. Both microalbuminuria and clinical proteinuria have been previously reported to be associated with a significant reduction in circulating i-Mg [18], and the results from the present study furtherly confirm that also the initial stages of diabetic nephropathy are associated with hypomagnesemia.

Some limitations of our study deserve to be acknowledged. First, since we performed a cross-sectional study we can not propose any prognostic role for hypomagnesemia in diabetic patients with metabolic syndrome. However, low serum t-Mg was independently associated with carotid wall thickness and coronary heart disease in the ARIC study [32,33]. Furthermore, low circulating Mg levels are associated with more rapid decline of renal function in patients with type 2 diabetes mellitus [34]. Thus, a prospective study would contribute to better define the potential role of hypomagnesemia as additional risk factor in metabolic syndrome patients. Furthermore, since we enrolled only patients with type 2 diabetes mellitus, the present findings can not be generalized to the entire population of non-diabetic subjects with metabolic syndrome.


   CONCLUSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
ACKNOWLEDGMENTS
 REFERENCES
 
Hypomagnesemia is highly prevalent in diabetic outpatients and is associated with the components of the metabolic syndrome. High plasma triglycerides and waist circumference are independently associated with low i-Mg concentrations. UAER also qualifies as independent correlate of hypomagnesemia. Our findings strengthen the need to address a greater attention to magnesium metabolism disturbances in patients with type 2 diabetes mellitus. Finally, since patients with diabetes mellitus and/or metabolic syndrome are especially at risk of developing hypomagnesemia, further studies are needed to investigate the prognostic value of low circulating i-Mg in both diabetic and non-diabetic patients with metabolic syndrome.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
REFERENCES
 
This work is partially supported by grants from the Italian Ministry for Education, University and Scientific Research (MIUR).

Received February 19, 2005. Accepted February 14, 2006.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 

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