|Year : 2021 | Volume
| Issue : 1 | Page : 29-32
Hypomagnesemia as a cardiometabolic risk marker in type 2 diabetes mellitus: Implications for Sub-Saharan Africa
Taoreed Adegoke Azeez1
, Oyebola Oluwagbemiga Sonuga2
1 Department of Medicine, Endocrinology Unit, University College Hospital, Ibadan, Nigeria
2 Department of Chemical Pathology, University College Hospital, Ibadan, Nigeria
|Date of Submission||10-Mar-2021|
|Date of Decision||09-Apr-2021|
|Date of Acceptance||11-Apr-2021|
|Date of Web Publication||28-May-2021|
Taoreed Adegoke Azeez
Department of Medicine, Endocrinology Unit, University College Hospital, Ibadan
Source of Support: None, Conflict of Interest: None
Background: Diabetes mellitus is a metabolic disorder associated with increased cardiovascular mortality. However, studies have suggested a possible link between hypomagnesemia and cardiovascular risk, but these studies are scanty in sub-Saharan Africa. This present study aimed to investigate the association between plasma magnesium and cardiovascular risk factors among type 2 diabetes patients. Methods: Seventy type 2 diabetes patients, with equal gender distribution, in a tertiary hospital in Nigeria were recruited. Ethical approval was obtained. Anthropometric measures were done as recommended. Plasma magnesium and fasting lipid profiles measured using standard protocols. Results: The mean age of the participants was 53.34 ± 9.57 years. The mean duration of diabetes mellitus among the participants was 6.29 ± 2.78 years. Central obesity and hypertension are the most prevalent cardiovascular risk factors among patients with type 2 diabetes. About 38.6% of the participants had suboptimal glycemic control. Nearly 64.3% had dyslipidemia. The frequency of hypomagnesemia among the participants was 25.7%. Hypomagnesemia was significantly associated with the presence of dyslipidemia (P = 0.042) and suboptimal glycemic control (P = 0.001). Conclusion: Hypomagnesemia is associated with cardiometabolic risk factors. Therefore, plasma magnesium could be used as a cheap marker of cardiovascular risk in low-resource settings like sub-Saharan Africa.
Keywords: Cardiometabolic risk, hypomagnesemia, plasma magnesium, sub-Saharan Africa, type 2 diabetes
|How to cite this article:|
Azeez TA, Sonuga OO. Hypomagnesemia as a cardiometabolic risk marker in type 2 diabetes mellitus: Implications for Sub-Saharan Africa. Ann Clin Cardiol 2021;3:29-32
|How to cite this URL:|
Azeez TA, Sonuga OO. Hypomagnesemia as a cardiometabolic risk marker in type 2 diabetes mellitus: Implications for Sub-Saharan Africa. Ann Clin Cardiol [serial online] 2021 [cited 2021 Nov 27];3:29-32. Available from: http://www.onlineacc.org/text.asp?2021/3/1/29/317104
| Introduction|| |
Magnesium is the fourth most abundant cation in the body and most abundant divalent cation in the cells where it plays a critical role in cellular metabolism and homeostasis. Hypomagnesemia is defined as serum or plasma magnesium level below the lower limit of reference interval which varies with the population and the methods used in assaying. At the cellular level, magnesium plays multiple roles in deoxyribonucleic acid stability, protein synthesis, and enzyme functions. Deranged plasma magnesium levels are associated with diabetes mellitus and its complications.
The incidence of hypomagnesemia in diabetes mellitus has been quoted as 13.5%–47.7%. This wide range was believed to be due to differences in sociodemographics and assay methodologies. There are multiple possible causes of hypomagnesemia in diabetes mellitus. Gastrointestinal causes include reduced intake from dietary restriction, esophageal motility dysfunction from autonomic neuropathy, and diabetic gastroparesis causing recurrent nausea and vomiting as well as diarrhea., Renal losses may be due to hyperfiltration, osmotic diuresis, recurrent metabolic acidosis, and hypoalbuminemia. Other proposed renal mechanisms of hypomagnesemia in type 2 diabetes are electrolyte disturbances such as hypokalemia and hypophosphatemia (which are relatively more common in diabetes), insulin resistance at the level of renal tubules, thereby enhancing magnesium wasting and the use of diuretics to control hypertension which often accompanies diabetes.,
Hypomagnesemia affects both insulin secretion and action. This assertion is supported by Guerrero-Romero et al., who demonstrated that magnesium supplementation improves insulin sensitivity in insulin-resistant participants. Glucokinase activity in pancreatic beta cells requires magnesium and this is believed to be a major pathway by which hypomagnesemia impairs insulin secretion. Similarly, magnesium is required for the various enzymes involved in the insulin signaling pathway and this is proposed to be the link between hypomagnesemia and insulin resistance.
Previous studies have documented an association between hypomagnesemia and elevated glycated hemoglobin (HbA1c) in patients with diabetes.,, Hypomagnesemia has also been associated with increased incidence of hypertension. Furthermore, Shamnani et al. have reported hypomagnesemia as a predictor of obesity in a cross-sectional study conducted in India. Similarly, other researchers have documented increased frequency of hypomagnesemia in patients with type 2 diabetes and dyslipidemia. Furthermore, smoking has been previously documented to be associated with hypomagnesemia.
In sub-Saharan Africa, the prevalence of diabetes mellitus and the associated cardiovascular risk factors are increasing but there is a paucity of information on the association between plasma magnesium and cardiometabolic risk factors in type 2 diabetes mellitus, hence the need for this study.
The objectives of the study were to determine the prevalence of hypomagnesemia in patients with type 2 diabetes and to evaluate the association between plasma magnesium and cardiometabolic risk factors such as hypertension, dyslipidemia, and obesity.
| Methods|| |
The study was carried out among patients attending the diabetes clinic of a tertiary hospital in Nigeria. It was a cross-sectional study design. It involved 70 patients (35 males and 35 female) with type 2 diabetes mellitus. The joint University College Hospital and University of Ibadan Ethical Review Committee gave the ethical approval for the study. Furthermore, the recruited participants gave written consent to partake in the study.
Individuals (30 years and above in age) who were previously diagnosed with type 2 diabetes, using the World Health Organization (WHO) criteria, were enrolled into the study.
Individuals diagnosed with any acute illness or hospitalized in the preceding 3 months to the study were excluded from the study. Other exclusion criteria were prior diagnosis with deranged magnesium levels, chronic diarrhea, usage of insulin or diuretics, magnesium-containing drugs, or supplements, and pregnancy.
Trained assistants obtained the socioeconomic data with pretested structured questionnaires. Height was measured with a stadiometer while the weight was determined with a D-339 Detecto Eye-level Physician Beam Scale. Body mass index (BMI) was computed with the equation given below. Waist circumference was measured following WHO recommendation.
BMI = weight (kg)/height2 (m2)
Blood pressure was measured with a mercury sphygmomanometer following the recommendations of the European Society of Hypertension. Using a fasting plasma sample, high-density lipoprotein-cholesterol (HDL-C), total cholesterol, and total glycerides were quantified using the enzymatic methods. Friedewald equation was employed in determining the low-density lipoprotein-cholesterol (LDL-C). HbA1c was measured using the high-performance liquid chromatography method.
Participants had venous blood sample collected following an overnight fast of about 8–12 h. Fasting plasma glucose was determined by glucose oxidase enzymatic method on automated chemistry analyzer Landwind C100 plus. Total cholesterol, total triglyceride, and HDL-C were determined using the enzymatic method on automated chemistry analyzer Landwind C100 plus. LDL-C was calculated using the Friedewald equation provided that the triglyceride was not >400 mg/dl.
LDL-C = Total cholesterol − HDL-C − total triglycerides/5.
Total cholesterol >200 mg/dl and/or total glyceride >150 mg/dl and/or HDL-C <40 mg/dl in males or <50 mg/dl in females is considered as dyslipidemia. HbA1c was determined using ion-exchange high-performance liquid chromatography method. Plasma magnesium was determined using Xylidyl Blue Monoreagent method on automated chemistry analyzer Landwind C100 plus.
The collected data were critically examined and were carefully entered into Microsoft Excel datasheet. The data were later analyzed the Statistical Package for the Social Sciences software, (SPSS) version 22 (IBM (International Business Machines Corporation), New York, USA). Quantitative variables were presented as mean ± standard deviation whereas categorical variables were presented as frequencies and percentages. The association between categorical variables was determined with the Chi-square test. P < 0.05 was considered to be statistically significant.
Definition of terms
Dyslipidemia – Fasting total cholesterol >200 mg/dl and/or fasting triglyceride >150 mg/dl and/or LDL-C >130 mg/dl and/or HDL-C <40 mg/dl (in males) or 50 mg/dl (in females).
Hypertension – Systolic blood pressure ≥140 mmHg and/or diastolic blood pressure ≥90 mmHg or being on antihypertensives.
Obesity – BMI ≥ 30 kg/m2.
Overweight – BMI 25–29.9 kg/m2.
Central obesity – Waist circumference ≥94 cm in males or 80 cm in females.
Hypomagnesemia – Plasma magnesium <1.7 mg/dl.
Suboptimal glycemic control – HbA1c above 7%.
| Results|| |
Seventy participants were involved in the study. There were 35 males and 35 females. The mean age of the participants was 53.34 ± 9.57 years. [Table 1] depicts the socioeconomic features of the participants. The mean duration of diabetes mellitus among the participants was 6.29 ± 2.78 years.
[Figure 1] shows the prevalence of cardiometabolic risk factors among the participants. Central obesity and hypertension are the most prevalent cardiovascular risk factors among patients with type 2 diabetes. Nearly 38.6% of the participants had suboptimal glycemic control.
|Figure 1: Prevalence of cardiometabolic risk factors among the participants|
Click here to view
The frequency of hypomagnesemia among the participants was 25.7%. [Table 2] shows the association between hypomagnesemia and cardiometabolic risk factors. Hypomagnesemia was significantly associated with the presence of dyslipidemia (P = 0.042) and suboptimal glycemic control (P = 0.001).
|Table 2: Association between hypomagnesemia and various cardiometabolic risk factors|
Click here to view
| Discussion|| |
The frequency of hypomagnesemia among patients with type 2 diabetes mellitus, in this study, was 25.7%. This is comparable to the findings of another study done among Nigerian patients with type 2 diabetes where a frequency of hypomagnesemia of 23.2% was reported. The various etiological links between hypomagnesemia and type 2 diabetes mellitus are dietary restrictions, autonomic gastrointestinal disorders, renal losses, and medications such as metformin.
There was a significant association between hypomagnesemia and dyslipidemia among patients with type 2 diabetes mellitus. Previous studies have also documented an association between hypomagnesemia and dyslipidemia among patients with type 2 diabetes mellitus.,, It has been documented that hypomagnesemia inhibits lipoprotein lipase and lecithin–cholesterol acyltransferase and enhances the effects of 3-hydroxy-3-methylglutaryl coenzyme A transferase, and these mechanisms have been hypothesized as the explanation for the association between hypomagnesemia and dyslipidemia.
Similarly, this study demonstrated a significant association between hypomagnesemia and suboptimal glycemic control. The findings of other previous studies are in keeping with this result.,, Osmotic diuresis from persistent hyperglycemia and gastrointestinal losses from gastroparesis and diarrhea are some of the documented explanations for this observation.,,
Magnesium is relatively cheap and simple to assay but it is often unchecked in patients with type 2 diabetes., In low-resource settings, like sub-Saharan Africa, the implications of this are that plasma magnesium should be routinely checked and those who have hypomagnesemia should have a further screening of their metabolic profiles. In other words, in resource-poor settings, as is obtainable in sub-Saharan Africa, hypomagnesemia could be used as a cheap and simple surrogate marker of poor metabolic control in patients with type 2 diabetes. Furthermore, since studies have shown a significant association between poor metabolic control and cardiovascular death, it can be concluded that plasma magnesium could be a reliable cardiovascular risk indicator in low-resource settings such as sub-Saharan Africa.,
| Conclusion|| |
Hypomagnesemia is a common in patients with type 2 diabetes and it is significantly associated with HbA1c and fasting lipid profile. It may be used as a marker of cardiometabolic risk in sub-Saharan Africa.
The sample size was small and it was a hospital-based study so the generalizability to the community may require some caution.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Barbagallo M, Dominguez LJ. Magnesium and type 2 diabetes. World J Diabetes 2015;6:1152-7.
Gommers LM, Hoenderop JG, Bindels RJ, de Baaij JH. Hypomagnesemia in type 2 diabetes: A vicious circle? Diabetes 2016;65:3-13.
Feng J, Wang H, Jing Z, Wang Y, Cheng Y, Wang W, et al
. Role of magnesium in type 2 diabetes mellitus. Biol Trace Elem Res 2020;196:74-85.
Pham PC, Pham PM, Pham SV, Miller JM, Pham PT. Hypomagnesemia in patients with type 2 diabetes. Clin J Am Soc Nephrol 2007;2:366-73.
Boulton AJ, Vinik AI, Arezzo JC, Bril V, Feldman EL, Freeman R, et al
. Diabetic neuropathies: A statement by the American Diabetes Association. Diabetes Care 2005;28:956-62.
Dai LJ, Ritchie G, Kerstan D, Kang HS, Cole DE, Quamme GA. Magnesium transport in the renal distal convoluted tubule. Physiol Rev 2001;81:51-84.
Lecube A, Baena-Fustegueras JA, Fort JM, Pelegrí D, Hernández C, Simó R. Diabetes is the main factor accounting for hypomagnesemia in obese subjects. PLoS One 2012;7:e30599.
Guerrero-Romero F, Tamez-Perez HE, González-González G, Salinas-Martínez AM, Montes-Villarreal J, Treviño-Ortiz JH, et al
. Oral magnesium supplementation improves insulin sensitivity in non-diabetic subjects with insulin resistance. A double-blind placebo-controlled randomized trial. Diabetes Metab 2004;30:253-8.
Azeez TA. Hypomagnesemia and insulin resistance: Gaining better understanding of the pathophysiology of type 2 diabetes. Diabetes Insights Biomed 2020;5:12.
Jahnen-Dechent W, Ketteler M. Magnesium basics. Clin Kidney J 2012;5:i3-14.
Bishwajit G, Seydou I. Hypomagnesemia and type 2 diabetes mellitus: A review of the literature. Austin J Nurition Food Sci 2014;2:1025.
Dasgupta A, Sarma D, Saikia UK. Hypomagnesemia in type 2 diabetes mellitus. Indian J Endocrinol Metab 2012;16:1000-3.
Chrysant SG, Chrysant GS. Association of hypomagnesemia with cardiovascular diseases and hypertension. Int J Cardiol Hypertens 2019;1:100005.
Shamnani G, Atul Rukadikar C, Gupta V, Singh S, Tiwari S, Singh Bhartiy S, et al
. Serum magnesium in relation with obesity. Natl J Physiol Pharm Pharmacol 2018;8:1074-7.
Deepti R, Nalini G, Ambazhagan. Hypomagnesaemia and dyslipidaemia in type 2 diabetes mellitus AJPRHC Research Article relationship between hypomagnesaemia Aand dyslipidaemia in type 2 diabetes mellitus. Res Heal Care 2014;6:32-6.
Yuyun MF, Sliwa K, Kengne AP, Mocumbi AO, Bukhman G. Cardiovascular diseases in sub-saharan Africa compared to high-income countries: An epidemiological perspective. Glob Heart 2020;15:15.
Adegoke O, Ozoh OB, Odeniyi IA, Bello BT, Akinkugbe AO, Ojo OO, et al
. Prevalence of obesity and an interrogation of the correlation between anthropometric indices and blood pressures in urban Lagos, Nigeria. Sci Rep 2021;11:3522.
Stergiou GS, Palatini P, Asmar R, Bilo G, de la Sierra A, Head G, et al
. Blood pressure monitoring: Theory and practice. European Society of Hypertension Working Group on Blood Pressure Monitoring and Cardiovascular Variability Teaching Course Proceedings. Blood Press Monit 2018;23:1-8.
Tsai CH, Wu HH, Weng SJ. Comparison of various formulae for estimating low-density lipoprotein cholesterol by a combination of ages and genders in Taiwanese adults. BMC Cardiovasc Disord 2014;14:113.
National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation 2002;106:3143-421.
Ayoade OG, Umoh I, Amadi C. Dyslipidemia and associated risk factors among Nigerians with hypertension. Dubai Med J 2020;3:155-61.
Amole IO, OlaOlorun AD, Odeigah LO, Adesina SA. The prevalence of abdominal obesity and hypertension amongst adults in Ogbomoso, Nigeria. Afr J Prim Health Care Fam Med 2011;3:188.
Gierach M, Gierach J, Ewertowska M, Arndt A, Junik R. Correlation between body mass index and waist circumference in patients with metabolic syndrome. ISRN Endocrinol 2014;2014:514589.
Odusan OO, Familoni OB, Odewabi AO, Idowu AO, Adekolade AS. Patterns and correlates of serum magnesium levels in subsets of type 2 diabetes mellitus patients in Nigeria. Indian J Endocrinol Metab 2017;21:439-42.
Sajjan N, Shamsuddin M. A study of serum magnesium and dyslipidemia in type 2 diabetes mellitus patients. Int J Orig Res Artic Clin Biochem Res 2016;3:36-41.
Waanders F, Dullaart RP, Vos MJ, Hendriks SH, van Goor H, Bilo HJ, et al
. Hypomagnesaemia and its determinants in a contemporary primary care cohort of persons with type 2 diabetes. Endocrine 2020;67:80-6.
Alshehri AM. Metabolic syndrome and cardiovascular risk. J Family Community Med 2010;17:73-8.
Isomaa B, Almgren P, Tuomi T, Forsén B, Lahti K, Nissén M, et al
. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care 2001;24:683-9.
[Table 1], [Table 2]