Year : 2018 | Volume : 6 | Issue : 2 | Page : 61 - 64  

Original Articles
Study of trace elements in type 2 diabetes mellitus with special Reference to iron and magnesium indicating significance for early detection of complications

Jhansi Rani Chalampalyam1, Vemula Solomon Sanjeeva Rao2, Sudhakar T3

1, 2, 3 Departments of Biochemistry, Chalmeda Anand Rao Institute of Medical Sciences, Karimnagar, Telangana, India

Corresponding Author



Background: Diabetes mellitus is a group of etiologically different metabolic defects characterized by hyperglycemia resulting from defect in insulin secretion as well as insulin action or both. The role of trace elements in type 2 diabetes like serum magnesium and total serum iron is essential in glucose homeostasis at multiple levels with complex interplay which exist between glucose and magnesium. The aim of the study was to determine the role of iron and magnesium in type 2 diabetes and its complications.

Objective: To identify the persons with type 2 diabetes mellitus and state their iron status, magnesium levels in serum for early detection of risk factors which indicate the severity of diabetes and its complications.

Methods: A total of 50 subjects aged >35 years were selected from Chalmeda Anand Rao institute of medical sciences, Bommakal, Karimnagar. Total serum iron is determined by Ferrozine method, serum magnesium is determined by xylidyl blue with ATCS method.

Results: The mean and SD of serum Random Blood Glucose in controls is 114.5+9.75 as compared to 207.5+31.5 in cases. The mean and S.D of serum Iron in control is 114.36+20.35 as compared to 286.08+96.35 in cases. The mean and S.D of serum Magnesium in control is 1.9+0.1 as compared to 0.88+0.1 in cases.

Conclusion: Our study was concluded that serum magnesium is decreased and serum total iron is increased in type 2 diabetes which plays a pathogenic role in diabetes and its complications.

Key words: Type 2 diabetes, Iron, Magnesium, Insulin Resistance


The WHO reports suggests that the prevalence of diabetes in worldwide would increases to 300 million in the year 2025. 1 It is one of the main threats to human health in the 21st century and is the fifth leading cause of death in most developed countries. 2 Magnesium is an important component of many unprocessed foods, such as whole grains, nuts, and green leafy vegetables, and it is largely lost during the processing of some foods. 3

The over- processing of food and adoption of western diets have contributed to the substantially reduced magnesium intake in industrialized countries during the last century. 4 Hypomagnesaemia is a common feature in patients with type 2 diabetes. 5 Effects of poor magnesium status on glucose homeostasis are plausible and may be mediated through oxidative stress, the role of magnesium as cofactor for enzymes involved in glucose metabolism, or the effects of intracellular ion levels on insulin sensitivity and insulin secretion. 6

Although the exact mechanism of iron-induced diabetes is uncertain, it is likely, as discussed below, to be mediated by three key mechanisms:1) insulin deficiency,2) insulin resistance, and 3) hepatic dysfunction. An understanding of the pathogenic pathways of iron-induced diabetes is derived mainly from studies on animal models of hemochromatosis. 7

Iron excess and oxidative stress mediate apoptosis of pancreatic islets with a resultant decrease in insulin secretory capacity. 8 Pancreatic islets have an extreme susceptibility to oxidative damage, perhaps because of the nearly exclusive reliance on mitochondrial metabolism of glucose for glucose-induced insulin secretion and low expression of the antioxidant defense system. 9 A high expression of divalent metal transporter additionally predisposes them for more accumulation of iron than other cells 10 and potentiates the danger from iron-catalyzed oxidative stress.


Subjects: The present study was carried out in the Department of Bio-chemistry C. A. R medical college, Karimnagar. The cases were selected from those attended, the medicine OPD at Chalmeda Medical college and hospital, Karimnagar. The Investigating were carried out in Bio-Chemistry laboratory Chalmeda medical college and hospital, Karimnagar.

Design: The total number of subjects included in the study was 50 and divided into two groups. Group Ι had 25 normal healthy subjects as controls while Group-ΙΙ had patients with obesity as cases. This is a case control study.

Criteria for Selection: A total of 50 subjects aged > 35 years were included in the study. Chronic diseases hepatitis, epilepsy, hemolytic diseases, anemia and renal diseases, were included in the exclusion criteria.

Blood Sample Collection: A venous blood sample was obtained from every volunteer into heparinized tubes (BD vacutainer system). All the blood samples were immediately carried to the Biochemistry Laboratory In a crushed ice block, Blood samples were centrifuged at 3000rpm for 10 minutes. The RBS was performed in fully automated analyzer (DS-302 vector Biotech); Glucose was estimated by GOD-PAP, enzymatic photometric test methodology.

Magnesium was estimated by Xylidyl blue with ATCS method where magnesium reacts with xylidyl blue to form a colored compound in alkaline solution. Total serum iron was estimated by Ferrozine method. Iron bound to transferrin is released in acidic medium and the ferric ions are reduced to ferrous ions. The ferrous ions react with Ferrozine to form a violet colored compound.

Ethics approval: The study protocol was reviewed and approved by the Institutional Ethics committee, at Chalmeda Anand Rao Institute of Medical Sciences, Karimnagar, 2015, and written informed consent form was obtained from all participants.


The total number of subjects included in the study was 50 and divided into two groups. Group Ι had 25 normal healthy subjects as controls while Group-ΙΙ had patients with obesity as cases. The mean and SD of serum Random Blood Glucose in controls is 114.5+9.75 as compared to 207.5+31.5 in cases. The mean and S.D of serum Iron in control is 114.36+20.35 as compared to 286.08+96.35 in cases. The mean and S.D of serum Magnesium in control is 1.9+0.1 as compared to 0.88+0.1 in cases.

Table 1: Comparison of Glucose, Serum Magnesium, Serum Iron in cases and controls


Random blood glucose

Serum magnesium

Serum iron









Table 1 shows increased Serum Glucose, increased serum iron decreased serum magnesium levels in cases compared to controls


Global statistics indicate that the prevalence of diabetes would nearly double by the year 2030. 11-12 The prevalence of Type-2 diabetes in India is highest among various Asian population. Number of deaths in adults due to diabetes among all age groups is 6.8% at global level. 13 Although diabetes can induce hypomagnesaemia, magnesium deficiency has also been proposed as a risk factor for type 2 diabetes 14 Magnesium is a necessary cofactor for several enzymes that play an important role in glucose metabolism. 15

However, the underlying cellular or molecular mechanisms by which magnesium intake influence insulin resistance are still not well understood. Abnormalities in intracellular magnesium homeostasis have been hypothesized to be the link between insulin resistance, type 2 diabetes, and cardiovascular disease. 6 First, magnesium functions as a cofactor for enzymes in glucose metabolism utilizing high-energy phosphate bonds. 3 Second, intracellular magnesium levels may be important for maintaining insulin sensitivity in skeletal muscle or adipose tissue. 16 Diminished levels of magnesium may decrease tyrosine kinase activity at insulin receptors 17 and increase intracellular calcium levels 6, leading to an impairment of insulin signaling. Third, intracellular magnesium levels may influence glucose-stimulated insulin secretion in pancreatic β-cells through altered cellular ion metabolism 6 or other pathways linked to oxidative stress and free radical formation. 18 In the present study also hypomagnesaemia is observed in cases compared to normal control group.

The central importance of iron in the pathophysiology of disease is derived from the ease with which iron is reversibly oxidized and reduced. This property, while essential for its metabolic functions, makes iron potentially hazardous because of its ability to participate in the generation of powerful oxidant species such as hydroxyl radical. 19 Iron participates in the formation of reactive oxygen species; organisms take great care in the handling of iron. Indeed, iron sequestration in transport and storage proteins may contribute to antioxidant defenses. It is now well established that oxidants can cause the release of catalytic iron 19 thus, a vicious cycle is initiated that leads to the formation of more reactive oxygen species. Evidence that systemic iron overload could contribute to abnormal glucose metabolism was first derived from the observation that the frequency of diabetes is increased in classic hereditary hemochromatosis (HH). 7

The importance of protein glycation is well known in the pathogenesis of diabetic vascular complications. Transition metals also play a role in protein glycation induced by hyperglycemia. It has been shown that glycated proteins have a substantial affinity for the transition metals, and the bound metal retains redox activity and participates in catalytic oxidation. 20 Thus, should similar glycochelates form in vivo; reactions mediated by the chelates could be involved in the vascular complications of diabetes. 21 Animal studies provide considerable evidence for the role of iron and oxidants in diabetic nephropathy. 22-26 Oxidative stress from factors such as hyperglycemia, advanced glycation end products, and hyperlipidemia further contribute to the availability of intracellular iron that can generate and viciously worsen oxidative stress and renal damage.

Iron content in the kidney has been shown to be increased in an animal model of diabetes 26, and urinary iron excretion is increased early in the course of diabetic renal disease in humans. 27 Most importantly, the pathogenic role of iron in progression is indicated by the observation that progression can be prevented either by an iron-deficient diet or chelators. 28-30 In human studies of end-stage renal disease patients, intravenous iron therapy has been shown to increase vascular and systemic oxidative stress 31-33, promote atherosclerosis 33, and increase the risk of arterial thrombosis. 32 In the present study also there is increased serum iron in cases compared to normal control group.


In the present study serum magnesium is decreased and serum total iron is increased in type 2 diabetes mellitus. Hypomagnesaemia and increased serum iron plays a pathogenic role in diabetes and its complications. So, the progression of complications in type 2 DM which cause morbidity and mortality can be reduced and contained with assessment by regular diabetic health checkups in building confidence and awareness for happenings to overt diabetes. May this work on complications of type 2 DM will bring in site to control complications of diabetes at an early stage of disease.


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