Serum Adenosine Deaminase Activity among Newly Diagnosed Patients with Type 2 Diabetes Mellitus and Its Correlation with Insulin Resistance

Aims: Insulin resistance is consistence feature in type 2 diabetes mellitus (DM). Several studies demonstrated that serum adenosine deaminase activity (ADA) is elevated in type 2 DM patients. The present study was conducted to estimate serum ADA activity in newly diagnosed type 2 DM patients, compared with control groups and to find out correlation of insulin resistance with serum ADA activity. Method: Fifty-one type 2DM patients were selected as cases and fifty healthy individuals served as controls. Their body mass index(BMI), fasting plasma glucose (FPG), fasting plasma insulin (FPI), homeostatic model for assessment of insulin resistance (HOMAIR), % beta cell activity, % sensitivity of insulin and serum ADA activity were measured using appropriate methods. Results: ADA activity was significantly increased among cases in comparison to controls (p value <0.001). Serum ADA activity was positively correlated with BMI (r=0.386; p=0.005); FPI (r=0.318; p=0.023); HOMAIR (r=0.363; p=0.009) & negatively correlated with % sensitivity (r=-0.381; p=0.006) among case group. Conclusion: ADA activity might be considered as a predictive marker of insulin resistance in obese or overweight type 2 DM. Key word: ADA activity, HOMA-IR, obesity, type 2 DM. Asia Pacific Journal of Research Vol: I Issue XV, July 2014 ISSN: 2320-5504, E-ISSN-2347-4793 Page | 2 INTRODUCTION: According to International Diabetes Federation 2012, in the world more than 371 million people suffer from diabetes mellitus (DM). 71.3 million Adults with diabetes in the world live in the South-East Asia Region, 61.3 million of whom are in India. The most common form of this epidemic is type 2 DM [1]. Type 2 DM consistently demonstrates three cardinal abnormalities: resistance to the action of insulin in peripheral tissues, particularly muscle and adipose tissue; decreased insulin secretion, and increased glucose production by the liver [2]. Insulin resistance is central to the pathophysiology of type 2 DM. It is defined as a decreased biological response to normal concentrations of circulating insulin [3]. Insulin resistance is manifested by decreased insulin-stimulated glucose uptake and its metabolism in adipocytes and skeletal muscle and by impaired suppression of hepatic glucose output resulting hyperglycemia [2]. However, the development of frank diabetes mellitus require insulin secretion defect also. In the absence of β-cell dysregulation, individuals can compensate indefinitely for insulin resistance with appropriate hyperinsulinemia [4]. GLUT4 is the main glucose transporter activated by insulin in skeletal muscle cells and adipocytes in maintaining blood sugar. Insulin sensitivity is influenced by a number of factors including age, weight, ethnicity, body fat (especially abdominal) [2], physical activity [5], dietary habits [6] (excessive carbohydrate diet), free fatty acid [2, 7], vitamin D deficiency [8], inflammation [9, 10] genetic factors and medications such as glucocorticoid. In addition to the above mentioned there are many more factors; such as adenosine molecule. Adenosine, a degradation product of adenine nucleotides, has been proven to play an important role in modulation of insulin action on glucose metabolism in different tissues. Some of the adenosine that is produced intracellularly is released into the extracellular space, where it interacts with adenosine receptors to regulate various physiological processes in an autocrine manner. One such action is to modulate insulinstimulated glucose transport (via GLUT4) in striated muscle and adipocytes [11]. Allan Green et al in 1987 demonstrated that adenosine and other A1 receptor agonists (N6 phenyl isopropyl adenosine, PIA), increases insulin sensitivity and inhibit lipolysis in adipocytes [12]. Intracellular adenosine concentration is maintained by adenosine deaminase enzyme. Adenosine deaminase (ADA 3.5.4.4) is a purine catabolic enzyme that catalyzes the deamination of adenosine to inosine and maintain cellular adenosine concentration. ADA was considered as good marker of cell mediated immunity. It plays a crucial role in lymphocyte proliferation and differentiation. Previously, ADA activity has been reported to be increased in type 2 DM [13-16]. But it is not yet established whether ADA activity rises at early phase of onset of type 2 DM or raised ADA activity is affected by therapy. It is also precisely not known whether there is any correlation between insulin resistance and serum ADA activity. This study was conducted to determine serum ADA activity in newly diagnosed patients with type 2 DM who have not started any treatment and its correlation with