Serum adiponectin among di erent stages of type 2 diabetes mellitus patients

Background: Type 2 diabetes mellitus is a chronic metabolic disorder that leads to micro and macrovascular complications. Nephropathy is the most common microvascular complication. For diagnosis of nephropathy in T2DM patients by using urinary albumin, this is not a sensitive and specific biomarker because it is elevated in other conditions. we aimed to evaluate the serum adiponectin for early detection of nephropathy in patients with type 2 diabetes mellitus. Methods: A total of 60 subjects were included in the present study and further subdivided into 30 patients T2DM with normoalbuminuria, 30 patients with microalbuminuria. All the patients were included after obtaining institutional ethical permission and consent forms. Blood and urine samples were collected from all the subjects and proceed with further analysis. Appropriate statistical analyses were used for different types of data analysis. Results: Increased levels of FBS, PPBS, HbA1C and serum adiponectin were observed in two groups of T2DM patients. Statistically elevated levels of serum Urea, Creatinine and Uric acid levels were observed in patients T2DM with microalbuminuria when compared to T2DM with normoalbuminuria. The serum adiponectin was positively correlated with FBS, PPBS, HbA1C, Urea, Creatinine, Uric Acid and Urinary Albumin in patients with two groups of T2DM. Conclusion: This study concluded that measuring the serum adiponectin levels may be useful for the early detection of nephropathy in patients with T2DM.


Introduction
Type 2 diabetes mellitus is a chronic metabolic disease due to both genetic and environmental factors play an important role in insulin resistance.
In this condition, β-cell function in the pancreas declines gradually over some time before the onset of clinical hyperglycemia. Several mechanisms have been proposed for insulin resistance, including stress, increased production of cytokines and growth factors and also by interacting with the renin-angiotensin-aldosterone system [10][11].
Adiponectin is an adipocytokine and it has antiinflammatory, antiatherogenic, and antidiabetic properties. It is also normally present on the endothelium and in the smooth muscle cells of intrarenal arteries and on the endothelium of glomerular and peritubular capillaries.
Circulating adiponectin exists mainly in three isoforms which include a low molecular weight trimeric form (LMW), a hexameric middle molecular form (MMW) and a high molecular weight form (HMW) consisting of 12-36 monomers; globular form and full-length form are the minor circulating fractions of adiponectin [12][13]. The mean plasma concentration of adiponectin was reported to be higher compared to other adipocytokines such as leptin and IL-6, ranging from 5-30 mg/L or 5-30 μg/mL, accounting for about 0.01% of all plasma proteins in humans [14]. The plasma half-life of adiponectin is seventy-five minutes and the protein is mainly cleared by the liver and also kidneys. The high molecular weight form has the slowest clearance rate and relatively constant serum levels.
Adiponectin plays an important role in metabolic regulation and energy homeostasis, mainly through its effects on carbohydrate and lipid metabolism [15]. Adiponectin inhibits hepatic gluconeogenesis by inhibiting genes involved in glucose production thereby decreasing glucose levels.
The glucose-lowering effect appears to be independent of insulin.     [26].
Similarly, another study reported that although serum adiponectin levels in the diabetic group did not show any significant difference as compared with the control group, the highest concentrations of adiponectin were observed in patients with macroalbuminuria when compared to those with normoalbuminuria and microalbuminuria, or the control group [27]. The serum total and HMW adiponectin levels correlated positively with the severity of diabetic nephropathy and retinopathy [28]. One more study found that diabetic patients with overt nephropathy had elevated serum levels of adiponectin that appear to be increased in proportion to the degree of renal tubular injury and tubulointerstitial inflammation [29]. According to them, the increase in circulating adiponectin in overt irrespective of the degree of diabetic nephropathy [31]. Thus, according to them, the increase in the serum adiponectin levels are caused by the increased synthesis in adipose tissue and secretion of the marker rather than reduced clearance due to impaired renal function [32]. They have also concluded that the reno protective role of adiponectin is mainly brought about by its effects on podocytes and is mediated by the AMPK pathway and also observed that overexpression of adiponectin in streptozotocin induced diabetics resulted in reduced proteinuria. Thus, these findings indicate that adiponectin exhibits renoprotective effects mainly through its action on podocytes [33].