The concentration of glycosylated haemoglobin (HbA1c) is taken as an index of protein glycosylation: it reflects the state of glycaemia over the preceding 2-3 months (Davidson, 2010; Tripathi, 2008).
Two major types of diabetes are- Type I or insulin dependent diabetes mellitus (IDDM), juvenile onset diabetes mellitus, which is caused due to the destruction of β- cells of pancreatic islets, majority of the cases are autoimmune (type 1A) antibodies that destroy β-cells and are detectable in blood. In all type I cases circulating insulin levels are low or very low and patients are more prone to ketosis. However this is less prevalent and has low degree of genetic predisposition (Davidson, 2010; Tripathi, 2008).
Type II diabetes or noninsulin-dependent diabetes (NIDDM), maturity onset diabetes mellitus. There is no loss or moderate reduction in β-cells mass; insulin in circulation is low, normal or even high, no anti-β-cell antibody is demonstrable; has a high degree of genetic predisposition; generally has a late onset (past middle age). Over 90% cases are type 2 DM. Causes may be- abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β-cell deficiency. Another cause that is related with DM comprise reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors. Many hypertensives are hyperinsulinaemic but normoglycaemic and exhibit insulin resistance associated with dyslipidaemia (metabolic syndrome). Hyperinsulinaemia per se has been implicated in causing angiopathy. Other contributing characteristics involves, excessive secretion of hyperglycaemic hormones (glucagon) or due to obesity that is responsible for relative insulin deficiency- the ?-cells lag behind (Davidson, 2010; Tripathi, 2008). Anatomy and Physiology of Insulin Blood glucose is highly regulated within a thin range. An equilibrium is conserved between the entry of glucose into the circulation from the liver, supplemented by intestinal absorption after meals as well as up[take of glucose by the peripheral tissues especially the skeletal muscle. Brain requires a constant supply of glucose and is not able to oxidize free fatty acids but is solely dependent on the glucose as the chief metabolic fuel. When there is decline in the intestinal glucose absorption between meals, hepatic glucose output is enhanced, this is in response to reduced insulin levels and elevated levels of the counter-regulatory hormones, glucagon and epinephrine (adrenaline). The liver produces glucose by the process of gluconeogenesis and glycogen breakdown. The chief components for gluconeogenesis are glycerol and amino acids (Davidson, 2010; Tripathi, 2008). After meals, blood insulin levels rise. insulin is an anabolic hormone with profound effects on the metabolism of carbohydrate, fat as well as protein. Insulin is secreted from pancreatic ? cells into the portal circulation. Various factors also influence and enhance insulin release encompassing amino acids and hormones like glucagon-like peptide 1 (GLP-1), released from the gut, incited by the food ingestion. Insulin on the other hand diminishes blood glucose by restraining hepatic glucose production and stimulating