Type 2 Diabetes Type 1 Research Paper

Type 2 Diabetes Mellitus is a chronic condition that is characterized by insulin resistance in the body and increased blood glucose levels, known as hyperglycemia (1, 2). Type 2 (T2) diabetes is more common than type 1, and its incidence worldwide is increasing (3). T2 diabetes mellitus commonly affects adults over the age of 45, however its prevalence in children is increasing (4). The cause of diabetes mellitus is multifactorial, and results in a complex pathophysiology (5). This essay will focus on the pathophysiology of type 2 diabetes and the range of associated presentations that result from these pathophysiological processes.

The aetiology of T2 diabetes is multifactorial, comprising of genetic makeup, often compounded by environmental

The beta cells of the islets of Langerhans, in the pancreas, are responsible for the regulation and secretion of insulin (8). The release of insulin from beta cells is stimulated when blood sugar levels rise (3, 6). In T2 diabetes, peripheral tissues, such as muscle and adipose tissue, become resistant to insulin, due to a lowered number of insulin receptors in the tissue, defective activation of the receptors or a combination of both (3). This decrease in sensitivity of peripheral tissues is one of the earliest pathophysiological changes to occurs in T2 diabetes (1, 2, 9). When these cells lose sensitivity to insulin, beta cells are increasingly stimulated to secrete more insulin, to maintain normal blood glucose levels, resulting in hyperinsulinemia (3, 9). This hypersecretion of insulin into circulation as compensation for tissue resistance, places excessive demand and stress on the beta cells, resulting in a deterioration in their ability to normally function (2, 5, 8). As insulin resistance worsens, progressive functional loss of beta cells occurs, eventually resulting in their failure (3, 6, 8). This progressive damage to pancreatic beta cells results in a decrease in insulin secretion into circulation, resulting in an increase in blood glucose levels (1). When failure occurs, the body can no longer

The development of neuropathy involves an increase in saturation of the polypol pathway, as well as increased oxidative stress, which contribute to changes in nerve structure and function (15). Increased blood sugar in diabetes mellitus results in a significant increase in cell glucose concentration, including in nerve tissues, due to the unregulated mechanism of cellular glucose uptake (8). The normal threshold of intracellular glucose rapidly becomes oversaturated, and the excess glucose becomes part of the polypol pathway (4). This pathway involves the conversion of large amounts of glucose into sorbitol and fructose (3, 16). These products of the polypol pathway then accumulate in cells and in nerve tissue. This build up leads to a change in the normal structure of nerve cell membranes, particularly through demyelination of nerves and reducing myoinositol in the membrane (16). Ion channels in degenerating nerve tissue will progressively lose their regulation ability, leading to abnormal action potential generation. A decrease in myelination of nerve fibers leads to a significant decrease in the fibers ability to correctly transmit and propagate forward (4). These changes can be managed in minor increases in blood sugar levels through regeneration and remyelination mechanisms, however in chronic high blood sugar, like