Pathophysiology of Diabetes
Diabetes mellitus (DM) is a metabolic disorder, associated with raised plasma glucose concentration and disturbance of glucose, carbohydrates, lipids, and protein metabolism. It is a various group of disorders identified by the presence of chronic hyperglycemia which can be categorized into type 1 diabetes mellitus (which is immune-mediated or idiopathic) and type 2 diabetes mellitus (also known as non-insulin dependent DM).
Type 1 DM results from the autoimmune destruction of insulin-producing pancreatic β cells of the endocrine pancreas. It is diagnosed after 80-90% of the beta cells are destroyed. This disease represents only around 10% of the diabetes cases worldwide, with no evidence of autoimmunity, and the pathogenesis in these cases is considered idiopathic. Type 1 DM previously encompassed insulin-dependent diabetes or juvenile-onset diabetes. It is the combination of chronic inflammatory infiltration and destruction of insulin-secreting beta cells of the islets of Langerhans in the pancreas, thus reducing the beta-cells and developing hyperglycemia. Type 1 diabetic patients need regular insulin doses exogenously to reverse this metabolic disorder which can also further prevent ketosis, reduce hyperglucagonemia, and control lipid and protein metabolism in them. Autoimmunity is another dogma considered to be a major factor involved in the pathophysiology of type 1 DM. It is strongly genetically linked with HLA on chromosome 6 which includes the generation of specific T cells, initiating an immune response to specific islet cells autoantigens. Islet cell antibodies (ICA), insulin autoantibodies (IAA), and anti-GAD antibodies are circulating antibodies that can be detected in the body fluids in type 1 diabetic patients. Other most common factors involved in the admittance of diabetes are viruses, chemicals, and even cow’s milk.
Type 2 diabetes is a complex disease critically determined by both genes and environmental factors. The former includes impaired insulin secretion and insulin resistance and the latter includes obesity, overeating, lack of exercise and stress, as well as aging. It is more prevalent than type 1 diabetes exhibiting intra-abdominal (visceral) obesity, which is closely related to the presence of insulin resistance. Type 2 diabetes comprises approximately 90% of all people with diabetes. Moreover, hypertension and dyslipidemia often are present in type 2 diabetic patients. Formerly it was known as adult-onset diabetes and factors highly associated with Type 2 DM are a family history of diabetes, older age, obesity, and lack of exercise. Obesity due to a lack of exercise is quite common leading to a decrease in muscle mass, induces insulin resistance and weight reduction ameliorates hyperglycemia. The pathogenesis of type 2 diabetes mellitus involves the synergistic role of both impaired insulin secretion and insulin resistance. It involves a genetic abnormality in the molecules related to the regulatory system of glucose metabolism such as molecules comprising the molecular mechanism for insulin action that have identified genetic abnormalities that can be independent causes of pathogenesis. Recently, a genome-wide association study (GWAS) has identified over 50 gene loci that have been linked to type 2 diabetes-related to insulin secretion abnormality associated with the pathogenesis of type 2 diabetes.
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