Type II diabetes: Pathophysiology, Diagnostic Tests, Medications, Clinical Manifestations, and etc.

Diabetes mellitus type 2 (also known as type 2 diabetes) is a long-term metabolic disorder that is characterized by high blood sugar, insulin resistance, and relative lack of insulin.[6] Common symptoms include increased thirst, frequent urination, and unexplained weight loss. Symptoms may also include increased hunger, feeling tired, and sores that do not heal.[3] Often symptoms come on slowly.[6] Long-term complications from high blood sugar include heart disease, strokes, diabetic retinopathy which can result in blindness, kidney failure, and poor blood flow in the limbs which may lead to amputations.[1] The sudden onset of hyperosmolar hyperglycemic state may occur; however, ketoacidosis is uncommon.[4][5]

Type 2 diabetes primarily occurs as a result of obesity and lack of exercise.[1] Some people are more genetically at risk than others.[6] Type 2 diabetes makes up about 90% of cases of diabetes, with the other 10% due primarily to diabetes mellitus type 1 and gestational diabetes.[1] In diabetes mellitus type 1 there is a lower total level of insulin to control blood glucose, due to an autoimmune induced loss of insulin-producing beta cells in the pancreas.[12][13] Diagnosis of diabetes is by blood tests such as fasting plasma glucose, oral glucose tolerance test, or glycated hemoglobin (A1C).[3]

Type 2 diabetes is partly preventable by staying a normal weight, exercising regularly, and eating properly. Treatment involves exercise and dietary changes.[1] If blood sugar levels are not adequately lowered, the medication metformin is typically recommended.[7][14] Many people may eventually also require insulin injections.[9] In those on insulin, routinely checking blood sugar levels is advised; however, this may not be needed in those taking pills.[15] Bariatric surgery often improves diabetes in those who are obese.[8][16]

Rates of type 2 diabetes have increased markedly since 1960 in parallel with obesity.[17] As of 2015 there were approximately 392 million people diagnosed with the disease compared to around 30 million in 1985.[11][18] Typically it begins in middle or older age,[6] although rates of type 2 diabetes are increasing in young people.[19][20] Type 2 diabetes is associated with a ten-year-shorter life expectancy. Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance.[13] Insulin resistance, which is the inability of cells to respond adequately to normal levels of insulin, occurs primarily within the muscles, liver, and fat tissue.[44] In the liver, insulin normally suppresses glucose release. However, in the setting of insulin resistance, the liver inappropriately releases glucose into the blood.[10] The proportion of insulin resistance versus beta cell dysfunction differs among individuals, with some having primarily insulin resistance and only a minor defect in insulin secretion and others with slight insulin resistance and primarily a lack of insulin secretion.[13]

Other potentially important mechanisms associated with type 2 diabetes and insulin resistance include: increased breakdown of lipids within fat cells, resistance to and lack of incretin, high glucagon levels in the blood, increased retention of salt and water by the kidneys, and inappropriate regulation of metabolism by the central nervous system.[10] However, not all people with insulin resistance develop diabetes, since an impairment of insulin secretion by pancreatic beta cells is also requ

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