The pathogenesis of type 2 diabetes is complicated, particularly as patients can present with differing degrees of insulin resistance. The disease can be due to a combination of genetic and environmental factors and is the most common type in the UK. The disease is characterised by either your body being unable to make enough insulin or your body unable to use the insulin which is produced effectively.
Type 2 diabetes doesn’t attack the beta cells, so it's not an autoimmune disease. The ineffectiveness of insulin (insulin resistance) is compensated by your body producing more of the hormone, but it can’t always produce enough. As the pancreatic beta cells are put under increasing pressure, the increased production of insulin can destroy them, stopping the production of insulin. This is a beta-cell failure. Over a prolonged period of time, it's possible to find yourself in a situation similar to that of a type 1 diabetic.
The changes in insulin secretion cause hyperglycaemia (high blood sugar) and eventually the need for insulin dependence. Obesity is a strong risk factor for becoming insulin resistant, alongside a lack of physical activity. Insulin action can be modulated by fat and muscle cells due to the origination of hormones, cytokines and metabolic fuels within these cells.
Kahn, S. E., Cooper, M. E., & Del Prato, S. (2014). Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future.Lancet (London, England),383(9922), 1068–1083. https://doi.org/10.1016/S0140-6736(13)62154-6