Type II Diabetes
Type II Diabetes is a progressive chronic disease stemming from multiple areas of metabolic dysfunction, including insulin resistance, declining insulin production, ineffective hepatic glucose production, and inappropriate hormone activity (Kahn et al., 2014). A healthy body has the ability to balance the neural, nutrient and hormonal components of glucose metabolism. The body has to adjust to altering metabolic demands, caloric intake and breakdown into glucose, with the subsequent uptake of glucose into muscle and adipose by means of insulin. The liver plays a role in gluconeogenesis or the production of glucose, which regulates the amount of glucose released into the bloodstream. Prominent hormone modulators in this process include insulin and glucagon, which work to perform opposite tasks (Kahn et al., 2014). Insulin originates from pancreatic beta cells and is responsible for the uptake of glucose into cells, while also delaying hepatic production of glucose and preventing hyperglycemia (Skyler et al., 2017). Glucagon, however, is from pancreatic alpha cells and stimulates the liver to undergo gluconeogenesis to increase glucose in the bloodstream and protect the body from entering hypoglycemic state (Kahn et al., 2014). In diabetes, however, the system is broken and the mechanism is altered.
The primary faults in the glucose metabolism is insulin resistance of body cells which leaves glucose in the blood stream and beta cell dysfunction resulting in decreasing amounts of insulin production (Kahn et al., 2014). In early stages, the insulin resistance causes the beta cells to go into overdrive to produce more insulin in response to the elevated serum glucose levels (Skyler et al., 2017). Over time, the beta cells lose functionality and insulin production becomes minimal. Due to insulin’s role in inactivating gluconeogenesis, the decline of insulin production leads to hepatic glucose production, increasing serum glucose even more. In sum, insulin resistance, insulin reduction, and hepatic glucagon secretion are the culprits in the unfortunate progression of type 2 diabetes (Kahn et al., 2014).
Reference:
Dodds, S. (2017). The How-To for Type 2 An Overview of Diagnosis and Management of
Type 2 Diabetes Meilitus. Nursing Clinics Of North America, 52(4), 513-522.
Kahn, S. E., Cooper, M. E., & Del Prato, S. (2014). Review: Pathophysiology and treatment
of type 2 diabetes: perspectives on the past, present, and future. The Lancet, 3831068-1083.
Laight, D. (2014). The pharmacology of oral antidiabetic agents. Nurse Prescribing, 12(12),
604-607.
Saenz, A. (2015). Metformin monotherapy for type 2 diabetes mellitus. Cochrane Database
Of Systematic Reviews, (9),
Skyler, J. S., Bakris, G. L., Bonifacio, E., Darsow, T., Eckel, R. H., Groop, L., & … Ratner,
- E. (2017). Differentiation of Diabetes by Pathophysiology, Natural History, and Prognosis. Diabetes, 66(2), 241.