Hormonal Alterations of the Endocrine Pancreas in the Case of Diabetes Mellitus
Diabetes mellitus (DM) may be regarded as a severe chronic illness that affects millions of people across the globe. It is a particular group of serious physiological dysfunctions “characterized by hyper-glycemia that results directly from inadequate insulin secretion, insulin resistance, and excessive glucagon secretion” (Blair, 2016). The pancreas is responsible for the secretion of insulin and glucagon for the regulation of blood glucose levels. The main function of insulin produced by β cells within the pancreas in response to food intake is to lower blood sugar levels by the facilitation of glucose uptake in the cells of the liver, fat, and muscle from the bloodstream (“Diabetes Mellitus,” n.d.).
Thus, being a metabolic disease characterized by the high levels of sugar in the blood over a long period of time, DM is defined as one of the global major health issues with life-threatening symptoms including renal failure, possible blindness, amputation of lower limbs due to poor blood circulation, heart attack, and stroke (Okur, Karantas, & Siafaka, 2017). As a matter of fact, all forms of DM are characterized by the pancreatic β cells’ inability to meet the demand of insulin secretion due to the functional β cells’ deficit in the peripheral insulin resistance’s setting or the cells’ almost complete loss (Saleh & Butler, 2019). In general, the deficit in β cell mass occurs due to the cell’s death, their degranulation that implies the depletion of insulin granules due to stresses, or their dedifferentiation or transdifferentiation – the alteration or loss of functional mature β cell identity (Saleh & Butler, 2019).
Type 1 Diabetes
This type, also known as insulin-dependent, childhood-onset or juvenile diabetes, is a result of β cell destruction that leads to deficient insulin production and complete insulin insufficiency n the body (Okur et al., 2017). Type 1 diabetes may be also defined as a particular autoimmune reaction characterized by the invasion of the immune system against functional mature β cell that produce insulin. Patients with this type of DM require the administration of insulin on a daily basis to control the blood sugar level, and non-administration is life-threatening. In general, the reasons for Type 1 diabetes are currently not identified and not preventable (Okur et al., 2017). However, such factors as viral infections and environmental risks may contribute to the occurrence of this disease.
Type 2 Diabetes
This most typical non-insulin-dependent or adult-onset type of diabetes is a result of a “continuous insulin secretory defect on the basis of insulin resistance in relation to the body’s inefficient use of insulin” (Okur et al., 2017). In the case of Type 2 diabetes, the body may produce insulin, however, it becomes so resistant that the hormone is inefficient (Okur et al., 2017). As a result, the pancreas produces more insulin in order to compensate its function’s reduction. Similar to Type 1 diabetes, the exact reason for non-insulin-dependent diabetes mellitus is unknown as well. However, the most significant factors that may contribute to its occurrence include poor nutrition, physical inactivity, and obesity.
Conclusion
It goes without saying that pathophysiology plays a highly significant role in advanced nursing practice as knowledge related to the mechanisms of the disease’s occurrence inevitably contributes to the understanding of its treatment. From a personal perspective, this research dedicated to the pathophysiology of diabetes mellitus is beneficial for me as a health care provider. I have extended my knowledge in the functionality of insulin and the differences between the two main types of diabetes mellitus.
References
Blair, M. (2016). Diabetes mellitus review. Urologic Nursing, 36(1), 27-36.
Diabetes Mellitus. (n.d.). 2021, Web.
Okur, M. E., Karantas, I. D., & Siafaka, P. I. (2017). Diabetes mellitus: A review on pathophysiology, current status of oral medications and future perspectives. Acta Pharmaceutica Siencia, 55(1), 61-82.
Saleh, A., & Butler, A. E. (2019). Alterations in beta cell identity in Type 1 and Type 2 diabetes. Current Diabetes Reports, 19(83), 1-12.