"Diabetes Risk Factors" is an outstanding example of a paper on diabetes mellitus. There are two core types of diabetes: diabetes mellitus type 1 ad type 2. In type 1 diabetes, immunological mechanisms stimulate the immune system to perceive the beta cells as being foreign, hence forming antibodies to destroy them. Beta cells will no longer produce insulin. In type 2, diabetes, the beta cells are physiologically active, and insulin production is normal. However, the body system's response to insulin is poor. This makes the beta cells to become hyperactive, as they respond to the situation by producing more insulin.
Such hyperactivity causes the beta cells to lose their ability to produce insulin. Diabetes type 2 crops in. Prior to the final diabetic diagnosis, the beta cells do undergo several stages of dysfunction. The five stages represent the developmental progression of diabetes. There is a marked change in the mass, physiological characteristics, and functioning of the Beta cells (Weir & Bonner-Weir, 2004). First, the compensation stage is characterized by a sudden increase in the insulin levels to match the escalating glucose levels in the body.
The stable adaptation stage entails a situation where the body's glucose levels rise to around 6 mmol/l. the third stage is the early unstable decompensation stage, where the glucose levels escalate to high levels. There is a stable decompensation in stage four and severe beta cells failure in the fifth stage, where several factors are well known to initiate the compromised functioning of the pancreatic beta cells in diabetes. Several factors may predispose a person to the progressive destruction of the beta cells. First, autoimmunity remains a threatening causative factor of the condition.
With reference to this, the body’ s immune system mistakes the pancreatic cells as foreign bodies or cells that are on the verge of bringing destruction to the body. Therefore, they form antibodies against the beta cells and destroy them. What triggers such a reaction is quite unknown, although viral infection is believed to be a triggering cause. Autoimmunity issue is also likely to run in families as an inherited condition (Shaw & Tanamas, 2012). Additionally, the aspect of increasing age puts one at risk of developing the condition.
At one age, there is a tendency to have an increase in both weight and performance of a few exercise patterns (d’ Emden et al. , 2012). The age factor does slow down the insulin production process, and the body becomes at risk of experiencing insulin resistance. Moreover, genetics also plays a key role in the destruction of the beta cells. A person with a close relative having the condition is at immense risk of inheriting the condition too. Genes are the components that carry instructional materials from parents to the offspring (Speight, Conn, Dunning, & Skinner, 2012).
They contain the essential proteins that are vital for body functioning. Gene variants do affect less than one percent of the total population. Human Leucocyte Antigen found in white blood cells has a close link to the development of type 1 diabetes. Furthermore, obesity or overweight people do release chemicals in their bodies, and such chemicals can disturb the cardiovascular and endocrine systems. It also increases the risks of developing coronary heart disease and cancer, as the body cells will respond to the chemicals immediately.
The chemicals also do alert the production of insulin (Reddy et al. , 2011). The obese nature of a person does stress the body cells and their operational mechanisms. The endoplasmic reticulum performs extraneous work, then it is deemed to handle. It then does send an alarm to the insulin receptors. The insulin receptors dampen up, leading to insulin resistance. Primarily, environmental factors such as a different variety of foods, occupational areas toxins, and viruses also trigger the destruction of the beta cells. Varieties of research do relate to the environmental factors with the autoimmune destruction of the cells.
People with viral infections such as cytomegalovirus, adenovirus, and mumps are also susceptible to the condition. Most significantly, all viral infections do attract and activate an immune response in a major way. A virus is also on the verge of autolyzing the beta cells (Weir & Bonner-Weir, 2013). They may also target the insulin receptors, leading to non-reversible reactions hence impeding the sugar regulation process. Lastly, medical conditions such as polycystic ovary syndrome and hypertension. Women with polycystic ovary syndrome have increased tendencies of having insulin resistance.
The two medical conditions escalate the risk of diabetes (Lee et al. , 2013). Regular insulin can be classified under short-acting soluble and crystalline zinc insulin, which has been, manufactured from the recombinant DNA techniques. Once a diabetic client is injected, regular insulin commences its effect in the body system within thirty minutes. The insulin molecules are diluted in the interstitial fluid to enable its transportation across the vascular endothelium. The peak effect is achieved within the duration of 2-3 hours immediately after the subcutaneous injection of the drug.
Administration at mealtime causes an increase in the risks of late postprandial hypoglycemia; therefore, it should be injected at least 30-45 minutes prior to meals. Short-acting insulin remains a great choice for a diabetic patient who is on diabetic ketoacidosis. It can also be administered intravenously. Essentially, it seeks to correct post-prandial hyperglycemia (Shaw & Tanamas, 2012). Metformin is classified under biguanides. Upon administration, they do reduce hepatic and renal gluconeogenesis to great levels; they slow down the rate of glucose absorption from the gastrointestinal tract, and they pose a direct stimulation of glycolysis in body tissues.
Additionally, they reduce plasma glucose levels. Its half-life is 1.5 to 3 hours, and its metabolism is through the kidney. Accumulation of metformin in the body may predispose one to lactic acidosis. In summation, the beta cell destruction is a non-reversible process, and the affected client has to rely on the anti-diabetic medication for the rest of his life.
Emden, M. C., Shaw, J. E., Colman, P. G., Colagiuri, S., Twigg, S. M., Jones, G. R. D., … Cheung, N. W. (2012). The role of HbA1c in the diagnosis of diabetes mellitus in Australia. The Medical Journal of Australia.
Lee, C. M. Y., Colagiuri, R., Magliano, D. J., Cameron, A. J., Shaw, J., Zimmet, P., & Colagiuri, S. (2013). The cost of diabetes in adults in Australia. Diabetes Research and Clinical Practice, 99, 385–390.
Reddy, P., Hernan, A. L., Vanderwood, K. K., Arave, D., Niebylski, M. L., Harwell, T. S., & Dunbar, J. A. (2011). Implementation of diabetes prevention programs in rural areas: Montana and south-eastern Australia compared. Australian Journal of Rural Health, 19, 125–134.
Shaw, J., & Tanamas, S. (2012). Diabetes: the silent pandemic and its impact on Australia. Baker IDI Heart and Diabetes Institute, 1–52.
Speight, J., Conn, J., Dunning, T., & Skinner, T. C. (2012). Diabetes Australia position statement. A new language for diabetes: Improving communications with and about people with diabetes. Diabetes Research and Clinical Practice, 97, 425–431.
Weir, G. C., & Bonner-Weir, S. (2004). Five stages of evolving beta-cell dysfunction during progression to diabetes. Diabetes, 53 (suppl 3), S16-S21.
Weir, G. C., & Bonner-Weir, S. (2013). Islet β cell mass in diabetes and how it relates to function, birth, and death. Annals of the New York Academy of Sciences, 1281, 92–105.