Insulin and Diabetes, Essay Example

Introduction

Insulin production in the human pancreas must be at an optimal level in order to sustain normal bodily functions and to prevent diabetes. However, glucagon must also be considered, as it performs a unique function when it is secreted from the liver during periods when blood glucose is low so that glucose levels are stabilized (Brown.edu). However, if there is dysfunction in insulin production and glucagon continues to be produced, the potential exists to develop an overabundance of glucose, thereby increasing the potential risk of diabetes in patients (Brown.edu). These factors require an analysis of the different systems and how they function in order to effectively stabilize glucose levels, while also considering that if this function does not occur in the normal fashion, there is a greater risk of developing complications in regards to insulin production, which may include a diagnosis of type 2 diabetes in some patients, particularly those who experience insulin resistance in some form. This condition has a trickle-down effect, as it also impacts the production of glucagon and causes a subsequent chain reaction of events that can no longer be managed without human intervention, such as medication or nutritional changes. Therefore, these factors must be considered as part of a larger approach in understanding insulin production and how it impacts routine function, and what occurs if this functionality is impaired for any reason, thereby causing other factors to occur and to complicate matters for the production of insulin in patients with this condition. The following discussion will address the role of insulin production and glucagon formation in the pancreas in order to better understand how these processes operate and the potential complications that may arise when patients experience dysfunction in these areas, including the potential risk of diabetes or the formation of type 2 diabetes in patients whose production of insulin is marked by dysfunction and poor production.

Analysis

Insulin production in its ideal form is produced within the pancreas and is used to stabilize blood sugar levels, particularly after eating foods. However, this process also requires a greater understanding of the different elements that have a tendency to impact insulin production in different forms, depending on individual circumstances. For example, it is known that “Oxidative stress has been implicated as a contributor to both the onset and the progression of diabetes and its associated complications. Some of the consequences of an oxidative environment are the development of insulin resistance, ?-cell dysfunction, impaired glucose tolerance, and mitochondrial dysfunction, which can lead ultimately to the diabetic disease state” (Rains & Jain, 2011, p. 567). Under these conditions, it is believed that there are significant factors that contribute to diabetes, including but not limited to oxidative stress; therefore, this mechanism must be evaluated more closely in order to better understand how to prevent diabetes using metabolic approaches to promote improved insulin regulation and reduced insulin resistance (Rains & Jain, 2011). It is important to identify the degree to which oxidative stress has an impact on insulin production and secretion and to determine if this production is dysfunctional in any way (Rains & Jain, 2011).

The metabolic stability of human organ and system function requires an understanding of glucagon and how it plays a potential role in the development of diabetes in patients (Lee et.al, 2012). It is believed that “glucagon suppression and blockade of its action correct the hyperglycemia of insulin deficiency, consistent with an essential role in the pathogenesis of diabetes. However, every glucagon-suppressing hormone also has antidiabetic actions unrelated to glucagon” (Lee et.al, 2012). This is an important step in the discovery of the relationship between glucagon and metabolism, as well as the relationship between glucagon and insulin in the prevention of diabetes (Lee et.al, 2012). These factors are critical because this process must determine if glucagon has sufficient functionality to prevent diabetes in patients (Lee et.al, 2012). There are considerable efforts required to ensure that insulin and glucagon production operate concurrently and cooperatively; however, if this is not the case, there is a potential risk of the development of diabetes in some patients (Lee et.al, 2012). Glucagon must be evaluated as a primary determining factor in diabetes and in evaluating whether or not patients are at risk for diabetes and whether or not their glucagon levels are appropriate to meet their needs effectively (Lee et.al, 2012). It is believed that glucagon is produced in response to insulin reduction in the pancreatic cells; therefore, when this relationship no longer occurs at the same level, it is possible to experience other factors that have a direct impact on patients and on the development of different factors that must be considered as part of a larger process in which type 2 diabetes is a reality (Lee et.al, 2012).

When insulin resistance is prevalent, it is important to identify the specific tools and resources that are required to determine its relationship to glucagon. It is believed that “subjects with type 1 diabetes and poor blood glucose control have even lower brain glycogen levels, and also that hypoglycemia in the type 1 diabetic population may increase brain glycogen relative to their own baseline. Thus, it is possible that diabetes itself alters brain glycogen content/metabolism in such a way as to confound the response to recurrent hypoglycemia” (Oz et.al, 2011). In this context, it is observed that patients require a balance between glycogen and insulin production, and when this occurs, there is a much higher risk of an imbalance that could ultimately contribute to poor outcomes in many patients in the form of hypoglycemia or hyperglycemia (Oz et.al, 2011).

It is also evident that insulin production may trigger response mechanisms in the brain, thereby creating an environment in which astrocytes, a type of glial cell, are able to accept glucose and form glycogen (Heni et.al, 2011). Furthermore, “insulin may be another inductor of astrocyte proliferation in the human brain. Whether astrocyte numbers are higher in persons with higher insulin levels (e.g. in obesity) has not been studied” (Heni et.al, 2011). This requires an understanding of the causes of this relationship and how it has a significant impact on the development of diabetes (Heni et.al, 2011). The ability to produce insulin must be fully operational and not dysfunctional in order to determine whether or not diabetes is a reality or if it is a preventable condition in some patients (Heni et.al, 2011). These factors must contribute to the overall direction of diagnostic tools and treatment to better understand diabetes and how it impacts many members of the population (Heni et.al, 2011).

There are considerable issues that must be addressed with respect to insulin dysfunction and resistance. It has long been believed that insulin resistance begins with an abundance of insulin production in pancreatic cells; however, ?-cells may also begin to malfunction in accordance with insulin overproduction and may even be a contributing factor in this resistance to begin with (Wahren & Kallas, 2012). ?-cell failure may be indicative of a challenging set of events that occur during the early stages of type 2 diabetes, thereby modifying the manner in which insulin is secreted by these cells (Wahren & Kallas, 2012). These factors represent a change in the composition of pancreatic insulin formation, thereby demonstrating a change in receptor function, which may also contribute to a suppression of insulin function in some patients (Wahren & Kallas, 2012). These findings suggest that insulin dysfunction may be attributed to a number of different factors that ultimately contribute to the formation of type 2 diabetes in different ways that impact patient health and wellbeing (Wahren & Kallas, 2012).

Patients with type 2 diabetes typically experience an increase in glucagon production in response to a lower level of blood glucose to reach a level of homeostasis (Diabetes.co.uk, 2014). Glucagon also promotes the breakdown of glycogen so that glucose formation takes place, it supports the development of gluconeogenesis, and it breaks down fat cells for use by the cells as a form of energy that services the body in different ways (Diabetes.co.uk, 2014). These factors promote an understanding of how glucagon is produced and typically functions in healthy patients without any complications that are related to insulin production, and if glucagon is produced in excess, there is a greater potential to develop type 2 diabetes (Diabetes.co.uk, 2014). This is an important step in the understanding of how glucagon and insulin production must work concurrently in order to promote survival and to provide a basis for examining new approaches to improve patient care outcomes in patients who may eventually develop insulin resistance in response to the development of new focus areas for research and evaluation (Diabetes.co.uk, 2014).

Insulin and glucagon production require a high level understanding of the different elements that contribute to this production. It is important to identify the specific factors that contribute to this state and that influence production. For example, it should be noted that “Markers of liver function, specifically g-glutamyltransferase (GGT) and alanine aminotransferase (ALT), predict incident type 2 diabetes in various populations…in healthy men and women, increased GGT and ALT activities within their physiological ranges are associated with peripheral but also hepatic insulin resistance, increased insulin secretion, and decreased hepatic insulin clearance” (Bonnet et.al, 2011). These factors contribute to the overall production of insulin and the development of new factors that demonstrate how liver function is of particular interest to scientists and clinicians in this area, due to its impact on insulin resistance (Bonnet et.al, 2011). This is an important step in the discovery of new ideas for consideration in the formation of insulin resistance within the pancreas and how this is likely to contribute to the formation of type 2 diabetes in patients (Bonnet et.al, 2011). This concurrent relationship also requires an understanding of the different elements that contribute to a homeostatic state and the steps that are required to ensure that patients receive the most effective treatment possible to manage type 2 diabetes if a diagnosis is made (Bonnet et.al, 2011).

Conclusion

The co-production of insulin and glucagon require an analysis of the different elements that contribute to the development of new directions in care and treatment to accommodate patients who have or at risk of developing type 2 diabetes. This process requires an analysis of the different elements that contribute to the formation of insulin resistance in patients and how this dysfunction may also lead to dysfunction in the production of glucagon in the same patient population. The relationship between these two substances is co-dependent in many ways in order to achieve the desired level of homeostasis that impacts overall health and routine function; however, when this is not achieved, it is likely that there is a greater risk of the development of type 2 diabetes, thereby increasing the health risk for patients. Maintaining the appropriate weight, having a healthy diet, and other contributing factors are necessary in order to support routine production of insulin and glucagon and to prevent additional complications from taking place within the affected patient population. These options provide a basis for exploring the different elements of patient care and treatment that impact patients and that support the development of new opportunities for treatment that may have a direct impact on patient health and wellbeing in different ways.

References

Bonnet, F., Ducluzeau, P. H., Gastaldelli, A., Laville, M., Anderwald, C. H., Konrad, T., … & Balkau, B. (2011). Liver enzymes are associated with hepatic insulin resistance, insulin secretion, and glucagon concentration in healthy men and women. Diabetes, 60(6), 1660-1667.

Brown.edu. Insulin/glucagon. Retrieved from http://biomed.brown.edu/Courses/BI108/BI108_2002_Groups/pancstems/stemcell/insulin_glucagon.htm

Diabetes.co.uk (2014). Glucagon. Retrieved from http://www.diabetes.co.uk/body/glucagon.html

Heni, M., Hennige, A. M., Peter, A., Siegel-Axel, D., Ordelheide, A. M., Krebs, N., … & Staiger, (2011). Insulin promotes glycogen storage and cell proliferation in primary human astrocytes. PLoS One, 6(6), e21594.

Lee, Y., Berglund, E. D., Wang, M. Y., Fu, X., Yu, X., Charron, M. J., … & Unger, R. H. (2012). Metabolic manifestations of insulin deficiency do not occur without glucagon action. Proceedings of the National Academy of Sciences, 109(37), 14972-14976.

Öz, G., Tesfaye, N., Kumar, A., Deelchand, D. K., Eberly, L. E., & Seaquist, E. R. (2011). Brain glycogen content and metabolism in subjects with type 1 diabetes and hypoglycemia unawareness. Journal of Cerebral Blood Flow & Metabolism, 32(2), 256-263.

Rains, J. L., & Jain, S. K. (2011). Oxidative stress, insulin signaling, and diabetes. Free Radical Biology and Medicine, 50(5), 567-575.

Wahren, J., & Kallas, Å. (2012). Loss of pulsatile insulin secretion: a factor in the pathogenesis of type 2 diabetes?. Diabetes, 61(9), 2228-2229.