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Protein's Role in Type 1 Diabetes Development and Management By Native Assignment Help
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According to the international diabetes community, protein is interlinked with demands of insulin followed by development of Type 1 diabetes (TID) (Diabetes.co.uk, 2019). Purpose of this assignment is to focus on protein-related diseases followed by Type-1 diabetes. Insulin loss diabetes or Type 1 Diabetes (T1D) is a protein-deficiency related disease, which is resulted due to loss of insulin generating Beta β cells and infiltration of islets (DiMeglio et al. 2018). This assignment is going to discuss the prevalence of Type-1 Diabetes (T1D) and an overview of insulin production. Pathophysiology of insulin deficiency diabetes is going to be covered in this study. Symptoms and possible treatment will also be covered in this study.
Insulin is a peptide hormone (protein), which is made up of an A chain and a B chain. Absence of insulin due to damage of the pancreatic beta cells is the main reason of the T1-diabetes mellitus. The prevalence ofType-1 Diabetes (T1D) is increasing in the UK based on an alarming rate. This section is going to cover provinces and the cost ofType-1 Diabetes (T1D) in United Kingdom (UK).
Above figure indicates that during 2008-2019 around 2.2 million people in England have been registered with Type-1 Diabetes (T1D) (Statista.com, 2018). The number of Type-1 Diabetes (T1D) has jumped to 2.9 million during 2014-2015. In addition, from 2016 to 2017, around 3.1 million people in the United Kingdom (UK) have faced the issue of Type-1 Diabetes (T1D). Approximately 3.2 million people in the United Kingdom (UK) have faced the issue of Type-1 Diabetes (T1D) during 2017-2018 (Statista.com, 2018). By focusing on the above information, it can be stated that the prevalence of Type-1 Diabetes (T1D) has gradually increased among United Kingdom (UK) people from 2008 to 2018.
In current situation, around 4.6 million people live in the United Kingdom (UK) with the issue of T1D. In addition, among 4.6 people, almost 3.7 people in the United Kingdom (UK) have been diagnosed with the issue of Type-1 Diabetes (T1D) (Diabetes.org.uk, 2018). However, the above figure indicates that 12.3 million people lived in the United Kingdom (UK) with the issue of Type 2 Diabetes (Diabetes.org.uk, 2018).
Above figure indicates that from 2019 to 2020, around 2.5% of people in the UK from 80 or above age group have been faced with the issue of Type-1 Diabetes (T1D) (Statista.com, 2020). However, around 11.5% of people among the 65-79 age groups have faced the problems of Type-1 Diabetes (T1D) in the United Kingdom (UK). Approximately 40.8% of people from 40-64 age group and 45.1% of people from 40 or under have faced the issue of Type-1 Diabetes (T1D) during 2019-2020 (Statista.com, 2020). By focusing on above focus information, it can be stated that 40 and under 40 age group in the United Kingdom (UK) have faced the issue of Type-1 Diabetes (T1D).
It has been identified that cases of diabetes progressively rise in the UK surrounded in every category of age. According to Diabetes UK, diabetes is correspondent with numerous obstacles, which may rise with a delay of interpretation.
Postprandial storage of nutrients played an emerging role to secrete insulin from pancreatic Beta cells (SkelinKlemen et al. 2017). This section is going to discuss insulin synthesized in beta cells under the pancreas and its act in regulating blood glucose altitude.
Pancreatic beta cell is a respond to blood circulating nutrients such as glucose. In the first stage of the glucose sensor pancreatic beta cell, it broadcast with one of its member Glucose carrier 2(GLUT 2). By taken advantage of the Glycolysis process, citric acid cycle and oxidative phosphorylation GLUT 2 trigger the import of glucose into pancreatic beta cells and develop ATP in the cell (SkelinKlemen et al. 2017). Need to understand that the glycolysis lane in the beta cell is actually diverse from ordinary glycolytic pathway in the context of the nature of hexokinase. The hexokinase enzyme is not symbiotic rather it follows Michaelis menten form of enzyme. This enzyme is not monitored by feedback inhibition of Glucose-6-phosphate. Here, the purpose of the Glycolysis process is to increase the number of Adenosine triphosphate (ATP) in the cell. Through the Glycolysis process low amounts of glucose in blood will develop a minimum amount of Adenosine triphosphate (ATP). At the last stage, innermost beta cells, elevated Adenosine triphosphate (ATP) inhibits Adenosine triphosphate (ATP) dependent K+ channels (KATP channels). As a result, it generates membrane depolarisation and decrees K+ efflux stated that depolarisation membranes switch on voltage-dependent calcium channels (SkelinKlemen et al. 2017). The calcium channels trigger insulin exocytosis and discharge insulin in the blood and it boost to control blood glucose levels.
On the other hand, if a low level of glucose enters into a beta cell and it develops a low level of Adenosine triphosphate (ATP), which fails to inhibit KATP channels. As a result, enhancement in the number of potassium and hyperpolarisation in the membrane to prohibit voltage vulnerable calcium channels (Chen et al. 2018). Consequently, it shorten the amount of calcium and decline to construct insulin, which alter the level of glucose in blood.
This section is going to cover pathophysiology of insulin deficiency diabetes.
In the first stage, destruction of the beta cell is identified due to the autoimmune process. During the cell destruction, beta-cell antigen and cellular fragments are released, and macrophages or dendritic cells engulf these. As per the above figure present as an Antigen presenting cell (APC). In pancreas, T-lymphocytes and B-lymphocytes bind with APC and T-lymphocytes activate immense responses on the another side B cells start producing antibodies (Burrack et al. 2017). Interleukin-12 (IL-12) was released from APCs, and it activated the CD4+T cell through the T helper 1 cell. This TH1 cell activates by cell–specific pre cytotoxic T cells through releasing IL-2, and it develops cytotoxic macrophages. In order to cytotoxic beta cells, T helper cells release cytokines. In the next phase, Cytotoxic T cell identified expression of beta cell and MHC class 1 molecule. Above figure, disclose that Cytotoxic T cell is a toxic beta cell through releasing enzymes and performance (Burrack et al. 2017). On other hand, TNFR and FAS apoptosis mediated destruction of pancreatic beta cells (Tomita, 2017). As a result, abnormalities are identified in the immune system because the immune system should not be triggered by outer antigen. Consequently, it destroys pancreatic beta cells and affects insulin production, followed by it developing autoimmune or insulin deficiency diabetes.
Based on symptoms, Type-1 Diabetes (T1D) can classified into two forms such as pre-symptomatic Type-1 Diabetes (T1D) and Symptomatic Type-1 Diabetes (T1D).
By focusing on the above figure, shows that in stage three, symptoms of Type-1 Diabetes (T1D) are identified (Katsarou et al. 2017). On the other hand, (Dheir et al. 2019) declared that frequent evacuation of urine, appetite, raised hunger, and fatigue are common symptoms identified with Type-1 Diabetes (T1D).
By obtaining insulin injection may control the risk arise from Type-1 Diabetes (T1D), which helps to maintain insulin levels in the body, followed by it maintaining blood glucose level (Heinemann et al. 2018). This form of treatment helps to lower the issue created or grown by Type-1 Diabetes (T1D). Insulin injection is one of the significant processes to control Type-1 Diabetes (T1D).
Replacement therapy of Beta cell is one of leading treatments of Type-1 Diabetes (T1D), which allow regulating insulin creation and level of blood glucose (Vantyghem et al. 2019). Beta cell therapy allows an individual to control insulin production, followed by maintaining blood glucose levels. Therefore, it can be stated that beta-cell therapy is one of common methods to control Type-1 Diabetes (T1D).
Conclusion
This study can be certified that Type-1 Diabetes (T1D) is an autoimmune disease, which is refined due to ruin in pancreatic beta cells. This study has determined the popularity and cost of Type-1 Diabetes (T1D). In this branch of study has identified that the prevalence of Type-1 Diabetes (T1D) has gradually raised in the United Kingdom (UK) since 2008. Overview of insulin formulation has been covered in this study. In this section, this study has identified that pancreatic beta cells develop insulin and control blood glucose levels. In next stage, this study has been analysed psychology of Type-1 Diabetes (T1D). In this section, this study has been identified that destruction of beta cells due to autoimmune reasons, apoptosis identified, and it develops Type-1 Diabetes (T1D). In final section, these reports discuss the treatment of Type-1 Diabetes (T1D) to improve health and wellbeing of people. This study has been identified insulin injection and beta cell replacements are a common therapy for controlling Type-1 Diabetes (T1D).
References
Journals
Burrack, A.L., Martinov, T. and Fife, B.T., 2017.T cell-mediated beta cell destruction: autoimmunity and alloimmunity in the context of type 1 diabetes. Frontiers in endocrinology, 8, p.343.
Chen, Z., Wang, J., Sun, W., Archibong, E., Kahkoska, A.R., Zhang, X., Lu, Y., Ligler, F.S., Buse, J.B. and Gu, Z., 2018. Synthetic beta cells for fusion-mediated dynamic insulin secretion. Nature chemical biology, 14(1), pp.86-93.
Dheir, I.M., Abu Mettleq, A.S., Elsharif, A.A., Abu Al-qumboz, M.N. and Abu-Naser, S.S., 2019. Knowledge Based System for Diabetes Diagnosis Using SL5 Object. International Journal of Academic Pedagogical Research (IJAPR).3(4).
DiMeglio, L.A., Evans-Molina, C. and Oram, R.A., 2018.Type 1 diabetes. The Lancet, 391(10138), pp.2449-2462.
Heinemann, L., Freckmann, G., Ehrmann, D., Faber-Heinemann, G., Guerra, S., Waldenmaier, D. and Hermanns, N., 2018. Real-time continuous glucose monitoring in adults with type 1 diabetes and impaired hypoglycaemia awareness or severe hypoglycaemia treated with multiple daily insulin injections (HypoDE): a multicentre, randomised controlled trial. The Lancet, 391(10128), pp.1367-1377.
Katsarou, A., Gudbjörnsdottir, S., Rawshani, A., Dabelea, D., Bonifacio, E., Anderson, B.J., Jacobsen, L.M., Schatz, D.A. and Lernmark, Å., 2017. Type 1 diabetes mellitus. Nature reviews Disease primers, 3(1), pp.1-17.
SkelinKlemen, M., Dolenšek, J., SlakRupnik, M. and Stoer, A., 2017.The triggering pathway to insulin secretion: functional similarities and differences between the human and the mouse β cells and their translational relevance. Islets, 9(6), pp.109-139.
Tomita, T., 2017.Apoptosis of pancreatic β-cells in type 1 diabetes. Bosnian journal of basic medical sciences, 17(3), p.183.
Vantyghem, M.C., de Koning, E.J., Pattou, F. and Rickels, M.R., 2019.Advances in β-cell replacement therapy for the treatment of type 1 diabetes. The Lancet, 394(10205), pp.1274-1285.
Websites
Diabetes.co.uk, 2019.Type 1 diabetes study shows dietary protein is linked with additional insulin need. Available from: [Accessed 26 November 2021].
Diabetes.org.uk, 2018.number of people living with diabetes doubles in twenty years. Available from:https://www.diabetes.org.uk/about_us/news/diabetes-prevalence-statistics /[Accessed 26 November 2021].
Diabetes.org.uk, 2019.diabetes statistics. Available from: https://www.diabetes.org.uk/professionals/position-statements-reports/statistics [Accessed 26 November 2021].
Statista.com, 2018.Number of patients on diabetes register in England from 2008/09 to 2017/18.Available from: https://www.statista.com/statistics/387322/individuals-with-type-1-diabetes-by-age-in-england-and-wales/[Accessed 26 November 2021].
Statista.com, 2020.Distribution of people registered with type 1 diabetes in England in 2019/20, by age*.Available from: https://www.statista.com/statistics/387322/individuals-with-type-1-diabetes-by-age-in-england-and-wales/ [Accessed 26 November 2021].
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