Cause of Type I Diabetes at the Cellular and Chemical Level - Research Paper Example

? Human Anatomy Type I Diabetes In an organism, rates of various metabolic processes depend on biological needs of the organism. The brain ensures that all processes occur at optimum conditions. A condition in which all body organs correctly functions is called homeostasis (Bronsen 6). Homeostatic balance is controlled by hormones and enzymes respectively. Any variation in the level of these chemicals leads to homeostatic imbalance. Diabetes mellitus type 1 is an example of a condition which results from an altered level of insulin in the body. Insulin is a hormone which regulates concentration of glucose in the blood. Destruction of insulin leads to Type I Diabetes. This paper explores type1 diabetes under various subheadings. Cause of Type I Diabetes at the Cellular and Chemical Level Type I Diabetes is caused by increase in glucose level in the blood. High glucose concentration results from decreased level of insulin in the blood. As mentioned by Kasper et al (p. 12) insulin reduces blood and urine sugar level. Insulin and glucagon are two hormones whose actions counter-effect one another in maintaining the right blood glucose level. Insulin suppresses glucose level when it is high, whereas glucagon raises glucose level when it is low. The two hormones are produced in the pancreatic cells. Beta cells in the pancreas secret insulin while pancreatic alpha cells secret glucagon. Secretion of insulin directly depends on glucose level in the blood and urine. That is when blood glucose level falls, insulin secretion also reduces and vice versa. Kasper et al (p. 13) argues that concentration of insulin decreases when the beta cells are destroyed. Destruction of beta cells results from autoimmune response of the body. Because of destroyed beta cells, secretion of glucose becomes abnormal and consequently, blood glucose level shoots up. Daneman (p. 847) explains that autoimmune action on beta cells triggers expansion of CD8+ T helper cells and autoreactive CD4+ cells. Also, innate immune system and autoantibody secreting B cells are activated in effect. It is the action of these activated chemicals that destroy the pancreatic beta cells. Several risk factors expose an individual to developing type I diabetes. The factors can be grouped as exposure to a driving antigen, a diabetogenic trigger, and a combination of genetic vulnerability. Genetically, type I diabetes is considered as a polygenic disease. Depending on a combination of loci in these genes, its presence can be recessive or dominant. The strongest gene, according to Kasper et al (p. 44), is the IDDM1, which is located on chromosome 6 of MHC Class II class at the straining region 6p21. There is, therefore, a chance of a child suffering from type I diabetes if one or both parents are diagnosed with type I diabetes. Aanstoot et al (pp. 12 & 13) gives an approximate statistics about chances of inheriting the diabetes. The probability of a child developing diabetes mellitus type I if a father has it is 0.1 and 0.04 if a mother has it (Aanstoot et al. 13). Knip et al (p. S127) argues that a virally triggered autoimmune response is another cause of type I diabetes. Introduction of virus into the body activates immune system, which attacks virus infected cells. The attack can extend to pancreatic beta cells resulting to suppression of insulin levels in the blood. Destruction of pancreatic beta cells of the Islet of the Langerhans decreases endogenous insulin production. Diet is another risk factor associated with type I diabetes (Knip et al. S129). Different people are allergic to different foodstuffs or food additives. An individual may be allergic to foodstuff(s) without his/her knowledge. Continual consumption of such foodstuff(s) results to inflammation, which is a characteristic of autoimmune disease. Apart from internally induced autoimmune response, Knip et al (p. S131) claim that certain chemicals and drugs destroy pancreatic cells. Drugs such as pyrinuron, a rotenticide, selectively destroy pancreatic cells when ingested. Streptozoticin is both an antineoplastic agent and an antibiotic used in pancreatic cancer chemotherapy. The drug kills pancreatic beta cells leading to low or zero production of insulin. Various factors, therefore, result to autoimmune response towards pancreatic cells. Hypotheses for Possible Triggers of Autoimmune Diseases Autoimmune diseases are imbalances or dysregulations in immune system of the body resulting to attack by the system on body’s own cells (Rose and Bona 426). That is, autoimmune diseases are conditions that follow an attack by immune system on body’s healthy tissues. Parham (p. 344), however, claims that a clear and specific trigger of autoimmune diseases is not known. Researchers, in effect, have developed hypotheses that attempt to explain or test specific triggers of autoimmune diseases. A unanimously accepted hypothesis is that autoimmune diseases are caused by a blend of genetic and environmental factors (Rose and Bona 429). Genetically, there is a chance of a child inheriting type I diabetes from a parent. The situation is possible if the child inherit, from a parent, a gene with a type I diabetes strain. Environmentally, factors such as agricultural chemicals and foodstuffs interfere with normal functioning of immune system in the body. Heavy metals such as lead, aluminum, mercury and chemicals like formaldehyde are other environmental factors that directly damage beta cells. Moreover, continual use of substance an individual is allergic to triggers autoimmune attack. Symptoms and Other Complications of Type I Diabetes Type I diabetes is characterized by three common symptoms, which are polyuria, polydipsia, and polyphagia (Daneman 849). Polyuria is a condition in which a type I diabetic patient experiences frequent urination. Frequent urination is a mechanism used by body to eliminate excess glucose level in the blood and in urine. Polydipsia is a condition in which a type I diabetes patient experiences increased thirst. As explained by Daneman (p. 849), because large volume of water is lost through urination, large amount of water should also be taken in. Polyphagia is, on the other hand, a condition in which an individual feels hungry more often. Other signs include weight loss and fatigue. Physiologic Explanation of the Symptoms and Complications Polyuria describes a condition where abnormal or excessive amount of urine is produced or passed out. In relation to diabetes mellitus type I, destruction of pancreatic beta cells leads to increase of blood glucose level than in the surrounding cells. Difference in glucose concentration in the blood and in the surrounding cells creates concentration gradient. Water molecules, consequently, move from regions of low glucose concentration to the blood, where glucose concentration is high. The body, in effect, uses urination to excrete excess water that has been drawn into the blood. Polydipsia immediately follows polyuria. Because of concentration gradient, which results to passage of large amount of water, an individual’s body will generally lose water. Since water is an essential substance for the normal functioning of body, an individual will, in effect, have a strong urge to drink water. Both polyuria and polydipsia require energy and therefore, digestion process will increase so that enough energy is provided. Consequently, an individual will feel hungry, a condition called polyphagia. Various processes depend on homeostatic balance. Quantitative growth is a vital process that strongly depends on ionic balance in the body. Therefore, any alteration of ionic concentration in blood interferes with weight gain of a person. Thus, autoimmune response towards pancreatic beta cells results to weight loss. Other common signs include abnormal blood pressure, blurred vision, and numbness. All these symptoms cause fatigue in a person. High blood glucose level is associated with other complications apart from type I diabetes. One complication is in the cardiovascular system. Excess blood glucose molecules attach themselves in the small, oxygen-delivering vessels resulting to a pathological change. The change causes severe effect on vital organs such as the heart and kidneys. In vision, high blood glucose level results to diabetic retinopathy, a loss in visual acuity. In the nervous system, type I diabetes results to peripheral neuropathy, which is a loss in feeling especially in the feet. A driver who suffers from type I diabetes is likely to cause accidents because of inability to read road signs and to regulate speed of a car by applying appropriate brake pressure. Hypoglycemia also results from elevated blood glucose level. The condition affects a person’s coordination, state of consciousness, and thinking process leading to a condition called neuroglycopenia. Disease Statistics Statistics from American Diabetes Association (ADA) confirms that type I diabetes varies with age and sex. While cross tabulating age and type I diabetes, the association had three age categories: less than 21 years old, 21-65 years, and above 65 years. The corresponding statistics were as follows; about 0.26% of the total population had diabetes, 11.3% of people in the middle age group had diabetes, while 26.9% in the third group had diabetes. From the statistics, it is evident that occurrence of type I diabetes increases with age. In sex, data released by ADA in 2011 showed that there is no significant difference in the occurrence of type I diabetes in men and women. The data showed that 11.8% of all men and 10.8% of all women aged above 20 had diabetes. Disease Management, Treatment and Possible Cure Even though exact cure of type I diabetes is not there, the disease can be prevented before destruction of beta cells begins. Immunosuppressive drugs and appropriate diet can effectively prevent destruction of the cells. According to Daneman (p. 855), cyclosporine A is a drug that stops destruction of beta cells. Anti-CD3 antibodies preserve regulatory T cells, which repress activate autoimmune response and create tolerance to self-antigens. Daneman (p. 856), nevertheless, warns that continual use of certain drugs has negative effect. Breastfeeding is an aspect of diet that lowers risks of a child suffering from type I diabetes at old ages. An individual should also take note on the amount of chemicals or types of foodstuffs he/she consumes. Three methods are used to manage type I diabetes; insulin therapy, pancreas transplantation, and islet cell transplantation (Daneman 857). Insulin replacement therapy involves increasing insulin levels either through insulin pump or via subcutaneous injection. Good dietary management is strongly recommended while undergoing insulin therapy. Pancreas transplantation involves replacing a destroyed pancreas with a new one. The procedure is, however, considered to be dangerous. That is, the accompanying immunosuppressants used in the surgery are unsafe. The transplantation is, therefore, done together with or some duration after kidney transplantation since almost similar drugs is used in the two surgeries. Islet cell transplantation involves replacement of destroyed beta cells. The replacement is done from stem cells or by transplant. A patient must, however, take some immunosuppressants to reduce autoimmune response. Conclusion In sum, type I diabetes is caused by high glucose concentration in the blood. High glucose concentration follows suppression in the level of insulin in the blood. Low insulin level results from destroyed pancreatic beta cells. The destruction is an autoimmune attack on healthy beta cells. Both environmental factors and genetic characteristics of an individual contribute to this autoimmune response. Common symptoms of the disease include polyuria, polydipsia, and polyphagia. Type I diabetes also results to complications, especially in the brain, kidney, heart, and eyes. Insulin therapy and transplantation of pancreas and islet cells are effective ways of managing the disease. Prevention can, however, be done before destruction of pancreatic cells begin. Works Cited Aanstoot, H. et al. The Global Burden of Youth Diabetes: Perspectives and Potential. Pediatric Diabetes 8.8 (2007): 1–44. American Diabetes Association (ADA). Diabetes Statistics: Data from the 2011 National Diabetes Fact Sheet (Released Jan. 26, 2011). Accessed April 23, 2012 from http://www.diabetes.org/diabetes-basics/diabetes-statistics/ Bronsen, H. Mental Health, Stress Forms and Emotional Reactions: Index of New Information with Authors, Research Categories and References. ABBE publishers association of Washington, 1996. Daneman, D. Type 1 Diabetes. Lancet 367.9513 (2006): 847–58. Kasper, Dennis L et al. Harrison's Principles of Internal Medicine. 16th Edition. New York: McGraw-Hill, 2005. Knip, M. et al. Environmental Triggers and Determinants of Type 1 Diabetes. Diabetes 54 (2005): S125–S136. Parham, Peter. The Immune System. New York: Garland Science, 2005. Rose, N. and Bona, C. Defining Criteria for Autoimmune Diseases: Witebsky's postulates revisited. Immunol Today 14.9 (1993): 426–30. 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