The Epidemic of Diabetes Mellitus - Essay Example

The world faced the challenge of the epidemic of diabetes mellitus. This disease was known even for ancient doctors, e.g. one of the Egyptian papyruses dated as 1552 BC (Patlak, 2002 ) mentioned the disease manifested with polyuria (excessive secretion of urine). The name of disease is derived from New Latin words "diabetes" (a siphon) and "mellitus" (honey-sweet). The last definition is related to the characteristic manifestation of the disease - patient's urine can have sweat test because of the presence of sugar (glucose). There are more than 20 million people suffering with diabetes mellitus in the United States (Center of Disease Control, 2005). In other words every 14th American has this serious health disorder. Furthermore, 29.8% of affected persons do not know about their disease - they have undiagnosed form (CDC, 2005). There are three main forms of diabetes mellitus (accordingly to International Classification of Diseases, 1994/2003): type I diabetes, type II diabetes and gestational diabetes. All these form has different etiology and only clinical manifestations are similar for them. But what is the distinct and what anatomical structures and physiological processes are responsible for normal regulations of carbohydrate metabolism. It's known that the first key discover in the clarification of diabetes etiology was made when German scientists von Mering and Minkowski proved that the pancreas play important role in preventing symptoms of diabetes. In 1910 British physiologist Sharpey-Schafer supposed the unknown chemical substance is responsible for normalizing blood sugar level. He called this agent as "insulin" (Patlak, 2002). Nevertheless insulin was discovered only in 12 years, thus there were no medicine before Banting and Best isolated insulin from canine and, later, bovine pancreas. They were first who used insulin for treatment of diabetic patients and they were awarded with Nobel prize for this invention (Patlak 2002, Porte et al., 2002). Anyway pancreatic secretion of insulin is one of the most important factors of diabetes developing. If the tissue of pancreas is changed due to congenital disease, toxic injury, inflammation or trauma than the quantity of insulin secreting by the islets of Langerhans (the groups of specialized cells of pancreas) will be decreased. Correspondingly the effects of insulin became weaker. The injection of insulin can treat this condition. This is the principal pathogenetic scheme of type I diabetes (Kahn, 2004). Another model is characteristic for type II diabetes. In this disease the level of insulin secretion is normal but there are the deficit of insulin receptors in the target cells. In other words, this condition is characterized with insulin resistance and there is no dependence on insulin level in the blood (Porte et al., 2002). Let's discuss the mentioned mechanisms in the details. Accordingly to the recent publications (Kahn et al., 2004) the most frequent cause of type 1 diabetes is an autoimmune destruction of -cells in the islets of Langherhans. 90% of type 1 diabetics have islet cell cytoplasmatic antibodies, 80% of them have islet cell surface antibodies. Thus presence of high titres of such antibodies are an important predictor of the risk of type 1 diabetes mellitus development. Other immunological indices also important for understanding pathogenesis and diagnostics of type 1 diabetes, e.g. anti-GAD (glutamic acid decarboxylase) antibodies and anti-insulin antibodies (Ishii et al., 2005 ). The active autoimmune processes result in a deficiency of insulin and occurrence of the clinical manifestations of diabetes mellitus. Nevertheless some cases of type 1 diabetes may not have autoimmune origin (Kahn et al., 2004). Recently conducted researches allowed to determine the role of heredity in the development of type 1 diabetes, particularly by detecting MODY (maturity onset diabetes) mutations responsible for some cases of the disease amongst young patients (Krzentowski, 2005; Arky, 2005). Type 2 diabetes has more complicate etiology. It is characterized with a strong correlation with genetic factor and obesity (Tirosh, 2005 ). Furthermore the lab studies (Gunton et al., 2005) demonstrated that the same genes could be responsible for type 2 diabetes as well as for obesity. The distinct of type 2 diabetes is the circumstance of existing detectable levels of circulating insulin. Nevertheless there are several variants of type 2 (or non-insulin dependent) diabetes mellitus classified dependently on the results of oral glucose tolerance test (Kahn et al., 2004). The risk of the second type of diabetes mellitus has significant genetic constituent. Thus genes determining the biosynthesis of such enzymes like pancreatic glucokinase (MODY 2), glucose transport protein (GLUT-2), glucagon-like protein-1 (GLIP-1) etc. The important role in the pathophysiology of type 2 diabetes is played by the superficial cellular receptors to insulin. To forestall the question of the therapeutic approaches in the management of diabetes there is expediently to make casual mention of the perspectives for further developing medicines increasing the sensitivity of somatic sells to insulin. This result could be achieved by blocking peroxisome proliferator-activated and retionoid X receptors (Kahn et al., 2004). The detailed explanation of the mechanisms of new drug action is outside the scope of this short review; nevertheless, it demonstrates the importance of understanding morphostructural (i.e. anatomical) and functional (i.e. physiological) peculiarities of the various health disorders. Because of insulin deficiency (type 1 diabetes) or insulin resistance (type 2 diabetes) the level of blood sugar (glycemia) is elevated. This circumstance could be related to the occurrence of polyuria (excessive secretion of urine) and polydipsia (excessive thirst and fluid intake). Because the level of metabolic disruptions is more expressed amongst type 1 diabetics the course of disease is more progredient, i.e. type 2 diabetes has slower onset and could be even unrecognized because of mild symptoms. In severe cases of disease the occurrence of emergency condition (e.g. diabetic coma) is possible, nevertheless the most of diabetic patients died due to the remoted complication (e.g. stroke, renal failure, severe infections, etc). The main criteria for diagnostics of diabetes mellitus are presented by the positive results of the tests for hyperglycemia (high level of blood sugar) or glucosuria (presence of glucose in urine) and the results of glucose tolerance test (WHO, 1999). Generally, the list of methods recommended for screening could be following: random glucose level, fasting glucose and insulin level, glucose level after sugar load, glucose tolerance test (Porte et al., 2002; Kahn et al., 2004). If patient has recurrent (changeable) or persistent (constant) hyperglycemia and any one of the symptoms of compromised glucose metabolism (e.g. high level (>7.0 mmol/l) of fasting plasma glucose or high (>11.1 mmol/l) plasma glucose level after glucose load or random plasma glucose level exceeding 11.1 mmol/l) than the diagnosis of diabetes mellitus is credited. If patient does not receive proper treatment his life quality is worsening and the risk of dangerous complications is increased. Decompensated diabetes can lead to diabetic ketoacidosis and hyperosmolar diabetic coma (Porte et al., 2002; Kahn et al., 2004). On the other hand overdose of insulin or oral hypoglycemic medicines leads to hypoglycemia, which could be very dangerous for patient life. But the major risks of diabetes are presented by long-term complications related to the systemic changes in the internal bodies. There are two groups of health conditions classified by the prevalence of macroscopic (macroangiopathy) and microscopic changes of the vessels (microangiopathy). Microangiopathy-related complications include retinopathy (disease of retina), peripheral neuropathy and diabetic nephropathy, while macroangiopathy is related to such diseases like ischaemic heart disease, stroke and peripheral vascular insufficiency. The modern therapeutic approaches correspond to the key features of pathophysiology of diabetes mellitus. The management of patients include lifestyle changes and, be necessity, administrtaion of antihyperglycemic (i.e. lowering blood sugar) medications. These medications are presented by insulin therapy for type 1 diabetes (Krzentowski, 2005) and oral medications for type 2 diabetes (Kahn, 2004). The oral medications can influence on the absorption of simple carbohydrates in the intestine, inducing the pancreatic release of endogenous insulin, enhancing insulin-stimulated glucose uptake by the skeletal muscle, inhibition of glucagon (insulin antagonist) secretion and sensitising cells to insulin impact. The biological approaches are developing currently - these promising methods are based on replacing the failed pancreas with more islet cells (Levisetti & Polonski, 2005). The last progress in gene engineering and stem cells technologies could be a solution of diabetes mellitus problem. Unfortunately, this disease is not curable today, but the rapid development of biology and medicine allows diabetic patients to keep their life quality on the highest possible level. References: 1. 5Arky RA. "Doctor, is my sugar normal". N Engl J Med. 353(14):1511-1513 2005 Oct 6; 2. CDC (2005) Diabetes Data Sheet Available at the web-site5 http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2005.pdf accessed on 12/07/2005 3. 5Department of Noncommunicable Disease Surveillance. Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications. Geneva: WHO, 1999 (Also available at http://whqlibdoc.who.int/hq/1999/WHO_NCD_NCS_99.2.pdf) Acessed on 12/06/2005 4. 5Gunton JE et al. Loss of ARNT/HIF1beta mediates altered gene expression and pancreatic-islet dysfunction in human type 2 diabetes. Cell. 122(3):337-349. 2005 Aug 12 5. 5Ishii M et al. Clinical and genetic characteristics of diabetic patients with high-titer (>10,000 U/ml) of antibodies to glutamic acid decarboxylase. Immunol Lett. 99(2):180-185 2005 Jul 15; 6. 5Kahn et al. Joslin's Diabetes Mellitus Lippincott Williams & Wilkins; 14th edition 2004 1224 pp. 7. 5Krzentowski G. [The new insulins] Rev Med Brux. 26(4):S241-245 2005 Sep; 8. 5Levisetti MG, Polonsky KS. Diabetic pancreatic beta cells ARNT all they should be. Cell Metab. 2(2):78-80. 2005 Aug; 9. Patlak M. New weapons to combat an ancient disease: treating diabetes. 5FASEB J. 16(14): 1853. 2002 Dec 10. 5Porte et al. Ellenberg and Rifkin's Diabetes Mellitus McGraw-Hill Professional; 6 edition 2002 1047 p. 11. 5Tirosh A et al. Normal fasting plasma glucose levels and type 2 diabetes in young men. N Engl J Med. 353(14):1454-1462. 2005 Oct 6; 12. WHO 5 (1994/2003) ICD X Available at http://www3.who.int/icd/vol1htm2003/fr-icd.htm accessed on 12/07/2005 Read More