Diabetes Mellitus- Type II - Essay Example

?Diabetes Mellitus- Type II INTRODUCTION: Diabetes Mellitus is a multigenic disease prevalent in a large number of people in the population. Genetic predisposition, environmental factors and a change in the lifestyle of the individual have caused the increased prevalence of diabetes mellitus. One of the deadly complications of diabetes is coronary artery disease which is attributed to imbalance in lifestyle. Diabetes has affected approximately 200 million individuals worldwide and expected to double by 2030 (Bottino & Trucco, 2005). Initial studies among 16917 individuals in Saudi Arabia (1995-2000) showed the prevalence of the disease in 26.2% of males and 21.5% of females (Al-Nozha, Al-Maatouq, Al-Mazrou, Al-Harthi, & Arafah, 2004). Similar study published in 2012 aimed at determining the prevalence of the disease in Arab countries between the years 1980-2009 showed that Bahrain had an increased prevalence of 5.17 percent, countries like Kuwait, UAE and Qatar showed lesser prevalence rate (Majeed, Alhyas, & McKay, 2012). There are two types of diabetes mellitus which are differentiated based on the aetiology and pathogenesis involved in the disease. They are classified as Type I Diabetes Mellitus (Insulin dependent diabetes mellitus or juvenile diabetes) and Type II Diabetes Mellitus (Non-insulin dependent diabetes) (Bottino & Trucco, 2005). It is noted that both have common symptoms and complications but differ in etio-pathogenesis. Type I Diabetes is an autoimmune disease caused due to the selective destruction of the Beta Cells in the pancreas which are responsible for the production of insulin. Type II diabetes is a metabolic disorder which results due to reduced production of insulin and insulin resistance. The commonly seen feature is insulin resistance in diabetes; but hyperglycemia which is also commonly seen in type II diabetes is not seen until there is disturbance in insulin production. Recent studies suggest that some factors that served as distinctive factors in determining the types of diabetes are now seen overlapping in both types. (Bottino & Trucco, 2005). The understanding of the pathogenesis of Type 2 Diabetes begins with the knowledge about the normal glucose homeostasis (DeFronzo, 2004). ROLE OF GLUCOSE AS THE MAJOR FUEL FOR THE BODY: Glucose is the major source of energy stored as glycogen in the human body. A large amount of the glycogen is seen predominantly in the liver and the skeletal muscles, approximately 500g in skeletal muscles and 100g in the liver. However, it is vital that glucose level should be within safety limit in order to stay healthy. When the body is provided with excess amount of glucose in the form of food, it is the function of the body to maintain the normal level needed for the body and also when there is a deficiency. Maintenance of physiological blood glucose concentration is the main function of glycogen present as a molecule in carbohydrates. As mentioned earlier, skeletal muscle and liver are the two main sources for glycogen. Significant amount of glycogen is present in the brain and heart for certain physiological functions. Approximately 80 percent of glycogen is stored in the skeletal muscles. They form a larger amount since skeletal tissues form 40-50 percent of the body weight. Liver is the most important and the only organ that directly helps in the release of glucose into the blood. Liver being a small organ weighing about 1.5 kg contributes to about 100g of glycogen. Skeletal muscle is unable to release glycogen from its storage into the blood due to the absence of Glucose 6 Phosphate. However, it serves as a source of supply of local energy during exercise. The glycogen so released during the exercise also breaks down into lactose and is then transported to the liver to maintain normal gylcemic level. This is called Cori cycle (Jensen, Rustad, Kolnes, & Lai, 2011). The glycogen stored in skeletal muscles is mainly used as energy source during flight or fright situations. Even when there is an increased amount of muscle glycogen, it is seen that there is a decrease in the glycogen levels in the liver during fasting. The body’s mechanism is to maintain normal levels of glycogen when they are reduced in production. Super compensation is a mechanism in which a glycogen depleting exercise can help stimulate the production of glycogen with increased intake of carbohydrates (Jensen, Rustad, Kolnes, & Lai, 2011). GLUCOSE HOMEOSTASIS: Major part of the glucose disposal takes place in the insulin dependent parts. Glucose uptake by the brain which is an insulin dependent takes approximately 50 percent and the insulin level becomes saturated at a concentration of about 40mg/dL. Liver and the gastrointestinal tract that forms the splanchnic area is also insulin dependent and about 25 percent glucose disposal takes place in this area. The remaining 25 percent of disposal is seen in the adipose tissue and skeletal muscles. Predominantly 85 percent of glucose production is by the liver and remaining by the kidney. Homeostatic mechanism in the body helps in maintaining the blood glucose. It is necessary that a normal balance is maintained between the entry of glucose from the liver into the circulation and the uptake of glucose by the tissues, especially the skeletal muscles. Low insulin levels and decreased glucose absorption in between meals stimulate the regulatory hormones like glucagon and epinephrine, thereby stimulating the liver to produce glucose as a result of gluconeogenesis and glycogen breakdown. Here, glucagon also plays a vital role in glucose homeostasis. Insulin is then released from pancreatic beta cells into the circulation as a response to increase in blood glucose. Insulin being a very potent agent in stimulating lipogenesis and inhibiting Lipolysis, causes decreased plasma concentration of free fatty acids (FFA). A change in the concentration of the FFA in response to concentration of insulin and glucose, plays an important role in the glucose homeostasis. PATHOGENESIS OF TYPE II DIABETES Pathogenesis of type II diabetes mellitus is more complex than type I as it is caused due to a combination of impaired beta cell function, action of insulin in liver and skeletal muscles leading to the deficit of insulin (Boon, Cumming, & John, n.d.). This multifaceted disease is present with several disturbances in the normal glucose homeostasis such as insulin resistance, impaired insulin secretion, abnormalities in the splanchnic glucose uptake (DeFronzo, 2004, p. 789). Insulin resistance is presented with hyperinsulinemia due to increased insulin secretion by pancreatic cells. This results in the inability of the Beta cells to function properly to compensate rise in blood glucose which causes hyperglycemia. The insulin resistance eventually results in the excess production of glucose in the liver and decreased usage in skeletal muscles. Furthermore, the beta cell failure results in the inability of the body to produce insulin for the body’s function. Type II diabetes is presented with a considerable amount of destruction of the pancreatic islet tissue in the early stages of the disease. The deposition of amyloid on the pancreatic tissue suggests a theory that the polypeptide amylin is produced due to increased insulin resistance. Further, the need for increased insulin secretion results in the formation of insoluble fibrils into amyloid which destroys the Beta cells. Type II diabetes is presented with 20-30 percent decrease in Beta cells. The level of alpha cells remains the same without any change and the level of glucagon secretion increases. A number of factors predisposing to type II diabetes are genetic factors, environmental factors (over eating, obesity, under activity), age, pregnancy etc. COMPLICATIONS SEEN IN DIABETES MELLITUS: Diabetes is a multifaceted disease with several systemic symptoms. Sometimes these symptoms are helpful in diagnosis of the disorder. Long term complications due to diabetes are sensory loss, retinopathy, foot ulcer, renal diseases etc (Boon, Cumming, & John, n.d.). Micro vascular and macro vascular complications in diabetes mellitus are associated with hyper-glycaemia (Neil, Adler, & Stratton, 2000). Micro-vascular defects include retinopathy, cataract, renal failure, sensory loss, motor weakness, postural hypertension, gastrointestinal complications like altered bowel habits, foot ulceration and arthropathy. Macro-vascular defects are myocardial infarction, stroke, ischemia and claudication (Boon, Cumming, & John, n.d.). OBESITY IN TYPE II DIABETES MELLITUS: Type II diabetes mellitus caused due to obesity among young individuals is a serious concern as it may result in several other systemic complications in later stages. It is seen that the lifestyle of an individual corresponds to the obese nature and a proper change in lifestyle will help in improving the condition. Apart from several other factors; obesity and lack of physical activities such as exercise are seen non-genetic risk factors of the disease. After a few studies that were conducted, it is noticeable that individuals who lacked any physical activity are obese and significant improvement is observed among the individuals who were involved in physical activities like running, jogging, gymnastics swimming, skiing. Another important area of advice for them is the dietary chart which guides in the consumption of fat, sugar, vegetables, salt etc. These dietary changes include decreased consumption of fat, sugar, salt, alcohol and increased consumption of vegetables. These changes in the lifestyle show significant decrease in the prevalence of the disease (Tuomilehto, Lindstrom, Eriksson, Valle, Hamalainen, & Parikka, 2001). The body mass index is a factor in the type 2 diabetes mellitus. Body mass index (BMI) of obese individuals is significantly different from lean individuals. Normal BMI 18-25. While overweight individuals have a BMI of 25-30, obese individuals have a BMI of 30 or more (Weinstein, et al., 2004). Increase in BMI more than 30 signifies that an obese individual is more likely to be affected with diabetes and therefore enough concern needs to be taken with increasing BMI as it is also a factor predisposing to diabetes mellitus. DIAGNOSIS AND TREATMENT OF DIABETES MELLITUS: Number laboratory diagnostic tests are available to determine the increased blood glucose level. Simple colorimetric tests are also used to determine the blood glucose level which depends on food intake of the individual. Recent improvements in diagnosis have helped in accurate determination of the disease. The HbA1c test helps in accurate determination of the glycemic level over a prolonged period. This glycated haemoglobin level is the most preferred lab test. Glucose concentration is directly proportional to the formation of HbA1c; An approximate increase of 2 mmol/l in blood glucose is seen with 1 percent increase in HbA1c (Boon, Cumming, & John, n.d.). Management of Type II diabetes mellitus is based on a proper lifestyle and medicine. Suphonylurea is used in the treatment of non-obese individuals whereas Metformin is the preferred drug for obese individuals. Combined therapy is also found to be helpful in the management of the disease. Other drugs used in the management are Thaizolidinedione, Alpha Glucosidase inhibitor, prandial glucose regulator, long acting insulin analogue etc. The most important factor in reducing the risk of type II diabetes is by changing the lifestyle of the individual based on the dietary changes and improvement of physical activity. Dietary management aims at achieving glycemic control, decreased hyperglycaemia, avoiding hypoglycaemia, weight management, reduced fat intake, improved protein intake and also reduced risk of micro and macro vascular complications. For patients with Type 2 diabetes, it is necessary to avoid excess carbohydrate intake and also to increase protein intake. Weight management can be achieved by increasing the physical activity like involving in sports and exercises like walking, swimming, jogging etc. Reduction in calorie intake along with physical activity helps in maintaining a good lipid profile and reduces the blood pressure. It is now very evident that along with the medicinal therapy, an improved lifestyle in the form of better dietary chart and weight management play a very important role in reducing the risk and complications involved in Type II diabetes mellitus (Boon, Cumming, & John, n.d.). CONCLUSION From the above discussion, it is clear that Type II Diabetes Mellitus is predominantly a life style disorder and it is treatable and not fatal with timely diagnosis and intervention and treatment as also life style changes. Reference List Al-Nozha,, M. M., Al-Maatouq, M. A., Al-Mazrou, Y. Y., Al-Harthi, S. S., & Arafah, M. R. (2004). Diabetes Mellitus in Saudi Arabia. Saudi Medical Journal, 25 (11), pp.1603-1610. Boon , N. A., Cumming, A. D., & John, G. (n.d.). Davidon's principles and practice of medicine (Vol. 20). Elsevier. Bottino, R., & Trucco, M. (2005). Multifaceted therapeutic approaches for a multigenic disease. Diabetic journal, 54 (2), pp.79-84. DeFronzo, R. A. (2004). Pathogenesis of type 2 diabetes mellitus. The Medical Clinics of North America, 88 (4), pp.787–835. Jensen, J., Rustad, P. I., Kolnes, A. J., & Lai, Y. C. (2011, December). The role of skeletal muscle glycogen breakdown for regulation of insulin sensitivty by exercise. Frontiers in physiology, pp.1-11. Majeed, A., Alhyas, L., & McKay, A. (2012). Prevalence of type 2 diabetes in the states of the co-operation council for the Arab states of the Gulf. Plose One, 7, pp.1-8. Neil, A. W., Adler, A. I., & Stratton, I. M. (2000). Association of glycaemia with macrovascular and microvascular complications of diabetes mellitus- type 2. BMJ, 321, pp.405-412. Tuomilehto, J., Lindstrom, J., Eriksson, J. G., Valle, T. T., Hamalainen, H., & Parikka, P. I. (2001). Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. The New England Journal of Medicine, 334, pp.1343-1349. Weinstein, A. R., Sesso, H. D., Lee, M. I., Cook, N. R., Manson, J. E., Buring, J. E., et al. (2004). Relationship of physical activity vs body mass index. Journal of American Medical Association, 292, pp.1188-1194. Read More