Diet and Exercise in Diabetes Mellitus - Research Paper Example

Research Paper: Diet and Exercise in Diabetes Mellitus Introduction A group of clinical syndromes characterized by hyperglycemia secondary to relative or absolute insulin deficiency is known as diabetes mellitus (DM) ((Edwards, 724) There are basically 2 types of diabetes mellitus and they are type-1 and type-2. In type-1 DM, the onset is in young age like childhood, adolescence or even early adulthood. It occurs due to absolute deficiency of insulin as a result of destruction of the beta-cells in the pancreas. On the other hand, type-2 DM occurs mainly in adults, especially in older people and is mainly predisposed by several factors including sedentary lifestyle and obesity. Hereditary factors play an important role in this type of diabetes, either due to genetic predisposition or due to similar behavioral patterns in the families like sedentary lifestyle and eating habits. DM-2 occurs due to a combination of decreased secretion of beta cells in the pancreas and increased peripheral resistance to insulin at tissue-receptor level (Kumar, p.1190). DM-2 is the most common type of diabetes. It is managed by pharmacotherapy and appropriate diet and exercise. Diet and exercise have a major role to play in the treatment of diabetes-2. In this research paper, the importance of diet and exercise in the management of diabetes will be discussed with reference to suitable literature. Pathophysiology of diabetes An understanding of the role of diet and exercise management therapy in diabetes can be enhanced by knowing the pathophysiology of diabetes type-2. As mentioned before, the main metabolic defects in type-2 are decreased ability of the tissues in the periphery to respond to insulin that is secreted in the body, along with decreased secretion of insulin from the beta cells located in the pancreas. The exact cause of insulin resistance is not yet clear. However, several factors have been incriminated in the development of the disease like inflammatory cytokines, esterified fatty acids, myocardial dysfunction and adipokines (Stumvoll, 1333). The only source of production of insulin in the body is the beta cells of Langerhans situated in the tail of the pancreas. Secretion from these glands decreases due to wear and tear, antibodies against it or due to failure in adaptation to the long term demands of peripheral insulin requirement and resistance (Kumar, p.1196). Failure of adaptation occurs due to lipotoxicity, glucotoxicity and formation of amyloid in the beta cells region. All these account to loss of pulsatile and oscillatory pattern of secretion of insulin by beta cells, thus causing loss of attenuation of the rapid phase of insulin secretion which, actually, is the normal response to elevated glucose levels in the blood. As age advances, the mass of beta cells also decrease along with degeneration of the islet, further contributing to decreased insulin secretion (Kumar, p.1196). Lipotoxicity is yet another cause of gradual decline in the function of beta cells because of inverse correlation between insulin sensitivity and levels of free fatty acids in the fasting plasma. There is immense research that supports a strong association between insulin resistance and obesity. Infact, central and visceral obesity is strongly associated with risk of diabetes-2 (Kumar, 1195). Also, intracellular triglycerides and raised free fatty acid levels in plasma are potent inhibitors of signaling of the insulin. Another important factor in obesity is dysregulation of the secretion of adipokine, which causes resistance of insulin at peripheral tissue level. For hyperglycemia to occur, both, decrease in insulin secretion and insulin resistance must be present. More often than not, insulin resistance develops much before the onset of decreased insulin secretion. Insulin resistance prevents uptake of glucose by various tissues like adipose tissue and muscles (Votey, eMedicine). Fasting insulin levels in those with DM-2 may either be increased or normal. In the initial stages, however, the insulin levels are actually increased (DeFronzo, p.117). Infact, the insulin levels gradually increase with rise in blood glucose levels upto 140mg/dl, following which, secretion of insulin is not sustained and infact, gradually decreases contributing to hyperglycemia. Since uptake of glucose is not possible, there is fall in the intracellular glucose levels and these prompt gluconeogenesis in the liver. Insulin will not be able to suppress the gluconeogenesis and this further contributes to hyperglycemia (Kumar, p.1196). Why is it important to treat diabetes mellitus promptly? Diabetes leads to increased catabolism and decreased anabolism. After reaching the renal threshold level of 180mg per dl, glucosuria occurs. This contributes to polyuria and polydipsia. Decreased levels of glucose in the cells contributes to delay in the healing of the wounds and also development of recurrent infections. it also causes lipolysis for generation of energy. Lipolysis causes an increase in the free fatty acid levels whih are taken up by the liver. Metabolism of free fatty acids in the liver yields ketone bodies, hydroxybutyric acid and acetoacetic acid. As the production of ketone bodies increases, metabolic acidosis ensues, resulting in dehydration. Infact, in many cases, diabetic ketoacidosis is the first presentation and it can turn fata due to development of cerebral edema. Increased lipolysis can contribute to weight loss and gluconeogenesis can cause muscle wasting. While these are the acute problems of diabetes, several long term complications can occur, which are associated with high mortality and morbidity. The 3 main complications of long term diabetes which merit importance are retinopathy, neuropathy and nephropathy. Other than these, diabetes contributes to cadiac morbidity and mortality. It also contributes to atherosclerosis nd increases the risk of stroke and myocardial infarction. Tissues like nerves, kidneys, lenses and blood vessels do not require insulin for transport of blood into their cells. Hence, when hyperglycemia is there, the cells, unlike other cells in the body are loaded with glucose. The glucose in the cells is metabolised to sorbitol and then to fructose by aldose reductase by using NADPH. Gradual decrease in NADPH causes oxidative stress to the cells, resulting in damage to the organs (Kumar, p.1195). In the retina, the raised intracellular glucose causes stimulation of the synthesis of diacyl glycerol, causing protein kinase C which revascularizes retina, causes deposition of the extracellular matrix, increases the production of cytokines which are proinflammatory and contributes to fibrinolysis. All these result in damage to various organs of the body (Kumar, p.1195). Management of diabetes: Role of diet and exercise Complications due to diabetes may be avoided by receiving appropriate medical care from a physician-coordinated team which includes physicians, nurse practitioners, physician’s assistants, nurses, dietitians, pharmacists, and mental health professionals with expertise and a special interest in diabetes (American Diabetes Association). The most important aspect in the management of diabetes is modification of lifestyle factors. This is because, unhealthy lifestyle like excessive eating, indulgence in excessive alcohol consumption, sedentary lifestyle and type-A personality behaviour cause initiation and propagation of type 2 diabetes mellitus. Diabetes self-management education is an integral component of care. Glycemic control This is fundamental to the management of diabetes. Research has shown that improved glycemic control is associated with sustained decreased rates of retinopathy, nephropathy, neuropathy (DCCT/EDIC Research Group, 2000, cited in American Diabetes Association) and cardiavascular complications (American Diabetes Association). The goal should be to achieve glycosylated hemoglobin of Read More