Eat Healthy to Prevent Type II Diabetes: Diet's Role in Diabetes Prevention - Research Paper

Introduction

Type II diabetes mellitus is one of the common heterogeneous diseases that has increasingly threatened the lives of many patients across the world. The benefits of observing a healthy diet are far more essential that daily training exercise, which helps maintain a healthy eating diet. However, despite the collective knowledge and increased awareness of the benefits of healthy eating, diabetes is still finding its way in the health of many Americans today (Shomali, 2012). Diabetes' threat has reduced since the invention of insulin in the 1920s, increasing the life span of the patients. Before the invention of insulin, the patient who has diabetes was left with only a few years to leave before dying, making diabetes one of the globe's threatening diseases. However, the risk has not reduced even with the invention of insulin to help mitigate the situation. As a result, diabetes is still a threat to the modern world, with greater emphasis and research being conducted across the world to help curb diabetes. Thus the essay will critically elucidate the pathophysiologic process of type II diabetes mellitus and underlying pathophysiological processes.

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According to Shomali, (2012), more than 150 million people have diabetes, with the number likely to double in the next twenty years, with type II diabetes mellitus being common in North America. The result of the increasing number of patients may be attributed to poor eating habits and a lack of observing healthy eating within our society. On the contrary, nearly 65% of our community is suffering from type II diabetes mellitus (T2DM). As Reinehr (2013) observes, the native Americans, Asian Americans, and Hispanic Americans are the most affected individuals in the United States (Fox et al., 2015). The pathophysiology of (T2DM) is highly characterized by an array of different characteristics such as impaired regulation in the production of hepatic glucose, peripheral insulin resistance, declining functionality on the v- cell, which later ushers the failure of v -cell.

Underlying Pathophysiological Process

The associated pathophysiology of T2DM varies distinctively with the functionality of the tissues and the different organs within the body. As Lin and Sun (2010) observe, skeletal muscles account for more than 75% of the entire body insulin intake, which stimulates glucose uptake. As a result, any possible defect in this tissue may result in the alteration of the patient's homeostasis process in the body, especially to patients with T2DM. Patients suffering from type II diabetes mellitus are faced with impaired insulin-stimulated tyrosine in their skeletal muscles. However, this does not subsequently alter the decrease in protein expression of IRS1.

The v-Cell dysfunction is profoundly characterized by a series of impairment, which is common in the first phase of insulin secretion that triggers glucose stimulation. On the contrary, the process may also trigger the stimulation of glucose intolerance in T2DM. The trans membranous transport of glucose defines the insulin response in the patient. However, the glucose sensor plays a vital role by inducing glucokinase to act as a stabilizing agent to the damaged degrading and protein.

The control of insulin secretion in patients with Type II diabetes mellitus tends to shift from glucokinase to the Glucose transport system, as the low level of glucose transport in v-Cell is experienced, hence secretion of glucose levels are mitigated in this process. The v-Cell is also prone to other defects, especially in type II diabetes mellitus condition, which includes defects like a reduced response to non-glucose insulin secretion. On the contrary, v-Cell experiences a decrease in its optimum conversion of insulin from proinsulin.

According to Schulz, et al., (2005), patients with prior gestational diabetes mellitus may perceive the presence of an impairment in their first phase of insulin secretion, which may be used to serve as a mark for T2DM. On the contrary, automated destruction may occur on pancreatic v-Cell, which may be a common factor in a minute subset of T2DM patients. However, the group possessing these traits may represent only a small fraction of the entire population, making their condition less significant to the compact population of the patients.

The Liver

According to Lin and Sun, (2010), the liver is the primary organ in the body that has the consume, produce and store lips and glucose. The formation of hepatic glucose in the body requires a metabolic reaction for the creation of glycogen. On the contrary, the generation of glucose to produce energy is supplied via glycolysis. The process of lipids metabolism in the body requires the synthesis of fatty acid through oxidation and bile acid. Never the less, the metabolic pathways are well coordinated to help regulate lipids and glucose under physiological conditions. Never the less, the liver remains a crucial target for the anabolic hormone insulin and glucagon (Lin, & Sun, 2010). The increased blood glucose concentration, triggers the release of insulin from pancreatic v-Cell, to help reduce the glucose concertation in the body, a step that is amplified under FFAs. However, impaired insulin sensitivity and lack of a proper regulation mechanism in the liver paves a path for the pathogenesis of type II diabetes mellitus.

During fasting, the glucose level in the body is highly regulated by the pancreatic a-cells, which releases glucagon, as a way of decreasing the blood glucose level. Members of the pancreatic a-cells perform a vital role by acting in a manner of slowing the absorption of carbohydrates, which results in minimizing any potential of rising blood glucose. On the contrary, this form of therapy may play a critical role in reducing body weight, which is a common trait to patients with type II diabetes mellitus. In this case, the glucose concentration in the blood is curbed. According to Lin and Sun (2010), glucagon significantly affects adipose tissue and the liver. The mobilization of fatty acids and the breakdown of glycogen is induced in this stage. The essence of mobilizing fatty acids in this process helps promote gluconeogenesis, a process involved in the formation of glucose from the lactate.

Presenting Signs and Symptoms

Patients diagnosed with T2DM experience an array of distinctive signs and symptoms that affects their health and lifestyle. According to Fox et al. (2015), most of the patients can experience weight loss, an early indication of type II diabetes mellitus. However, most of the signs and symptoms of T2DM may be subtle. Patients with T2DM experience a higher rate of thirst and a sense of feeling hungry than usual, a concept that many patients fail to understand.

The higher concentration of sugar (glucose) in the blood is a clear indication that kidneys have to work extra hard to help balance the fluids in the body. In this case, the fluids in the body are pulled by the kidneys to help return the blood sugar level into optimum. As a result, the body responds by triggering a counter mechanism to request for more fluids, which results in frequent thirst of the patient. Diabetes insulates glucose from reaching every cell of the body, a step that may force the body to request for more glucose to help support the optimum functioning of the cells. In this case, patients may feel hungry even after shorter moments after having their meals.

According to Reinehr, (2013), over 7.3 million out of the 30.7 million Americans with diabetes, leave with undiagnosed diabetes, a concept that is fatal and threatening to their life span. On the contrary, there are numerous cases of patients with prediabetes, a condition where the patient's blood sugar is higher than the normal but not higher enough to be classified as diabetes.

The dangers of undiagnosed diabetes are by far worse if the condition is not diagnosed to help control the sugar levels. T2DM can cause severe damages to the heart and other blood vessels, gastrointestinal tract, kidney, gums, teeth, and eyes. On the contrary, there is an increase in the risk of higher increased cardiovascular-related diseases such as coronary artery disease.

Patients with type II diabetes mellitus experience slow healing of sores, blurred vision, which makes it cumbersome for the patient to see at night. Additionally, patients with T2DM, experience higher levels of fatigue, and frequent urination, that result in higher levels of non-concentrated urine. Due to lack of using the provided glucose b the cell, it is typical for the body of the patient to feel fatigued because there are little metabolic reactions at the cells to transform the glucose into energy, which will support the entire body functioning.

Diagnostic Abnormalities

Type II diabetes mellitus is diagnosed by glycated hemoglobin (A1C) test, which aims at indicating the patient's blood sugar levels for the past two or three months. The essence of considering a higher range, such as three months, is to establish the actual patterns of blood sugar levels in the body. Normal blood sugar levels should be less than 5.7% (Reinehr, 2013). However, abnormalities are detected at the range between 5.7 and 6.4 percent, a condition that may be considered as prediabetes. On the contrary, any possible scores of 6.5 % within two distinctive tests indicate the presence of diabetes.

Current Research

With the increasing levels of type II diabetes mellitus, there is a need for increased research to help protect the dramatic prevalence of the disease. The development and advancement in treatment, which includes extensive investigations, will play a critical role in curbing the growth of the condition. Research on the efforts towards finding a suitable solution is currently being conducted under three distinctive fields which include pharmacological, biological, and technological.

The focus of technological research is geared towards finding a positive solution that will help in the medical breakthrough to help deliver glucagon via an artificial pancreas. Even though the components of this technology are already in use, the perfection through research is still needed, a step that may see this technology available for clinical use in the next ten years (Shomali, 2012).

The increased number of T2DM cases are pushing the boundaries of research in the field. The advances in therapy concepts of type II diabetes mellitus are pushing for research in type I diabetes mellitus since they are both significant disorders of glucose management. As Shomali, (2012) observes, both T1DM and T2DM, are highly characterized by the higher abnormalities in the rise of glucose in the bloodstream. The advancement in technology had seen a breakthrough in differentiating the different types of Diabetes, when insulin-sensitive and insensitive were finally differentiated, giving the background cause of the epidemic.

Through the differentiation between sensitive and insensitive insulin, the pathophysiological backgrounds of the two diseases have been widely researched, making T1DM a relatively understood epidemic. In this case, the patient's immune system is responsible for attacking the beta cells in the islets, which are destroyed, triggering a shift in insulin. However, the fact behind the aggressive response of the immune and their behavior on the beta cells is still unknown, despite being linked with several factors such as the environmental factors and genetic composition of the patient.

Despite the extensive technological research, the pathophysiology of type II diabetes Mellitus remains ununderstood since there is a higher degree of camouflaging results such as the presence of insulin resistance during the patient's diagnosis. In this case, the body fails to use the produced insulin effectively, yet the pancreas is producing enough...