The Patient With Diabetes Mellitus

Type II Diabetes, also known as diabetes mellitus, is also called non-insulin-dependent diabetes or aadult onset diabetes. It is a medical disorder that, due to a number of factors codependent with the modern world, is characterized by higher than normal blood glucose levels that play havoc with insulin deficiency and resistance. Insulin resistance means that cells do not respond appropriately when there is free insulin in the blood system. Essentially, they body is reacting to an improper balance of sugars and insulin. Because obesity is often present, research suggests that even thought the mechanisms controling glucose and insulin are unclear, the adopose tissue likely

Everybody knows that obesity is a big factor in developing type-2 diabetes, and that part of coping with this metabolic disorder is lifestyle change. If blood glucose does not go down, then medicines are introduced. Some type-2 diabetics even have to administer insulin in order to keep their blood glucose levels

Type 2 diabetes mellitus (T2D) is the most common form of diabetes (American Diabetes Association, 2012). T2D is so prevalent that it is estimated to be the fifth most common cause of death worldwide (Yates, Jarvis, Troughton, and JaneDavies, 2009, p. 1). T2D manifests when the body is unable to metabolize glucose properly, resulting in elevated blood sugar, debilitating fatigue, and other serious complications such as distal limb amputations, kidney failure, and blindness. The generally accepted causes of T2D include diet, sedentary lifestyle, and obesity.

Treatment of diabetes is important to minimize the harm that is done to the body by diabetes. In addition to exercise and a special diet, type 1 diabetes patients need regular insulin injections to lower the blood sugar levels, while people with type 2 diabetes usually don’t need insulin shots, most of them require insulin tablets in addition to healthy diets and regular exercise and a few don’t even need the insulin tablets. (2, 7)

Insulin resistance is the first physiological change occurring in type two diabetes. In these type two diabetic patients, insulin is unable to move glucose into liver, kidney and muscle cells although insulin is able to attach properly to the cell surface receptors. In order to rectify this, most patients with type two diabetes start secreting normal to very high levels of insulin, which can initially overcome this resistance. After a while, the pancreas cannot keep up with this high insulin production and the cells become resistant to glucose intake. Persistent hyperglycemia or high blood glucose levels are not desirable since this causes damage to the beta cells of the pancreas that produces the insulin hormone. This damage to beta cells further hampers insulin synthesis and patients at this stage are categorized as full-blown diabetic. Such patients consistently show a hyperglycemia state even after hours of fasting ( Hinkle & Cheever,

Diabetes is a problem that is expanding across the nation due to various factors that may be avoided such as bad eating habits, lack of exercise and education. These components can all be reversed, which will result to a diabetic free life. According to Diabetes Research Institute, “the most common form of diabetes is called type 2, or non-insulin dependent diabetes”. People with type 2 are able to produce some of their own insulin, yet often, it’s not enough (Diabetes Research Institute, 2016). Diabetes is the 7th leading cause of death in the United States and effects over 23.6 million people (Healthy People, 2014).

Interventions used in treatment of type 2 diabetes should be those that improve the probability that the patient will have better long term control of diabetes. It is therefore imperative that early diagnosis is given fast priority especially when metabolic abnormalities of diabetes are less severe. Lifestyle interventions are key in containing type 2 diabetes. It is common knowledge that sedentary lifestyle and over nutrition which lead to obesity and overweight increase the risk of type 2 diabetes (Peters & Davidson, 1996). Interventions that reverse or improve these factors have beneficial effects on control of glycemia in established type 2 diabetes.

Considerable advances in the past treatment of type II diabetes include the application of lifestyle intervention and prevention efforts aimed at delaying development of glucose intolerance in order to evade diabetes and the progression of new curricula of glucose in the blood-lowering prescriptions to appendage current treatments (DeFronzo, 2010) (Mazzola, 2012). Presently, the control and maintenance of type II diabetes centres on control of glucose by the decrease of haemoglobin and glucose in the blood (DeFronzo, 2010). Current treatment strategies focus on the progression of therapeutic factors that affect the defects contributing to type II diabetes and thus, provide sustainable glucose control through a delaying of disease development

Type 2 diabetes is a chronic disorder in which the body does not properly respond to insulin well, thus allowing high concentrations of glucose to

This is usually caused by a positive energy balance, and more relevantly a sedentary lifestyle. Increased amounts of visceral fat can be detrimental to the anti-inflammatory phenotype of adipose tissue, which is normally characterised by small adipocytes and the presence of anti-inflammatory immune cells, or adipokines, such as M2-macrophages and CD4-regulatory T-cells (Bishop et al., 2011). These cells release the anti-inflammatory cytokine adiponectin. The presence of visceral fat causes these adipocytes to expand, and then infiltrated by pro-inflammatory adipokines, such as M1-macrophages. This causes the secretion of pro-inflammatory cytokines, such as CRP and TNF (Bishop et al., 2011). These cause a state of low-grade systemic inflammation, which can cause vascular damage and disrupt regular metabolism (Canino et al., 2011)

Fat: Decreased triglyceride synthesis in adipose tissue. Increased triglyceride breakdown in adipose tissue, fatty acid and triglyceride levels in blood, and production of ketone bodies in

Type 2 diabetes results from a multitude of defects: impaired insulin secretion, insulin resistance, and defects in GLP-1 secretion and action. Prior to the onset and throughout the course of the disease, beta cell function and pancreatic mass deteriorate; causes may be lipotoxicity, glucose toxicity, increased age, genetics, insulin resistance, and incretin deficiency. Insulin resistance takes place in the liver, adipose, and skeletal tissues (1), ultimately leading to decreased peripheral uptake and hyperglycemia. In the liver, lack of insulin action results in gluconeogenesis and glycogenolysis, further potentiating the hyperglycemia. In fat cells, decreased GLUT4 leads to excessive release of free fatty acids and adipocytokines (2). Because

Luckily, there are treatments out in the medical industry that can help manage the lack of insulin.  Patients with Type 1 diabetes will be given either insulin injections or oral medications to help control the amount of insulin being produced within the pancreas.  The procedure to helping glucose levels stay balanced is a whole different story for people diagnosed with Type 2 diabetes.  Doctors recommend for these patients to change their diet, start exercising, and take the prescribed pills to keep levels homeostatic (Rosen, 2006) (Congcong, 2012).  With every positive outlook must come with negative effects that can make the situation even worse if not treated

The primary goal of diabetes management is to maintain near-normal plasma glucose levels in order to prevent or reduce complications. The administration of insulin is required for type 1 diabetic patients. The management of type 2 diabetes; however, is based on behavioural changes with lifestyle modifications and pharmacological measures. Diet, exercise, and weight loss ( in the obese) are the cornerstones of

Diabetes Mellitus, more commonly known as type 1 diabetes and type 2 diabetes, is a disease that causes destruction or dysfunction of β cells, which are cells in the pancreas that secrete insulin (1). Having dysfunctional β cells leads to a deficiency in insulin, which in turn limits the uptake of glucose into the cells (2). Currently, diabetes does not have a cure; it is managed by close glucose monitoring and injection of exogenous insulin (1). However, only with these methods, it is difficult to control the blood glucose levels in a range that is considered normal (3). As low blood sugar poses an immediate danger, and continued high blood sugar leads to serious life threatening consequences – such as cardiovascular disease, diabetic