Diabetes mellitus is a metabolic disorder characterized by chronic hyperglycemia (WHO, 2006). This chronic hyperglycemia comes from problems with insulin secretion and action which lead to disturbances in the metabolism of fats, proteins and carbohydrates (WHO, 1999; ADA, 2011). Diabetes can be credited with causing long-term damage, dysfunction and failure of multiple organs: primarily the eyes (retinopathy), nerves (neuropathy), kidneys (nephropathy), heart and blood vessels (metabolic syndrome). and cardiovascular diseases) (ADA, 2011). Without effective treatment, it can become very serious, with a risk of death due to ketoacidosis or a non-ketotic hyperosmolar state (WHO, 1999). Say no to plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”? Get an original essay There are two types of diabetes: insulin-dependent diabetes mellitus (IDDM) and insulin-independent diabetes mellitus (IIDM). Diabetes mellitus affects approximately 20 million people worldwide and is due to a defect in insulin secretion which results in a lack of secretion by cells? of the pancreas (ADA, 2001). IIDM is the most common form of diabetes, accounting for 90% of all diabetes cases worldwide (Gonzalez et al, 2009). An impairment of insulin secretion due to cell dysfunction? of the pancreas and impaired insulin action due to insulin resistance can all be considered characteristic defects of IIDM (Holt, 2004). Epidemiology. According to the Chronic Diseases Unit, in 2012, diabetes was the ninth leading cause of death worldwide and is expected to become the seventh leading cause of death worldwide by 2030 according to the World Health Organization (WHO) in 2015. In 2000, an estimated 171,000,000 people were living with some type of diabetes and the WHO predicted that by 2030, 366,000,000 people worldwide would be living with this metabolic disorder (WHO, 2015). In Europe; there was a prevalence rate of 8.5% among adults aged 20 to 79 living with diabetes (Human Intelligence, 2013). According to the WHO, 86,000 people across Ireland were living with diabetes in 2000, and this figure is expected to rise to 157,000 by 2030. It is estimated that 10-15% of the population have diabetes and are diagnosed with it. type 1 diabetes. which means they are insulin dependent (Diabetes Ireland, 2015). In Ireland, 854,165 adults over the age of forty currently have type 2 diabetes or are at risk of developing it. That's not even the worst part, because what's even scarier is that 304,382 adults between the ages of 30 and 39 are also at risk of developing type 2 diabetes because they are considered overweight and don't meet the recommended guidelines of 150 minutes of physical exercise. activity per week. In doing so, these people put themselves at high risk of developing chronic poor health (Diabetes Ireland, 2015). The prevalence of diabetes is increasing every year and is a growing problem that must be addressed. A major factor driving this is the growing sedentary culture being inculcated in Ireland and around the world. Cost. In 2012, in a document published by the American Diabetes Association (ADA), it was estimated that diabetes costs reached $245 billion in 2012, an increase of 41% from $174 billion in 2007 ( ADA, 2013). An accredited international study in 1999 examined the costs of type 2 diabetes in Ireland and found that 10% of the Irish national budget was spent on treating the disease; 49% were spent on hospitalization forcomplications and salaries, 42% to the cost of medicines, 8-9% to outpatient care and consultation with non-diabetic specialists for diabetes-related problems) (Diabetes Ireland, 2015). It is not feasible to continue to spend such a large part of the budget on one condition, which looks like the costs will only increase when there are free ways to solve the problem, such as exercise and proper diet. healthy. Part of the costs should be devoted to educating the population about the risks of being overweight or obese, as well as the risk of maintaining low levels of physical activity. Workshops on healthy eating and exercise should be held in every workplace and school in the country to curb the sedentary culture we currently live in; with the emergence of this culture, we would see a change in the prevalence of type 2 diabetes. Current exercise guidelines. Current exercise guidelines in effect by the ADA are that 30 minutes of moderate-to-vigorous intensity aerobic exercise should be performed at least 5 days per week, or a total of 150 minutes per week, which should be performed to function as a management strategy for people with diabetes. “Moderate intensity” can be described as working hard enough that you can complete the exercise without being able to sing. Whereas “vigorous activity” can be described as exercise in which you are unable to say more than a few words without needing to take a break (ADA, 2015). The benefits of practicing physical activity when you have diabetes are essential. Performing aerobic exercise has been shown to improve the body's use of insulin; it improves cholesterol levels while lowering blood sugar and blood pressure. It is also advisable to participate in resistance training accompanied by aerobic exercise, in order to see an improvement in their insulin sensitivity and significantly reduce their blood glucose concentration (ADA, 2015). Pathophysiology of DII; Insulin secretion, insulin resistance and subsequent B cell dysfunction can be defined as the factors characterizing type 2 diabetes mellitus (Olokoba, 2012). These defects usually exist together in an individual and the causation can be primarily based on genetic and environmental factors (Kosma, 2010). Impaired insulin secretion. Insulin release from pancreatic islet beta cells is in response to changes in blood glucose concentration (Kosma et al, 2010). GLUT2 transporters facilitate the diffusion of glucose into beta cells (Kosma et al, 2010). In beta cells, adenosine triphosphate (ATP) is created by glucose metabolism. This creation of ATP causes an increase in the ATP/ADP ratio, which leads to depolarization of the cell because it induces the closure of potassium channels. Depolarization of the cell results in the opening of voltage-gated calcium channels that allow the influx of extracellular calcium into the pancreatic beta cell. Insulin exocytosis occurs due to this increase in free cytosolic calcium (Seino et al, 2002). Insulin release occurs biphasically from the beta cells of the pancreas in response to the sharp increase in blood glucose concentration. The first and second phases of insulin release are considerably weaker and may often be absent in people with type 2 diabetes compared to healthy individuals. This insulin release defect can be observed in parentsfirst-degree normoglycemic in type 2 diabetic patients (Henriksen et al, 1994). Insulin Resistance According to Kahn, insulin resistance can be considered the main predictor of type 2 diabetes. Insulin performs its biological function by interacting with an insulin receptor (IR). After insulin binds to the IR, auto-phosphorylation takes place, which consists of the binding of scaffolding proteins such as insulin receptor substrate (IRS) proteins. Following phosphorylation of IRS proteins, they interact with and activate the p85 regulatory subunit of phosphatidylinositol 3-kinase (PI3K). The resulting action of PI3K leads to accommodation of the translocation of GLUT4-containing vesicles to the cell surface (Muoio et al, 2008). Glucose is then transported into the cell via the GLUT4 transporter. Insulin resistance can be characterized as the inability of the liver, adipose tissues, and skeletal muscle cells to respond properly to circulating insulin concentrations. In order to maintain normal levels of blood glucose concentration, the pancreas must compensate by secreting increased levels of insulin. However, this boosted insulin level can only be maintained for a short time. After this compensatory period, the development of prediabetes and diabetes typically occurs, particularly in individuals in whom beta cell dysfunction is also significant (Vaag et al, 1992; Kosma et al, 2010). Beta cell dysfunction One of the most serious contributing factors to type 2 diabetes is beta cell dysfunction, triggered by insulin resistance (Ashcroft et al, 2012). Beta cell dysfunction is more serious than insulin resistance because it impairs insulin secretion while resistance allows secretion but insulin insensitivity develops in the tissues. For the body to meet the ever-changing metabolic demand for insulin, normal beta cell integrity is necessary (Cerf, 2013). Hormones, neuronal inputs and nutrient availability contribute to maintaining blood glucose levels through careful management of insulin secretion (Schrimpe-Rutledge et al, 2012). Glucose is of considerable physiological importance with respect to beta cell function and stimulation of insulin genes, beta cell insulin secretion and proinsulin biosynthesis (Henquin et al, 2006). Although the important role of insulin resistance and beta cell dysfunction in type 2 diabetes is better understood, it must be remembered that the metabolic process of the disease is inherently heterogeneous and that many Other pathogenic considerations must be taken into account (McCulloch et al, 2014). ). Diet, obesity and inflammation. Two of the most visible risk factors associated with increased prevalence of impaired glucose tolerance (IGT) and type 2 diabetes are increased weight gain and decreased physical activity (Engelgau et al, 2004; Sullivan et al, 2004; al, 2005). In general, people diagnosed with type 2 diabetes tend to be overweight or obese and have excessive central visceral adiposity. This reinforces the idea that adipose tissue is involved in the pathophysiology of type 2 diabetes (Olokoba et al, 2012). Obesity is one of the main causes of resistance to insulin-mediated glucose absorption. It also leads beta cells to become less sensitive to glucose (McCulloch et al, 2014). Fortunately, the solution is simple and inexpensive: active weight loss has been shown to have the ability to largely reversethese effects and bring blood sugar levels close to normal (McCulloch et al, 2014). Hirosumi speculates that the c-Jun amino-terminal kinase (JNK) pathway may be a central facilitator of the relationship between insulin resistance and visceral adiposity, because JNK activity is amplified under conditions of High visceral adiposity, an effect that can inhibit insulin activity. In animals, the absence of JNK1 results in reduced adiposity and increased insulin sensitivity (Hirosumi et al., 2002). Obese patients tend to have a high concentration of free fatty acids, which poses a serious risk for patients with type 2 diabetes (McCulloch et al, 2014). This high level of free fatty acids they harbor may inhibit insulin secretion and insulin-stimulated glucose uptake in people with type 2 diabetes. This can lead to metabolic overload of the liver and muscles, leading to mitochondrial dysfunction as well as impaired fatty acid oxidation. This metabolic overload associated with physical inactivity leads to the collection of lipid-derived intermediates in mitochondria, further adding to mitochondrial stress and insulin resistance. The development of hepatic insulin resistance and hepatic steatosis is promoted by the rerouting of free fatty acids to the endoplasmic reticulum and cytoplasm due to impaired fatty acid oxidation (Muoio et al, 2008). This increase in fatty acid level leads to disruption of the insulin signaling cascade, which eliminates insulin activation associated with PI3K activity (Dresner et al, 1999). Adiponectin has been shown to decrease free fatty acid levels in the blood and is linked to improved lipid profiles. It has been shown to improve glycemic control and decrease inflammation in diabetic patients (Mantzaros et al, 2005). It has been shown that adiponectin deficiency is linked to the development of insulin resistance and therefore type 2 diabetes (Kadowaki et al, 2006). Leptin has been linked to obese people and increased insulin resistance. As adipocyte mass and stored fat increase, the magnitude of leptin secretion also increases (McCulloch et al, 2014). In a study done on mice, an increase in glucose tolerance could be observed in the absence of leptin when the mice were fed their usual diet. However, once a high-fat diet was introduced to the mice, they were found to gain weight and increased insulin resistance occurred. With this valuable information, it can be suggested that leptin may play a role in the development of obesity-related type 2 diabetes (McCulloch et al, 2014). Adipocytes also release a protein called retinol binding protein 4 (RBP4). In obese patients with type 2 diabetes or glucose intolerance, there is a correlation between RBP4 and insulin resistance. RBP4 has been shown to decrease in patients who have increased their level of physical activity due to decreased insulin resistance. Effect of Exercise on Type 2 Diabetes. As I mentioned before, over 80% of the diabetic population is considered overweight or obese. Inevitably, a link has been made between type 2 diabetes and obesity, as we can see that there is a strong correlation between the two. Effect of exercise on blood sugar and insulin levels Exercise has been shown to have a positive effect on blood sugar levels and insulin levels, thus having a positive effect on people with type 2 diabetes. As we already know, at rest,Glucose absorption tends to be more reliable with insulin. Glucose transport into the cell cytoplasm is facilitated by the translocation of GLUT-4 to the cell membrane (Suh et al, 2007). With the initiation of exercise, if the duration is long enough and the intensity high enough, there is a significant improvement in glucose absorption and utilization. The more intense the exercise, the greater its effect on blood sugar levels, as an increased amount of carbohydrates will be metabolized to meet the energy needs associated with the increased intensity (Suh et al, 2007). As we know, abnormal amounts of blood glucose concentration lead to defects in insulin secretion which are the cause of type 2 diabetes. Decreased blood glucose concentrations help prevent this impairment. insulin secretion and can be used as an effective method of treatment and prevention of type 2 diabetes. Effect of exercise on carbohydrate and fat oxidation in type 2 diabetes. It has been shown that Carbohydrate oxidation improves in people with type 2 diabetes with increased physical activity, although glucose absorption is impaired through insulin-dependent pathways. This is true since the majority of glucose absorbed during exercise is via insulin-independent pathways (Sigal et al, 2006). Most of the carbohydrate oxidation that occurs during exercise in people with type 2 diabetes is thought to be independent of the actual intensity of the exercise. Carbohydrates are used as a substrate during exercise and are readily available as an energy source in the form of muscle glycogen and blood glycogen. It is considered to depend on the intensity of the exercise and the amount you use (Colberg et al, 2010). In a study conducted by Lima, a cycle ergometer test was performed and fat oxidation levels were measured. The study showed that fat oxidation was increased in people with type 2 diabetes, while high-intensity exercise prolonged this exercise further. Fat oxidation was also increased after exercise in people with type 2 diabetes compared to those who were not diagnosed with type 2 diabetes. From the above we can see the positive effects that exercise can have on people with type 2 diabetes. The increase in the oxidation of carbohydrates and fats has positive effects on the factors that characterize diabetes type 2, such as obesity and abnormal glycogen levels. The oxidation of carbohydrates helps reduce glycogen levels through oxidation and also their use as an energy source. As we know, high blood sugar leads to insulin deficiencies which can trigger the onset of type 2 diabetes. Therefore, exercise is an effective way to prevent and treat people with pre-diabetes or diabetes. They are able to do this because they both help increase insulin sensitivity and reduce body fat, which would reduce adipocytes, which would help prevent the onset of type 2 diabetes and help treat it. Effect of exercise on blood pressure. People with type 2 diabetes are also at high risk of developing hypertension. However, it has been shown that hypertension can be treated with single bouts of exercise, whether aerobic or resistance, while increasing the risk of hypotension. Exercise stimulates the release of nitric oxide, which helps lower blood pressure after exercise. The benefits of hypotension following exercise are..