Diabetes mellitus is a metabolic disease characterized by chronic hyperglycemia (WHO, 2006). This chronic hyperglycemia results from problems with insulin secretion and action leading to disturbances in fat, protein and carbohydrate metabolism (WHO, 1999; ADA, 2011). Diabetes is believed to cause 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 disease) (ADA, 2011) . Without effective treatment, it can become very serious with the possibility of death from ketoacidosis or a non-ketotic hyperosmolar state (WHO, 1999). Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay There are two types of diabetes: insulin-dependent diabetes mellitus (IDDM) and insulin-independent diabetes mellitus (IIDM). IDDM affects approximately 20 million people worldwide and is caused by a defect in insulin secretion that leads to a failure of secretion by the β cells of the pancreas (ADA, 2001). IIDM is the most prevalent form of diabetes and accounts for 90% of all diabetes cases worldwide (Gonzalez et al, 2009). Impaired insulin secretion due to pancreatic β-cell dysfunction and impaired insulin action due to insulin resistance can all be considered defects that characterize IIDM (Holt, 2004). Epidemiology. According to the 2012 Chronic Disease Hub, diabetes was the ninth leading cause of death globally, and is expected to become the seventh leading cause of death globally by 2030, according to the World Health Organization (WHO) in 2015. In 2000, it was estimated that 171,000,000 people were living with some type of diabetes and the WHO predicted that by 2030, 366,000,000 people worldwide will be living with this metabolic disorder (WHO, 2015). In Europe; there was a prevalence rate of 8.5% of adults ages 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 the number is expected to rise to 157,000 by 2030. An estimated 10-15% of the population have diabetes and have been diagnosed with type 1 diabetes. which means they are insulin dependent (Diabetes Ireland, 2015). In Ireland, there are 854,165 adults over the age of forty who currently suffer from type 2 diabetes or are at risk of developing it. That's not even the worst part, even more frighteningly 304,382 adults between the ages of 30 and 39 are at risk of developing type 2 diabetes as they are considered overweight and do not reach the recommended guidelines of 150 minutes of physical activity. activities per week. These individuals, in doing so, put themselves at high risk of developing chronic diseases (Diabetes Ireland, 2015). The prevalence of diabetes amplifies every year and represents a growing problem that must be addressed. An important factor behind this is the growing sedentary culture that is spreading in Ireland and around the world. Cost. In 2012, in a paper published by the American Diabetes Association (ADA), diabetes costs were estimated to have risen to $245 billion in 2012, a 41 percent increase from $174 billion in 2007 (ADA , 2013). An internationally accredited study conducted in 1999 examined the costs of type 2 diabetes in Ireland and found that 10% of Ireland's national budget was spent on treating the condition; 49% was spent on hospital admissions for complications and salaries, 42% on the cost of drugs, 8-9% on outpatient care andon visiting non-diabetes specialists for diabetes-related problems) (Diabetes Ireland, 2015). It is not possible to continue spending such a large part of the budget on just one condition, as it seems the costs will only increase when free solutions to address the problem, such as exercise and healthy eating, become available. A portion of the costs should be spent on educating the population about the risks of being overweight or obese, as well as the risk of maintaining low levels of physical activity. Seminars on healthy eating and exercise should be organized in every workplace and every school across the country to curb the sedentary culture we currently live in; with the curbing of this culture, we would see a change in the prevalence of type 2 diabetes. Current exercise guidelines. The current exercise guidelines in place by the ADA call for 30 minutes of moderate to vigorous intensity aerobic exercise to be performed at least 5 days per week, or a total of 150 minutes per week to be performed for work as a management for people with diabetes. “Moderate intensity” can be described as working hard enough that you can complete the exercise but not be able to sing. While “vigorous activity” can be described as exercise where you cannot say more than a few words without needing to take a break (ADA, 2015). The benefits of doing physical activity when you have diabetes are fundamental. Completing aerobic exercise has been shown to improve the body's use of insulin; improves cholesterol levels while also lowering blood glucose levels and blood pressure. It is also recommended to participate in resistance training along with aerobic exercise, to observe an improvement in insulin sensitivity and significantly reduce blood glucose concentrations (ADA, 2015). Pathophysiology of IIDM; Insulin secretion, insulin resistance and subsequent B cell dysfunction can be defined as the characterizing factors of type 2 diabetes mellitus (Olokoba, 2012). These defects usually coexist in an individual and the cause may be based mainly on genetic and environmental factors (Kosma, 2010). Impaired insulin secretion. The release of insulin from pancreatic islet beta cells is in response to alterations in blood glucose concentration (Kosma et al, 2010). GLUT2 transporters help the diffusion of glucose into beta cells (Kosma et al, 2010). In beta cells, adenosine triphosphate (ATP) is created through glucose metabolism. This creation of ATP leads to an increase in the ATP/ADP ratio, which causes the cell to depolarize as it induces the closure of potassium channels. Depolarization of the cell leads to the opening of voltage-gated calcium channels that allow influx of extracellular calcium into pancreatic beta cells. 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 significantly lower and can often be absent in people with type 2 diabetes compared to healthy individuals. This defect in insulin release can be observed in normoglycemic first-degree relatives of type 2 diabetic patients (Henriksen et al, 1994). Insulin resistance According to Kahn, insulin resistance can be considered the main predictive factor of type 2 diabetes. Insulin carries out its biological function by interacting with ainsulin receptor (IR). After binding of insulin to the IR, autophosphorylation occurs which consists of the binding of scaffold proteins such as insulin receptor substrate (IRS) proteins. Following phosphorylation of IRS proteins, they interact with the p85 regulatory subunit of phosphatidylinositol 3-kinase (PI3K) and its activation. The resulting action of PI3K leads to the 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 react properly to circulating concentrations of insulin. To maintain normal blood glucose levels, the pancreas must compensate by secreting increased levels of insulin. However, this amplified level of insulin can only be sustained for a short period of time. After this compensatory period, the development of pre-diabetes and diabetes usually occurs, especially in individuals where beta cell dysfunction is also prominent (Vaag et al, 1992; Kosma et al, 2010). Beta Cell Dysfunction One of the most severe contributors to type 2 diabetes is beta cell dysfunction and is triggered by insulin resistance (Ashcroft et al, 2012). Beta cell dysfunction is more serious than insulin resistance as it impairs insulin secretion while resistance allows secretion but insulin insensitivity develops in the tissues. In order for the body to meet the ever-changing metabolic demand for insulin, normal beta cell integrity is required (Cerf, 2013). Hormones, neural inputs and nutrient availability help to support blood glucose levels through careful management of insulin secretion (Schrimpe-Rutledge et al, 2012). Glucose is of enormous physiological importance when it comes to beta cell function and stimulation of insulin genes, beta cell insulin secretion and proinsulin biosynthesis (Henquin et al, 2006). Although understanding has increased of the significant role that insulin resistance and beta cell dysfunction play in type 2 diabetes, it must be remembered that the metabolic disease process is inherently heterogeneous and other pathogenetic considerations must be taken into account ( McCulloch et al, 2014). ). Diet, obesity and inflammation. Two of the most obvious risk factors associated with a greater prevalence of impaired glucose tolerance (IGT) and type 2 diabetes are increased weight and decreased physical activity (Engelgau et al, 2004; Sullivan et al, 2005 ). Generally, individuals diagnosed with type 2 diabetes tend to be overweight or obese and have excess central visceral adiposity. This consolidates the idea that adipose tissue is involved in the pathophysiology of type 2 diabetes (Olokoba et al, 2012). A major cause of resistance to insulin-mediated glucose uptake is obesity and also leads to beta cells becoming less sensitive to glucose (McCulloch et al, 2014). Fortunately, the solution is simple and economical: active weight loss has been shown to have the ability to largely reverse these effects and return blood glucose concentrations to near-normal levels (McCulloch et al, 2014). Hirosumi believes that the c-Jun amino-terminal kinase (JNK) pathway could be a central facilitator of the relationship between insulin resistance and visceral adiposity, as JNK activity is amplified in cases of high visceral adiposity, aeffect that can inhibit the activity of insulin. 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 pose a serious risk to patients with type 2 diabetes (McCulloch et al, 2014). This high level of hosting free fatty acids can inhibit insulin secretion and insulin-stimulated glucose uptake in individuals with type 2 diabetes. This can lead to metabolic overload of the liver and muscles causing mitochondrial dysfunction together to impaired fatty acid oxidation. This metabolic overload coupled with physical inactivity leads to the collection of lipid-derived intermediates in the mitochondria which further adds to mitochondrial stress and insulin resistance. The development of hepatic insulin resistance and hepatic steatosis is favored by the re-routing of free fatty acids into the endoplasmic reticulum and cytoplasm due to reduced 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 levels of free fatty acids in the blood and is related to improved lipid profiles, has been shown to improve glycemic control and decrease inflammation in patients with diabetes (Mantzaros et al, 2005). It has been shown that adiponectin deficiency is related to the development of insulin resistance and therefore type 2 diabetes (Kadowaki et al, 2006). Leptin has been linked to obese individuals and increased insulin resistance. As adipocyte mass and stored fat increases, the extent of leptin secretion also increases (McCulloch et al, 2014). In a study conducted on mice, an increase in glucose tolerance was observed in the absence of leptin when the mice were fed their regular diet. However, once the mice were introduced to a high-fat diet, they were found to gain weight and experience increased insulin resistance. Through this valuable insight, it can be suggested that leptin might 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 who suffer from type 2 diabetes or are glucose intolerant, there is a correlation between RBP4 and insulin resistance. RBP4 has been shown to decrease in patients who have increased levels of physical activity due to decreased insulin resistance. Effect of Exercise on Type 2 Diabetes. As I already mentioned, 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 physical exercise on blood sugar and insulin levels Physical exercise has been shown to have a positive effect on both blood sugar and insulin levels, thus having a positive effect on individuals suffering from type 2 diabetes. As we already know, in resting conditions, glucose absorption tends to be more reliable than insulin. Glucose transport into the cell cytoplasm is facilitated by the translocation of GLUT-4 into the cell membrane (Suh et al, 2007). With the onset of exercise, if the duration is long enough and the intensity high enough, there is a significant improvement in glucose absorption and utilization. Moreintense the exercise, the greater the effect it has on blood sugar as more carbohydrates will be metabolised to meet the energy needs associated with the increased intensity (Suh et al, 2007). As we know, abnormal amounts of blood glucose concentrations lead to defects in insulin secretion that are the cause of type 2 diabetes. A decrease in blood glucose concentrations helps prevent this impairment of insulin secretion and can be used as a effective for treating and preventing type 2 diabetes. Effect of exercise on carbohydrate and fat oxidation in type 2 diabetes. Carbohydrate oxidation has been shown to improve in individuals with type 2 diabetes with aid of increased exercise, even with impaired glucose absorption through insulin-dependent pathways. This is true as the majority of glucose intake during exercise occurs through insulin-independent pathways (Sigal et al, 2006). Most of the carbohydrate oxidation that occurs during exercise in individuals 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 glycogen in muscle and glycogen in blood. It is believed to depend on the intensity of the exercise and the amount used (Colberg et al, 2010). In a study conducted by Lima, a cycle ergometer was tested and fat oxidation levels were measured. The study showed that fat oxidation was increased in individuals with type 2 diabetes while high-intensity exercises further prolonged this exercise. Fat oxidation was also increased after exercise in subjects with type 2 diabetes compared to those who were not diagnosed. From the above, we can see the positive effects that exercise can have on those suffering from type 2 diabetes. Increased oxidation of carbohydrates and fats has positive effects on the factors that characterize type 2 diabetes such as l obesity and abnormal glycogen levels. Carbohydrate oxidation helps lower glycogen levels through oxidation and also through using it as an energy source. As we know, high blood glucose levels lead to insulin problems that can initiate the onset of type 2 diabetes, so exercise is an effective way to prevent and treat those who are pre-diabetic or diabetic. They are able to do this as 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 physical exercise on blood pressure. Individuals with type 2 diabetes are at high risk of also developing hypertension. However, it has been shown that hypertension can be treated with individual exercises, whether aerobic or resistance, also increasing the likelihood of hypotension. Exercise stimulates the release of nitric oxide which helps lower blood pressure after exercise. The benefits of hypotension after exercise are numerous and highly beneficial, but may depend on the intensity of the exercise performed. An individual with type 2 diabetes appears to respond better to high-intensity exercise, which causes him or her to work above the lactate threshold. Completing exercise at this intensity has been shown to reduce systolic blood pressure much more significantly than exercise at a lower intensity (Lima et al, 2008). The above demonstrates that.