Preventing Diabetes and Obesity - Research Paper Example

?Samantha Wahrsager 7 August Preventing Diabetes and Obesity Introduction Type T1D) and type 2 (T2D) diabetes, which are autoimmune disorders, are most common. Nonetheless, gestational diabetes mellitus (GDM) is increasingly becoming prevalent among pregnant women. Chronic insulin resistance tends to catalyze occurrence of beta-cell dysfunction. Type 1 diabetes destroys pancreatic beta cells, thus compromising generation of insulin. Insulin is a hormone that plays a significant role in metabolism of glucose. Environmental and genetic factors tend to influence the destruction of pancreatic beta cells. T1D results when the immune system destroys beta cells. Pre-emption and treatment of type 1 diabetes is possible, but more research is necessary to gain full understanding and identify accurately the activating factors causing autoimmunity. Type 2 diabetes and gestational diabetes mellitus have similar pathophysiological aspects. This paper discusses the causes of diabetes in relation to environmental and genetic factors. It also discusses the possible treatment for diabetes. Epidemiology of Diabetes Diabetes is increasingly becoming prevalent globally and statistics project that 5.4% of world population will be diabetic by 2025. Prevalence tends to increase with age. Approximately 40% of people receive no diagnosis. T2D is the most common diabetes, as it accounts for approximately 90% of incident rates (IR), whereas T1D accounts for large proportion of the remainder. GDM affects pregnant women of reproductive age commonly obese and overweight (Kaaja & Ronnemaa 195). Approximately 12% of people aged between 40 and 75 are diabetic with about 19% comprising people older than 75. T2D is increasingly becoming prevalent among young people too. Africans, Latinos, South Asians, and First Nations are more vulnerable to diabetes. The rising IR of diabetes implies that there is an increase in yearly rate of heart diseases, two to three times in the coming years (Woo and Yang 2). Etiology of Diabetes The interplay between gene and environment tend to cause type 1 diabetes mellitus (T1D). Empirical evidence has not fully established the root causes of this disorder. According to Ehehalt et al. (2009), diet is an environmental factor that plays significant role in rising incidence rate of T1D with meat consumption partly responsible for rising prevalence of T1D. Research on migration determinants elicits mixed reactions. Migration research investigates and evaluates the rate of T1D disorder before and after migration, so that shift in rate subsequent to immigration signifies predominance of environmental factors. People with high-risk HLA genotypes are more susceptible to T1D. Statistical evidence indicates that people diagnosed with high-risk HLA genotypes for TID have been decreasing recently (Ehehalt et al. 614). Researchers have investigated environmental factors that cause diabetes; they include viruses, climate changes, toxins, fats, soy products, whole milk, wheat gluten, coffee, and tea (Moran, Omen & Pietropaolo 321). On the contrary, the incident rate of a country tends to emphasize the genetic predisposition as a factor (Ehehalt et al. 614). Environmental and genetic factors tend to cause increase in T1D rate among adolescents and children. In fact, children and adolescents tend to undergo similar risk factors for developing T1D symptoms despite residing either in their native countries or abroad. The widespread variability of incident rate (IR) of T1D indicates involvement of genetic factors. Conversely, the rising prevalence rates of T1D among general population indicate that there is involvement of environmental factors (Ehehalt et al. 616). Genetic research links leukocyte antigens, especially class II alleles, to predisposition to Type 1 diabetes. The insulin gene located on chromosome 11p15, and the human leukocyte antigen (HLA) located on chromosome 6p21 play role in familial heredity. The HLA genes confer greater risk to T1D because these genes specifically tend to encode class II alleles, which tend to trigger autoimmune response. Genetic factors play greater role in T1D than environmental factors. Environmental factors tend to contribute to at least 50% discordance rate in homozygotic twins, although tend to play few underlying roles in the development of autoimmunity. Conversely, genetic semblance in dizygotic twins contributes significantly to the understanding vulnerability to diabetes (Morran, Omenn & Pietropaolo 318). Some environmental factors, such as viruses, may catalyze the disorder. Research, however, remains scanty in this area. Immune imbalances tend to trigger autoimmunity, although impede immune regulation. Consequently, this allows the development of autoimmune disorders (Morran, Omenn & Pietropaolo 314). The failure by immune system to perform distinct act of balancing predisposes the system to autoimmunity. A normal functioning immune system is balanced and can trigger or suppress responses of cells to pathogens. Unbalanced immune system tends to promote redundancy in cellular responses, which favors development of T1D. The production of autoantibodies and their gradual permeation into the islets of Langerhans in the pancreas leads to destruction of the islets and beta cells. The infiltration of immune system into lesions of the islet causes insulitis. Macrophages, CD+4, and CD+8 T cells tend to pile up at the islet lesion, which aids destruction of beta cells by the immune system. In this way, T-cells mediate beta-cell obliteration, but are not destructive themselves. Furthermore, these immune cells tend to trigger each other through cytokines and surface receptors. The concentration of these cells in islet lesions permits rapid communication of activation signals, which promote destruction (Morran, Omenn & Pietropaolo 316). Research (Hussein, Ventura, Grima & Felice, 2011) on roles of hereditary bio-makers in evaluating risks for ultimate development of type 2 diabetes mellitus (T2DM) indicate that rising incidences of obesity characterize rising acuteness of existing intolerance to carbohydrates. The ultimate severity of aberrations in carbohydrate metabolism tends to correlate with the status of genetic allele. The clinical features, such as T2DM, lipid profile disorders, and hypertension are manifestations of metabolic signifiers (Hussein et al. 119). Gestational diabetes mellitus (GDM) occur in pregnant women when elevated insulin level compensates insulin resistance at the periphery to sustain glucose homeostasis. Obesity and overweight before pregnancy causes susceptibility to GDM (Kaaja & Ronnemaa 194). Insulin resistance and beta cell anomalies tend to cause T2D. At least 90% of T2D patients have insulin resistance, which case correlates with dysfunction of beta cells (Woo and Yang 3). T2D GDM has close correlation with susceptibility to onset of T2D in pregnant women. GDM and T2D have similar characteristics, such as insulin resistance, impediment of insulin production, and glucose intolerance. They also share similar risk determinant, such as familial inheritance and obesity. A body of evidence suggests that GDM is hereditary, but no research has evaluated GDM heritability. Family history of T2D tends to determine GDM. The interplay between numerous genes and environment tend to cause T2D (Pappa et al. 267). Treatment of Diabetes Treatment involves regulation of glycemic levels, although one can regulate lipids, blood pressure, quit smoking, and other treatment to forestall macrovascular and microvascular ramifications of diabetes. In addition, exercise, weight loss, and diet are crucial aspects of GDM and T2D therapy. Nonetheless, treatment with at least one dose of anti-diabetic oral agents can supplement these (Rhoades & Bell 662). Sulfonylurea agents, such as gliclazide and glimepiride are administered orally and once per day. Insulin sensitizing medication thiazolidinediones (TZDs) includes pioglitazone and rosiglitazone. These medications help to reduce insulin resistance in adipose tissue and muscles as well as reduce output of hepatic glucose (Woo and Yang 3). The peroxisome proliferator-activated protein receptor gamma (PPAR-gamma), an intranuclear receptor in adipose tissue and muscles, provides mechanism of action of TZDs. This is because it plays crucial role in regulating genes that increase insulin sensitivity. One administers rosiglitazone TZDs together with metformin or sulfonylurea during monotherapy. Pioglitazone is used as a signifier in monotherapy only. The TZDs also rosiglitazone tend to lower microalbuminiria. It also improves the patient’s lipid profile, so that HDL cholesterol level increases, and decrease blood pressure. When used in monotherapy, TZDs reduce likelihood of diabetic patient developing hypoglycemia. The patient can, however, conduct alanine aminotransferase level (ALT) diagnosis before monotherapy, and subsequently every 60 days during the first year of the patient’s monotherapy (Woo and Yang 4). One should not begin medication if diagnostic level of ALT is two and a half times greater than normal. Nevertheless, if diagnostic ALT level is greater than normal in the course of therapy, one should discontinue administration of therapy. Metformin is also another medication administered orally and reduces hyperglycemia. Metformin is a more appropriate therapy for patients with obesity. Furthermore, it is a more effective treatment than sulfonylurea because it minimizes weight gain significantly and reduces probability of hypoglycemia. Other oral anti-diabetic agents include nateglinide, repaglinide, and orlistat. Orlistat is suitable for obese patients with T2D disorder, and is used together with multivitamins. T2D patients can receive oral treatment if exercise, oral agents, and diet have been unsuccessful in reducing hypergycemia. A combination of insulin and oral agents is through one injection dosage before sleeping. T2D often use neutral protamine hagedorn (NPH) at bedtime, although presents risks of developing hypoglycemia (Woo and Yang 5). To sum up, T1D and T2D diabetes are becoming increasingly prevalent globally. Diabetes results when immune system. GDM is also becoming increasingly prevalent among pregnant women. GDM and T2D share common characteristics with insulin resistance and beta dysfunction being the most significant causes. Women with GDM have likelihood of developing T2D in the future. Exercise, weight loss, and proper diet are essential in treatment of diabetes. Oral agents may supplement these. In case the patient fails to meet glycemic goals, insulin treatment may become necessary. These medications help to reduce insulin resistance in adipose tissue and muscles as well as reduce output of hepatic glucose. Works Cited Ehehalt, Stefan, et al. "Incidence of Diabetes Mellitus among Children of Italian Migrants Substantiates the Role of Genetic Factors in the Pathogenesis of Type 1 Diabetes." European Journal of Pediatrics 168 (2009): 613-617. Hussein, Abou S, et al. "Genetic Factors in Risk Assessment for the Development of Type 2 Diabetes Mellitus in a Small Case Series." International Journal of Risk & Safety in Medicine 23 (2011): 119-123. Kaaja, Risto and Tapani Ronnemaa. "Gestational Diabetes: Pathogenesis and Consequences to Mother and Offspring." The Review of Diabetic Studies 5.4 (2008): 194-202. Morran, Michael P, Gilbert S Omenn and Massimo Pietropaolo. "Immunology and Genetics of Type 1 Diabetes." Mount Sinai Journal of Medicine 75 (2008): 314-327. Pappa, Kalliopi I, et al. "Gestational Diabetes Mellitus Shares Polymorphisms of Genes Associated with Insulin Resistance and Type 2 Diabetes in the Greek Population." Gynecological Endocrinology 27.4 (2011): 267-272. Rhoades, Rodney and David R Bell. Medical Physiology: Principles for Clinical Medicine. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2012. Woo, Vincent and Kwang Yang. " The Future of Diabetes Management." Clinical Focus. n.d. 8 August 2012. Web. Available from, . Read More