Diabetes entails a collection of metabolic disorders which are usually characterized by prolonged high sugar levels in an individual’s blood. For instance, both type 1 diabetes (T1D) and type 2 diabetes (T2D) are characterized with hyperglycemia. This condition is referred as hyperglycemia, and it has been found to cause debilitating health consequences. Van Belle, Coppieters and von Herrath (2011) report reaffirm that chronic hyperglycemic conditions may lead to health complications including heart disease, blindness, kidney failure, stroke, and ketoacidosis. Ordinarily, T2D occurs due to insulin resistance in which adipose or muscle cells exhibit low response to insulin. This phenomenon is associated to old age or obesity. In contrast, T1D is caused by autoimmune destruction of pancreatic beta-cells which are responsible for the production of insulin (Ozougwu, Obimba, Belonwu & Unakalamba, 2013). Currently, diabetes presents an immense challenge to the global public health system (Kimuyu, 2018). Therefore, this discussion focuses on the key aspects of type 1 diabetes.
Table of Contents
Introduction
Epidemiology
Impact of T1D on Life
Disease Process
Signs of T1D
Etiology of T1D
Genetics of T1D
Cause of Beta Cells Destruction
Environmental Triggers
Nutritional Triggers of T1D
Protective Dietary Components
Pathophysiology of T1D
Effect of T1D on Body Systems
Conclusion
References
Introduction
Diabetes entails a collection of metabolic disorders which are usually characterized by prolonged high sugar levels in an individual’s blood. For instance, both type 1 diabetes (T1D) and type 2 diabetes (T2D) are characterized with hyperglycemia. This condition is referred as hyperglycemia, and it has been found to cause debilitating health consequences. Van Belle, Coppieters and von Herrath (2011) report reaffirm that chronic hyperglycemic conditions may lead to health complications including heart disease, blindness, kidney failure, stroke, and ketoacidosis. Ordinarily, T2D occurs due to insulin resistance in which adipose or muscle cells exhibit low response to insulin. This phenomenon is associated to old age or obesity. In contrast, T1D is caused by autoimmune destruction of pancreatic beta-cells which are responsible for the production of insulin (Ozougwu, Obimba, Belonwu & Unakalamba, 2013). Currently, diabetes presents an immense challenge to the global public health system (Kimuyu, 2018). Therefore, this discussion focuses on the key aspects of type 1 diabetes.
Epidemiology
In the US, T1D is common among children than adults. Overall, T1D has been found to occur at a prevalence rate of 1.7 per 1,000 children, primarily within 0 to 19 years age bracket (Van Belle, Coppieters & von Herrath, 2011). However, its prevalence exhibits demographic disparities. Evidence indicates that T1D affects non-Hispanic whites more than any other ethnic population (Chiang, Kirkman, Laffel & Peters, 2014).
Impact of T1D on Life
From a health lens, diabetes impacts life, adversely. Foremost, it lowers an individual’s life expectancy, more or less the same as other chronic noncommunicable illnesses such as cancer, obesity and cardiovascular disease. Second, diabetes affects an individual’s social life, including daily activities and career. It is also worth noting that diabetic patients experience psychosocial stress. Evidence reveals that adolescents with T1D have a high risk of developing psychosocial factors (Kakleas, Kandyla, Karayianni & Karavanaki, 2009).
Disease Process
In T1D, the disease progression is attributable to the progressive beta-cells destruction. This destruction is carried out by the body’s immune system in which immune cells target Insulin-producing Islets of Langerhans, primarily the beta-cells. This autoimmune destruction leads to a decrease in the production of insulin; thus, it does not reach its normal levels in the blood. In turn, this phenomenon causes a physiological imbalance in which glucose accumulates in blood. As a result, the patient presents with T1D signs.
Signs of T1D
In practice, the onset of T1D in children is characterized by the occurrence of the principal signs. These include hunger (polyphagia), frequent urination (polyuria), accumulation of ketones in the blood (ketonemia), and excessive thirst (polydipsia). Adults present with similar signs, although it is not as acute as it is the case in children. According to clinical reports, the onset of T1D is similar to that of T2D. As such, it is relatively difficulty to diagnose T1D in adults (Chiang, Kirkman, Laffel & Peters, 2014).
Etiology of T1D
In retrospect, different epidemiological models have described the etiology of T1D. Therefore, it is apparent that that the cause of this condition has been studied extensively, in order, to understand the underlying pathophysiology of the disorder. Overall, the etiology of T1D is associated with genetic factors. However, there are environmental factors which precipitate genetic predispositions to T1D.
Genetics of T1D
Being at autoimmune disorder, T1D occurs due to changes in the genetic components in an individual’s genome. Genetic mutations in the chromosomal regions involved in the production of insulin-producing genes. According to Chiang, Kirkman, Laffel and Peters (2014), there is an array of genes involved in the etiology of T1D. These include a rare monogenic forms, HLA gene, insulin gene, PTPN22 gene, IL2RA gene, and CTLA-4 gene. It is reported that T1D, hardly occurs due the mutation of a single gene, but rather a collection of genetic defects. In most cases, a single mutation combines with other autoimmune factors that are involved in the regulatory pathway to cause the disorder. For instance, genetic changes in Foxp3 transcription factor impairs the regulation of T cells; thus, leading to multiorgan autoimmunity. This phenomenon is evidenced in IPEX syndrome, as well as autoimmune polyendocrine syndrome type 1. It is estimated that 80% of children with Foxp3 mutations die early due the severity of the autoimmunity. On the other hand, genetic changes in autoimmune regulator (AIRE) have been found to cause 20% of T1D (Van Belle, Coppieters & von Herrath, 2011).
Genetic changes in HLA gene have also been found to be responsible for the onset of T1D (Todd, 2010). Research indicates that more than 60% of patients with T1D posses a mutant form of HLA gene, HLA-A *0201, which increases the susceptibility for T1D. On the other hand, genetic changes in the insulin gene locus have been found to predispose individuals to T1D. Tandem repeats of VNTR type I on insulin gene locus, located on chromosome 11 impair the binding of AIRE to the promoter region, leading dysregulation. In this context, clinical studies indicate that VNTR type I is responsible for the reduced tolerance in the thymus, which is in turn caused by low transcription of insulin protein. Another essential gene involved in the development of T1D is PTPN22. This gene is concerned with the production of tyrosine phosphatase (LYP), a lymphoid protein which down regulate T cell receptor signaling. Therefore, mutations in this gene lead to the development of autoreactive T cells which are involved in the beta cells destruction (Van Belle, Coppieters & von Herrath, 2011).
Cause of Beta Cells Destruction
From a pathological perspective, the destruction of beta cells is caused by autoreactive T cells in the body. These destructive cells are known to escape from the secondary lymphoid organs, primarily the thymus where selective elimination occurs. As such, the autoreactivity of these T cells is responsible for their beta cells invasion. Therefore, it is apparent that beta cells destruction is associated to genetic factors, but not nutritional or environmental factors.
Environmental Triggers
Despite the evidence that genetic factors are responsible for the etiology of T1D, it is suggestive that environmental factors precipitate the onset of T1D. For instance, bacterial and viral infections have been found to precipitate genetic mutations into T1D. Bacteria have long been associated with physiological changes in humans, especially changes in metabolism. This phenomenon is acknowledged by Van Belle, Coppieters and von Herrath (2011) who report that microbial imbalance in the gastrointestinal tract triggers autoimmunity. It is also reported that the intestinal wall does not provide adequate protection to the immune system; thus, bacteria are able to activate the immune system. Evidence for bacterial activation of the immune system is usually provided by the presence of distorted Treg subset in the intestines of TID patients. From a pathological perspective, the elimination of the normal intestinal microbiota exposes the immune system to activation by pathogenic bacteria.
An outstanding example of invasive bacteria that trigger the onset of T1D is the Mycobacterium avium subspecies paratuberculosis (MAP). This bacterium infects ruminants such as cows, and it can resist high temperatures. In humans, MAP has been found to trigger humoral responses, and its consequences include the development of mutations in SLC11A1 gene. Therefore, the expression MAP DNA in T1D patients suggests its involvement in diabetogenic responses (Dai et al., 2009).
On the other hand, some viruses have been found to trigger the onset of T1D. For instance, enteroviruses are believed to cause changes in the processing and function of the pancreatic islets. In some clinical studies, enteroviruses are isolated from the pancreatic islets, and this suggests that the infection of the beta cells by these particles results into T1D. Research indicates that enteroviruses induce the upregulation of the key proteins, primarily chemokines CXCL10. Rotaviruses are also associated with the onset of T1D. This has been reaffirmed by the presence of congenital rubella diabetes among children (Van Belle, Coppieters & von Herrath, 2011).
Nutritional Triggers of T1D
Evidence indicates that some foods or nutritional components play significant roles in the development of T1D. For instance, cow’s milk is known to contain protein components that trigger autoimmunity. According to clinical reports, cross-reactivity by antibodies to beta cell surface protein (p69) and albumin occurs in infants during the early developmental stages. Therefore, feeding children with cow’s milk during their early developmental stages, rather than breastfeeding predisposes them to T1D. On the other hand, wheat proteins, primarily gluten trigger T cell reactivity. According to Van Belle, Coppieters and von Herrath, (2011), gluten is linked to the onset of T1D because it initiates autoimmunity. Therefore, cow’s milk and gluten-rich wheat products should be avoided in child’s diet.
[...]
- Quote paper
- Patrick Kimuyu (Author), 2018, Understanding Type I Diabetes and the Underlying Physiological Mechanisms, Munich, GRIN Verlag, https://www.grin.com/document/411946
-
Upload your own papers! Earn money and win an iPhone X. -
Upload your own papers! Earn money and win an iPhone X. -
Upload your own papers! Earn money and win an iPhone X. -
Upload your own papers! Earn money and win an iPhone X. -
Upload your own papers! Earn money and win an iPhone X.