There are 4 main types of diabetes:
1.Type 1 or Juvenile Onset Diabetes (JOD) that starts mostly in early age and results from failure of pancreas to produce sufficient insulin to carry on the sugar to different body organs and parts. As discussed in the “Autoimmune Disorders” section, this type of diabetes is immune-mediated. Here a T-cell mediated autoimmune attack leads to the loss of beta cells of the islets of pancreas where the insulin is produced. This type of diabetes that is less than 10% of the whole diabetes, has been associated to Coxsackie B4 and most recently B1 Viruses that invade the pancreas and through “molecular mimicry”, trick the host immune system to recognize its own tissue as foreign, antigen or eiptope, and the occupying virus as the host, antibody or paratope. This deceives the immune system to produce HLA (Human Leukocyte Antigen),e.g. types DR3 and DR4 by T-cells against the pancreas to fail the production of insulin!
Coxsackievirus that belongs to a family of single strand RNA enterovirused, that also includes poliovirus and echovirus. There is estimated that there are at lease 68 human enterovirus subtypes, affecting millions of people worldwide each year, some as epidemies. These viruses often found in the respiratory secretions (e.g., saliva, sputum, or nasal mucus) and stool of an infected person and are the causes such common infections as nonspecific febrile illness, aseptic meningits and epidemic pleurodynia in children. In the United States, enteroviruses are responsible for 30 to 50 million infections in children per year and in 2007, an outbreak of coxsackievirus in China, cost the death of 22 children and affecting more than 800, leading to hospitalization of 200 children.
We stress on the above statistics not for their immediate significant common morbidities and mortalities, but for their long lasting future effects that these viruses could create in the host, e.g. causing autoimmune disorders such as diabetes mellitus type 1. These viruses as we know so far, after infecting the host cell, their genomes are translated in a cap-independent manner into single polyproteins, and subsequently by virus-encoded proteases causing their own replications and later on affecting our immune system for their generations to come.
So in the near future, hopefully the management of diabetes type 1 or juvenile onset, will be not its treatment with insulin that is already too late, but will be its prevention, by identifying, preventing the above viral infections. Or by advancing our knowledge and techniques in immunology and genetic engineering, we hopefully will be able to treat the conditions such as diabetes type 1, by reversing its genetic impact on our genome and HLA system! Vaccination or Autoantigen-specific immunotherapy with alum-formulated GAD65 (Glutamic Acid Decarboxylase) has already shown some promise to reduce the loss of beta-cell function after the clinical onset of type 1 diabetes.
2.Type 2 or Mature Onset Diabetes (MOD) that starts in adult age, mostly middle age and results from overwhelming pancreatic islet cells by overeating, specially carbohydrates, thus suppressing the production of insulin, or sensitivity of insulin to blood sugar. This type of diabetes comprises the majority of diabetic cases in more than 90% and is a result of sedentary and overeating life styles that causes obesity. This type could be insulin resistant due to the loss of sensitivity of insulin to regulate blood sugar.
3.Gestational Diabetes which could resemble and be a subtype and is some cases will evolve into type 2, happens during pregnancy in some women. This condition could be temporary, treatable and may not last after delivery.
4. Latent Autoimmune Diabetes of Adults(LADA) that is a subtype of type 1 , developing in adults and is similarly an autoimmune disorder! The immunological evidence, common in both type 1 diabetes and LADA, is demonstrated by the presence of autoantibodies against islet cell antigens in the patients’ sera. Specifically, these antigens include 65kDa glutamic acid decarboxylase (GAD65) and insulinoma-associated antigen (IA2). While type 1 diabetes shows both these autoantibodies, LADA typically demonstrates production of GAD65 autoantibodies. An association between “Cytomegalovirus” (CMV) infection and the pathogenesis of some neuroendocrine autoimmune diseases, such as LADA and Stiff Man Syndrome, through T cell crossreactivity with GAD65 has already been substantiated. Primary prevention of these autoimmune diseases therefore might be attempted by targeting the CMV virus by vaccination or tolerance-inducing induction strategies.
Dr.Mostafa Showraki, MD, FRCPC Lecturer, University of Toronto,School of Medicine,Author: “ADHD:Revisited” Book “adhdrevisited.com”/”medicinerevisited.com”
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