Diabetes (or Diabetes mellitus) is a complex group of diseases caused by a number of reasons. Individuals suffering from diabetes have hyperglycemia (high blood sugar) either because there is low production of insulin or body cells do not use the produced insulin. About 350 million people suffer from diabetes globally (Danaei et al., 2011). The World Health Organization (1999) has predicted that diabetes will rise to the top seventh cause of death worldwide by 2030. There are three common forms of diabetes: type 1 diabetes, type 2 diabetes and gestational diabetes. This paper mainly discusses these major forms of diabetes considering their causes and consequences.
Type 1 Diabetes
In type 1 diabetes mellitus, body cells fail to produce insulin due to compromised immune system causing damage to the cells where production of insulin takes place. The cause and prevention of type 1 diabetes are not particularly known; however, it is suspected to be a consequence of certain genetic factors.
Type 2 Diabetes
In type 2 diabetes mellitus, there is low production of insulin by the body cells or the body does not effectively make use of the produced insulin. Type 2 diabetes is known to be the commonest type of diabetes; in fact, 90% of diabetes sufferers have type 2 diabetes (World Health Organization, 1999). The cause and cure of type 2 diabetes remains unknown; however, genetic factors and manner of living take part in its causes, and watching blood sugar level can control the disease.
Gestational diabetes happens when there is a development of high blood sugar level in pregnant women not previously diagnosed of diabetes. For mothers who had gestational diabetes during their first pregnancy, the probability that it will occur in subsequent pregnancies is approximately two-thirds. Furthermore, some patients may subsequently develop type 2 diabetes. After pregnancy, diabetes type 1 or 2 may occur and will require obligatory treatment.
Genetic Factors and Markers
The role of genetic factors as a cause of diabetes has been proven definitively. This is the main etiological factor for diabetes.
IDDM is considered to be a polygenic disease which is based on at least two of the mutant genes in diabetic chromosome 6. They are associated with the HLA system (D-locus), which determines the individual, genetically determined response of the body and B cells to various antigens.
The hypothesis of polygenic inheritance of IDDM suggests that diabetes is caused from two mutant genes (or two groups of genes) that have a recessive inherited predisposition to autoimmune lesions of the insular apparatus or increased sensitivity of B cells to viral antigens or attenuated antiviral immunity.
Genetic susceptibility is linked with particular genes of HLA systems, which are considered markers of such a predisposition.
Patients with a genetic predisposition to IDDM have an altered response to environmental factors. They have weakened antiviral immunity, and they are extremely susceptible to cytotoxic damage to the B cells by viruses and chemical agents.
Viral infection may be a factor that provokes the development of IDDM. The most common occurrence of IDDM clinically is preceded by the following viral infections: measles (rubella virus has a tropism to the islets of the pancreas, accumulates, and can be replicated in them), Coxsackievirus and hepatitis B virus (can be replicated in the insular apparatus), mumps (1-2 years after the epidemic of mumps, the incidence of IDDM in children dramatically increases), infectious mononucleosis, cytomegalovirus, influenza virus, etc. The role of viral infection is confirmed by seasonality in the incidence of IDDM development (often, the first diagnosed cases of IDDM among children occur in autumn and winter months, with a peak incidence in October and January), the detection of high titers of antibodies to the virus in the blood of patients with IDDM, and the detection by immunofluorescent methods for studying viral particles in the islets of Langerhans in people who have died of IDDM. The role of viral infections in the development of IDDM is confirmed in experimental studies. Viral infections among individuals with a genetic predisposition to IDDM are involved in the development of the disease as follows:
- the cause of acute injury to B cells (Coxsackievirus);
- leads to viral persistence (congenital cytomegalovirus infection, rubella) with the development of autoimmune reactions in the islet tissue.
In modern diabetology, the next staging of IDDM is expected.
First stage – a genetic predisposition, due to the presence of certain antigens in the HLA system, as well as genes of chromosomes 11 and 10.
Second stage – the initiation of the autoimmune process in islands of B cells influenced with viruses, cytotoxic agents and any other unknown factors. A crucial point in this step is the expression of B cells HLA-DR-antigen and glutamic acid, and therefore, they become autoantigens that cause the development of autoimmune response reactions.
Third stage – the stage of the active immunological process with formation of antibodies to B cells, insulin and autoimmune insulitis development.
Fourth stage – the progressive reduction of insulin secretion stimulated by glucose (1-phase secretion of insulin).
Fifth stage – clinical diabetes (the manifestation of diabetes). This step develops during the occurrence of the degradation and death of 85-90% of the B cells.
Many patients after the insulin treatment fall into remission of the disease (the “diabetic honeymoon”). Its length depends on the severity and degree of B cell damage, their ability to regenerate, and the level of residual insulin secretion, as well as the severity and frequency of related viral infections.
Sixth stage – the complete destruction of b-cells, and a complete lack of insulin secretion and C-peptide. Clinical signs of diabetes form and insulin treatment becomes necessary again.”
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