Altered level of inflammatory markers in relation to glycemic status associated with adolescent diabetic patients

Abstract

Diabetes mellitus is considered to be one of the most common public health disorders which have a wide range of distribution all over the globes. For development of adolescent diabetes mellitus, the major etiological factors are the synergistic effects of environmental, genetic and immunological factors which used to destruct the pancreatic β-cells mass. The main contributing factor for occurrence of type 1 diabetes in individuals of genetic susceptibility is due to process of autoimmunity that used to develop several months or even years which used to destroy the β-cells mass.1 Immunological markers are used to consider as main precipitating agent before diabetic condition is clinically overt. Although there was a well-maintained normal tolerance level of glucose but due drastically decline of mass of β cells, insulin secretion is gradually decreasing. Clinical sign and symptom of diabetes mellitus usually caused when about 80% of β cell mass used to destroy. At this point of time the number of residual functioning β cells is insufficient to maintain the glucose tolerance. The triggering factor for transition from impaired glucose tolerance to frank diabetes are very frequently associated with requirement of more amount of insulin that may occur in infections or puberty. In human leukocyte antigen region (HLA region) on chromosome no 6 the major susceptibility gene of type 1 diabetes mellitus is located and this inheritance is mainly is of polygenic variety which used to account for 40% to 50% of genetic risk for developing of type 1 diabetes mellitus. Class II major histocompatibility complex (class II MHC) is encoded by genes which are situated in this region. The strongest association is with the DQ locus within this region and this locus is again further subtyped into α and β loci. The haplotypes DQ A1*0301, DQ B1*0302, DQ A1*501 and DQ B1* 201 have the strongest association with type1 diabetes that have shown after refinement in genotyping of HLA loci. It has been found that the amino acid in position 57 of the N-terminal β-1 domain of the HLA-DQ β chain is directly related to susceptibility of type 1 diabetes although analysis of DNA sequence from patients with type 1 diabetes mellitus has not so far shown unique class II sequence.2 If individuals undergone infection or toxic insult, their immune system generally susceptible to develop a vigorous autoimmune process either against molecule of β cell resembling the viral protein or against altered pancreatic β cell antigens is felt to develop immune mediated type 1 diabetes mellitus. Although other types of islets cell are inexplicably spared from the autoimmune process though they are functionally and embryological similar to β cells and expresses maximum of the similar proteins in β cells. By the process called “Insulitis” the pancreatic islets are infiltrated with leucocytes.3