**Genetics**

**Chapter 3**

**Update of Type 1 Diabetes**

Additional information is available at the end of the chapter

in patients who are prone to diabetic complications.

Diabetes is one of the fastest growing diseases. World health organization estimates that approximately 340 million people have type 1 diabetes and this number increases by 3-5% each year so the type 1 diabetes population reached 25 million by 2010. Type 1 diabetes is an autoimmune disease that is caused as a result of destruction of pancreatic β-cells. Several factors may contribute to the pathogenesis of type 1 diabetes. Genetic susceptibility of type 1 diabetes is determined by polymorphisms/mutations in multiple genes in both human and

The Major Histocomapatibility Complex (MHC) accounts for approximately 40% of the familial aggregation of type 1 diabetes and the insulin gene for only 10 % suggesting the existence of additional loci. The gene for "Protein Tyrosine Phosphatase, Non-receptor type 22 (lymphoid)."PTPN22, the lymphocyte signaling molecule, on chromosome 1p13.3–p13.1 is a confirmed locus that contributes to multiple autoimmune disorders, including type 1 diabetes. Diabetes associated Cytotoxic T - Lymphocyte Antigen 4 (CTLA-4) locus polymor‐ phisms in most populations have relative risks less than 1.5. A fundamental question is whether there are genetic polymorphisms that confer major risk for type 1 diabetes, other than the Human Leukocyte Antigen (HLA) DR and DQ alleles (class II HLA alleles). Recently, genes outside MHC region have considered playing an important role in the onset of diabetes.

As accumulative report suggest the role of olfactory receptor in the pathogenesis of diabetic microvascular and other diabetic complications, undoubtedly, this haplotype specific altera‐ tion of type 1 diabetes risk is an independent risk for the disease and can address the promising MHC-linked gene other than DR/DQ. Moreover, there is nothing to hinder for that this might be a signal that identify the role of olfactory receptor gene in the pathogenesis of type 1 diabetes

> © 2013 Jahromi; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use,

© 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,

distribution, and reproduction in any medium, provided the original work is properly cited.

and reproduction in any medium, provided the original work is properly cited.

Mohamed M. Jahromi

http://dx.doi.org/10.5772/55960

**1. Introduction**

animal models.
