**1. Introduction**

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 animal models.

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 in patients who are prone to diabetic complications.

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

Diabetes is one of the fastest growing diseases. Diabetes affects today an estimated 371 million people world-wide compared to 366 million by the end of 2011. Of course this includes 20 million to 40 million of patients with type 1 diabetes. While type 1 diabetes accounts for 5% to 20% of those with diabetes, it is associated with higher morbidity, mortality and health care cost than the more prevalent type 2 diabetes. Overall, 4.8 million people died and \$ 471 billion were spent due to diabetes in 2012 [1-2].

New figures indicate that the number of people living with diabetes is expected to rise from 371 million in 2012 to 552 million by 2030, if no urgent action is taken. This equates to approx‐ imately three new cases every ten seconds or almost ten million per year. International diabetes federation also estimated that almost half of the people with diabetes are unaware that they have diabetes [2].

In some of the poorest regions in the world such as Africa, where infectious diseases have traditionally been the focus of health care systems, diabetes cases are expected to increase by 90% by 2030. At least 78% of people in Africa are undiagnosed and do not know they are living with diabetes (Figure 1):

