Type 1 Diabetes
Type 1 Diabetes:
Causes:
Autoimmune Response
Type 1 diabetes is usually a progressive autoimmune disease, in which the beta cells that produce insulin are slowly destroyed by the body's own immune system. It is unknown what first starts this cascade of immune events, but evidence suggests that both a genetic predisposition and environmental factors, such as a viral infection, are involved.
Islets of Langerhans contain beta cells and are located within the pancreas. Beta cells produce insulin which is needed to metabolize glucose within the body.
Genetic Factors
Researchers have found at least 18 genetic locations, labeled IDDM1 - IDDM18, that are related to type 1 diabetes. The IDDM1 region contains the HLA genes that encode proteins called major histocompatibility complex. The genes in this region affect the immune response. New advances in genetic research are identifying other genetic components of type 1 diabetes. Other chromosomes and genes continue to be identified.
Most people who develop type 1 diabetes, however, do not have a family history of the disease. The odds of inheriting the disease are only 10% if a first-degree relative has diabetes, and even in identical twins, one twin has only a 33% chance of having type 1 diabetes if the other has it. Children are more likely to inherit the disease from a father with type 1 diabetes than from a mother with the disorder.
Genetic factors cannot fully explain the development of diabetes. Over the past 40 years, a major increase in the incidence of type 1 diabetes has been reported in certain European countries, and the incidence has tripled in the U.S.
Viruses
Some research suggests that viral infections may trigger the disease in genetically susceptible individuals.
Among the viruses under scrutiny are enteric viruses, which attack the intestinal tract. Coxsackieviruses are a family of enteric viruses of particular interest. Epidemics of Coxsackie virus, as well as mumps and
Causes:
Autoimmune Response
Type 1 diabetes is usually a progressive autoimmune disease, in which the beta cells that produce insulin are slowly destroyed by the body's own immune system. It is unknown what first starts this cascade of immune events, but evidence suggests that both a genetic predisposition and environmental factors, such as a viral infection, are involved.
Islets of Langerhans contain beta cells and are located within the pancreas. Beta cells produce insulin which is needed to metabolize glucose within the body.
Genetic Factors
Researchers have found at least 18 genetic locations, labeled IDDM1 - IDDM18, that are related to type 1 diabetes. The IDDM1 region contains the HLA genes that encode proteins called major histocompatibility complex. The genes in this region affect the immune response. New advances in genetic research are identifying other genetic components of type 1 diabetes. Other chromosomes and genes continue to be identified.
Most people who develop type 1 diabetes, however, do not have a family history of the disease. The odds of inheriting the disease are only 10% if a first-degree relative has diabetes, and even in identical twins, one twin has only a 33% chance of having type 1 diabetes if the other has it. Children are more likely to inherit the disease from a father with type 1 diabetes than from a mother with the disorder.
Genetic factors cannot fully explain the development of diabetes. Over the past 40 years, a major increase in the incidence of type 1 diabetes has been reported in certain European countries, and the incidence has tripled in the U.S.
Viruses
Some research suggests that viral infections may trigger the disease in genetically susceptible individuals.
Among the viruses under scrutiny are enteric viruses, which attack the intestinal tract. Coxsackieviruses are a family of enteric viruses of particular interest. Epidemics of Coxsackie virus, as well as mumps and
References: American Diabetes Association. Standards of medical care in diabetes -- 2009. Diabetes Care. 2009 Jan;32 Suppl 1:S13-61. Bakris GL, Sowers JR; American Society of Hypertension Writing Group. ASH position paper: treatment of hypertension in patients with diabetes-an update. J Clin Hypertens (Greenwich). 2008 Sep;10(9):707-13; discussion 714-5. Camilleri M. Clinical practice. Diabetic gastroparesis. N Engl J Med. 2007 Feb 22;356(8):820-9. Farrar D, Tuffnell DJ, West J. Continuous subcutaneous insulin infusion versus multiple daily injections of insulin for pregnant women with diabetes. Cochrane Database Syst Rev. 2007 Jul 18;(3):CD005542. Fiorina P, Secchi A. Pancreatic islet cell transplant for treatment of diabetes. Endocrinol Metab Clin North Am. 2007 Dec;36(4):999-1013; ix. Drueke TB, Locatelli F, Clyne N, Eckardt KU, Macdougall IC, Tsakiris D, et al. Normalization of hemoglobin level in patients with chronic kidney disease and anemia. N Engl J Med. 2006 Nov 16;355(20):2071-84. Hunt D. Foot ulcers and amputations in diabetes. Clin Evid. 2006 Jun;(15):576-84. Retnakaran R, Zinman B. Type 1 diabetes, hyperglycaemia, and the heart. Lancet. 2008 May 24;371(9626):1790-9. Shapiro AM, Ricordi C, Hering BJ, Auchincloss H, Lindblad R, Robertson RP, et al. International trial of the Edmonton protocol for islet transplantation. N Engl J Med. 2006 Sep 28;355(13):1318-30. Skyler JS. Cellular therapy for type 1 diabetes: has the time come? JAMA. 2007 Apr 11;297(14):1599-600. Vardi M, Nini A. Phosphodiesterase inhibitors for erectile dysfunction in patients with diabetes mellitus. Cochrane Database Syst Rev. 2007 Jan 24(1):CD002187. Voltarelli JC, Couri CE, Stracieri AB, Oliveira MC, Moraes DA, Pieroni F, et al. Autologous nonmyeloablative hematopoietic stem cell transplantation in newly diagnosed type 1 diabetes mellitus. JAMA. 2007 Apr 11;297(14):1568-76. Writing Group for the SEARCH for Diabetes in Youth Study Group , Dabelea D, Bell RA, D 'Agostino RB, Imperatore G, Johansen JM, et al. Incidence of diabetes in youth in the United States. JAMA. 2007 Jun 27;297(24):2716-24.