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Type I Diabetes: Selenium and Folic Acid effects on Type I Diabetes Introduction: Type I Diabetes is an autoimmune disease; in diabetes the body turns against the beta cells in the pancreas which produce insulin. The pancreas then doesn’t produce any or very little insulin. Glucose builds up in the blood, overflows in the urine, and out of the body losing its main source of fuel even though the blood contains large amounts of sugar. It is unknown what causes the immune system to attack the beta cells but they think that autoimmune, genetic, environmental factors, and possibly viruses are involved. Type I diabetes is shows up in children and young adults but can appear at any age and symptoms can develop in a short period of time. Symptoms of Type I diabetes are: excessive thirst/appetite, increased urination, unusual weight loss or gain, fatigue, nausea, blurred vision, dry mouth, slow healing sores, itching skin in the vaginal/groin area, and yeast infections (1). Objective: Selenium: To help prevent the onset of diabetes-accelerated atherosclerosis (3). Folic Acid: To normalize endothelial progenitor cells that play a role in vascular wall repair (2). Materials/Methods: Selenium: Human umbilical vein endothelial cells were pretreated with Se (100 nmol/L) and stimulated by high glucose or high insulin. Expression of adhesion molecules was measured by Western blot (3). Folic Acid: Microarray analysis was used to investigate gene expression profiles of endothelial progenitor cells from type 1 diabetes patients before and after a four week period of folic acid supplementation compared to the gene expression profiles of those from healthy subjects. The probability of genes being expressed differently was computed using a random-variance t-test. A multivariate permutation test was used to identify genes that were expressed. Functional classification of genes was done by using ontology in the Gene Ontology database (2). Results: Selenium: Se significantly inhibited glucose induced expression of vascular cell adhesion molecule-1 (VCAM- 1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin (3). Folic Acid: Type 1 diabetes significantly modulated the expression of 1591 genes compared to healthy controls. These genes were found to be involved in processes regulating development, cell communication, cell adhesion and localization. Genes that were normalized by folic acid played a major role in development, such as the transcription factors ID1 and MAFF (2). Summary: Selenium: These results suggest that Se can inhibit high glucose- and high insulin-induced expression of adhesion molecules. Therefore, Se may be considered as a potential preventive intervention for diabetes-accelerated atherosclerosis (3). Folic Acid: Folic acid normalizes endothelial progenitor cell gene expression profiles of patients with type 1 diabetes. Signaling pathways modulated by folic acid may be potential therapeutic targets to improve endothelial progenitor cell function (2). Discussion: Both selenium and folic acid show the ability to help reduce common abnormalities in the human body from type I diabetes. Selenium is shown to reduce the risk of atherosclerosis and with folic acid treatment endothelial progenitor cell gene expression profiles from diabetic patients are similar to those of healthy controls (3). Because the cause of diabetes is unknown there is no real prevention and to help prevent the other problems associated with it is the next best thing (2). References: (1)”Diabetes Overview.” WebMD Diabetes Center: Types, Causes, Symptoms, Tests, and Treatments. Web. 21 Feb. 2010. <http://diabetes.webmd.com/guide/diabetes-overview>. (2)”Folic acid supplementation normalizes the endothel… [Cardiovasc Diabetol. 2009] – PubMed result.” National Center for Biotechnology Information. Web. 21 March. 2010. <http://www.ncbi.nlm.nih.gov/pubmed/19706161?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.P ubmed_RVDocSum&ordinalpos=5>. (3)"Selenium Inhibits High Glucose- and High Insulin-i... [Arch Med Res. 2008] - PubMed Result." National Center for Biotechnology Information. Web. 21 Mar. 2010. <http://www.ncbi.nlm.nih.gov/pubmed/18375247>.
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