Diabetes: Difference between revisions
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Nephrogenic diabetes insipidus is caused by mutations in aquaporin 2 . Usually AQP2 is trafficked to the cell membrane where it facilitates the reabsorption of water into the cell. In the diseased state there the channels are retianed inside the cell resulting in the inability to control the concentration of urine being produced. | Nephrogenic diabetes insipidus is caused by mutations in aquaporin 2 . Usually AQP2 is trafficked to the cell membrane where it facilitates the reabsorption of water into the cell. In the diseased state there the channels are retianed inside the cell resulting in the inability to control the concentration of urine being produced. <ref>The Journal of Cell Biology. (2003). Reversed polarized delivery of an aquaporin-2 mutant causes dominant nephrogenic diabetes insipidus 163(5):1099-109</ref> | ||
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Revision as of 15:36, 12 November 2010
There are five types of diabetes; types 1-5:
Type 1 Diabetes [1] - is also known as insulin-dependent diabetes melitus and is caused due to the immune system destroying pancratic beta cells and so preventing them producing insulin.
Type 2 Diabetes[2] - is also known as non-insulin dependent diabetes mellitus and is caused due to insulin no longer triggering its signalling cascade. Increasing obestiy in the world is making this type of diabetes increasingly common.
Type 3 Diabetes - other specific types of diabetes
Type 4 Diabetes [3]- gestational diabetes mellitus (GDM)
Type 5 Diabetes [4]- impaired glucose tolerance (IGT) and impaired fasting glucose (IFG)
Nephrogenic diabetes insipidus is caused by mutations in aquaporin 2 . Usually AQP2 is trafficked to the cell membrane where it facilitates the reabsorption of water into the cell. In the diseased state there the channels are retianed inside the cell resulting in the inability to control the concentration of urine being produced. [5]
- ↑ Surg Annu. 1978;10:1-21. Replacement of pancreatic beta cells as treatment for diabetes mellitus: a review. Jonasson O, Hoversten GH.
- ↑ Acta Med Indones. 2010 Oct;42(4):204-8. Insulin resistance profile among siblings of type 2 diabetes mellitus (preliminary study). Purnamasari D, Soegondo S, Oemardi M, Gumiwang I. Department of Internal Medicine, Faculty of Medicine, University of Indonesia - dr. Cipto Mangunkusumo Hospital. Jl. Diponegoro no. 71, Jakarta Pusat 10430, Indonesia.
- ↑ Diabetes Care. 2010 Oct 26. [Epub ahead of print] Body and Liver Fat Mass Rather Than Muscle Mitochondrial Function Determines Glucose Metabolism in Women with a History of Gestational Diabetes. Prikoszovich T, Winzer C, Schmid AI, Szendroedi J, Chmelik M, Pacini G, Krssák M, Moser E, Funahashi T, Waldhäusl W, Kautzky-Willer A, Roden M. Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
- ↑ Clin Chem. 2010 Nov 9. [Epub ahead of print] Prediabetes as a Therapeutic Target. Pour OR, Dagogo-Jack S. Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center, Memphis, TN.
- ↑ The Journal of Cell Biology. (2003). Reversed polarized delivery of an aquaporin-2 mutant causes dominant nephrogenic diabetes insipidus 163(5):1099-109