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"Mitochondria and the Pathogenesis of Type 2 Diabetes Mellitus"Prof. J.A. Maassen (biography)
English - 2006-09-15 - 57 minutes
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Summary :
In this presentation Prof. Maassen talks about the role of mitochondria in the development of glucose intolerance, in tissues such as adipose tissue, liver, muscle and pancreatic beta cells.
Mitochondria have their own DNA (mtDNA), which is about 16.5kb in length. This DNA is maternally inherited, and a number of clinical syndromes are associated with mtDNA mutations. One mutation at the 3243 position, for example, leads to a diabetic subtype called Maternally Inherited Diabetes and Deafness (MIDD) (1, 2). What is thought to occur in these patients is that due to a reduced storage capacity for triglycerides in their adipocytes, and less efficient scavenging of liberated fatty acids by beta-oxidation, a chronic elevation of fatty acids in the circulation occurs, which induces lipotoxicity in the beta-cell. Enhanced lipotoxicity in the beta-cell, together with enhanced reactive oxygen species production leads to an accelerated decline in beta-cell mass, and eventually the development of diabetes. There are also known mutations in nuclear-encoded mitochondrial proteins which modulate the risk for diabetes.
Is there a relation between common type 2 diabetes and mitochondrial dysfunction? There is evidence from studies in muscle to suggest this is the case (3,4). Prof. Maassen also discusses insulin sensitivity in carriers of the 3243A>G mutation, and ends by presenting a model illustrating how mitochondrial dysfunction plays a role in the development of type 2 diabetes.
Copyright © 2006 E-MedHosting.com Inc.
Learning objectives :
After viewing this presentation, the participant will be able to discuss:
- The life style factors that contribute to the development of common type 2 diabetes
- Why triglycerides and in particular fatty acids are major players in the development of type 2 diabetes
- The role of mitochondria in the pathogenesis of the metabolic syndrome and the development of type 2 diabetes
- Why hyperglycemia is a late event in the metabolic syndrome and why thiazolidinediones (TZDs, glitazones) and physical exercise have a beneficial effect in slowing down the disease process
Bibliographic references :
1. van den Ouweland JM, Lemkes HH, Ruitenbeek W, Sandkuijl LA, de Vijlder MF,
Struyvenberg PA, van de Kamp JJ, Maassen JA.Mutation in mitochondrial tRNALeu(UUR) gene in a large pedigree with maternally transmitted type II diabetes mellitus and deafness Nature Genetics 1, 368 - 371 (1992).
2. Takashi Kadowaki, Hiroko Kadowaki, Yasumichi Mori, Kazuyuki Tobe, Ryoichi Sakuta, Yoshihiko Suzuki, Yuzo Tanabe, Hiroshi Sakura, Takuya Awata, Yu-ichi Goto, Takaki Hayakawa, Kenpei Matsuoka, Ryuzo Kawamori, Takenobu Kamada, Satoshi Horai, Ikuya Nonaka, Ryoko Hagura, Yasuo Akanuma, and Yoshio YazakiA Subtype of Diabetes Mellitus Associated with a Mutation of Mitochondrial DNA N Engl J Med. 1994 Apr 7;330(14):962-8.
3. Mootha VK, Lindgren CM, Eriksson KF, Subramanian A, Sihag S, Lehar J, Puigserver
P, Carlsson E, Ridderstrale M, Laurila E, Houstis N, Daly MJ, Patterson N,
Mesirov JP, Golub TR, Tamayo P, Spiegelman B, Lander ES, Hirschhorn JN,
Altshuler D, Groop LC.PGC-1alpha-responsive genes involved in oxidative phosphorylation are coordinately downregulated in human diabetes Nature Genetics 34, 267 - 273 (2003).
4. Petersen KF, Dufour S, Befroy D, Garcia R, Shulman GI.Impaired Mitochondrial Activity in the Insulin-Resistant Offspring of Patients with Type 2 Diabetes N Engl J Med. 2004 Feb 12;350(7):664-71.
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