Journal of Regional Section of Serbian Medical Association in Zajecar

Year 2006     Volumen 31     No 4
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UDK: 616.379-008.64-02; 612.349.8 ISSN 0350-2899 31 (2006) 4 p. 180-185
   
Review

Insulin signalling pathway in skeletal muscles

Emina Sudar, Jelena Velebit, Esma R. Isenović
Institut za nuklearne nauke "Vinča" - Laboratorija za radiobiologiju i molekularnu genetiku, Beograd

  
 

 

  
  Summary:
Insulin (INS), the hormone of endocrine pancreas, is one of the most important vertebrate proteins. Increased circulating levels of glucose (Glu) stimulate pancreatic β cells to secrete INS by exocytosis. Insulin receptor (IR) belongs to the group of membrane receptors with tyrosine kinase activity. Skeletal muscles (SM) account for about 85% of total Glu disposal under INS stimulated conditions where it is incorporated and stored as glycogen. Glu entry into cells is a process that requires the involvement of a carrier protein in order to facilitate the movement of Glu across the plasma membrane of a cell and they are identified as glucose transporters (GLUT). In SMs, GLUT1 and GLUT4 are the primary GLUTs expressed. In SMs, INS stimulated Glu disposal is mediated via translocation of GLUT4 from intracellular storage site to the plasma membrane and GLUT1 primary mediates basal, rather than INS mediated Glu uptake. Impairment of the mechanisms responsible for this translocation leads to INS resistance. Peripheral INS resistance is a key factor in the pathogenesis of type 2 Diabetes Mellitus (DMT2) and involves defects in Glu transport system in adipocytes and SM. SM is the principal site of Glu uptake under INS stimulated conditions and INS resistance in SM has been identified as the most important site for INS resistance in DMT2 and may result from a defect at the level of Glu transport, Glu phosphorylation or glycogen synthesis. Glu transport is one of the first steps in INS stimulated Glu uptake in SM and it is a rate limiting factor in the whole Glu metabolism.
Key words: insulin, skeletal muscles, insulin resistance, Diabetes Mellitus Type 2.

Napomena: kompletan tekst rada na srpskom jeziku
Note: full text in Serbian
 		  
 

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  Acknowledgment
This work was supported by Ministry of science and protection of the environment, Serbia; project grant No 143030
 		  
  Corresponding Address:
Emina Sudar
Institut za nuklearne nauke "Vinča"
Laboratorija za radiobiologiju i molekularnu genetiku
P.O. Box 522
11001 Beograd, Srbija
Tel/Fax: 011-244-75-85
e-mail: sudare@vin.bg.ac.yu

Paper received: 12.09.2006.
Paper accepted: 12.10.2006.
Published online: 31.01.2007.		  
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