By Antje Sander, Stefan Schwarz
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refs: http://www. dft. gov. uk/mca/mcga-seafarer_information/mcga-dqs_st_shs_seafarer_information-medical/mcga-dqs_st_shs_ships_capt_medical_guide. htm
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Additional resources for Anatomie fast. Der Crashkurs
The insulin effect on the glucose transport system is mediated by a translocation of glucose transporters from the intracellular pools to the plasma membrane and activation of these transporters in the plasma membrane. The glucose transporter GLUT-4 plays a major role. A reduced capacity of insulin-dependent translocation of GLUT-4 to the plasma membrane is observed as a consequence of insulin resistance. Concerning the crosstalk between various tissues, the adipose tissue and adipocytes contribute to the development of insulin resistance by producing and secreting mediators such as adipokines and cytokines that act on the muscle and other target tissues of insulin action.
141 NAFLD is the most common liver disease and, along with the worldwide increase in prevalence of general and abdominal obesity, NAFLD has become a prevalent general health problem in many industrialized countries. NAFLD represents a continuum of liver disease from simple steatosis to NASH and cirrhosis. 63,143 However, this endeavor might not be sufficient to completely understand the pathophysiology of NAFLD. During conditions of a positive energy balance, subcutaneous and visceral adipose tissues expand in a manner that is predominantly genetically determined.
4,54,63,106–109 Free fatty acids are important mediators in central obesity. Elevated free fatty acid concentrations in plasma are found in insulin resistance and in type 2 diabetes. These free fatty acids are most likely liberated by an increased lipolytic activity of the central and visceral fat depots and facilitate insulin resistance through an increased rate of fatty acid oxidation of the involved organs. Insulin and the sympathetic nervous system are important regulators of lipolysis. In central obesity, the increased sympathetic activity and a reduced 15 Normal Insulin Resistant Insulin Resistance Insulin 2 GLUT-4 Insulin receptor Flotillin P P P P CAP Cbl P P Flotillin CAP P P CbI P P Translocation of GLUT-4 CAP Cbl Insulin signalling via PI3 kinase, PDK1 AKT/PKB No translocation of GLUT-4 CAP CbI Stimulation of conduction system–driven contractile activity Insulin signalling via PI3 kinase, PDK1 AKT/PKB Lack of contractile activity FIGURE 2-3 Differences in the regulation of GLUT-4 translocation in cardiac myocytes under normal conditions and in insulin resistance.
Anatomie fast. Der Crashkurs by Antje Sander, Stefan Schwarz