The metabolic disturbances and their consequences in diabetes mellitus are well known more or less in details too. However, our knowledge on the diabetic disorders in membrane functions are limited. These damages are connected mostly with the disregulation of the membrane protein syntheses due to deficiency of insulin. In this review the impairments of the Na(+)-pump and the Ca(2+)-transport mechanisms as well as the insulin-dependent glucose transporter GLUT4 will be discussed in diabetes. The capacity of these transporters could be decreased even more than 50 percent in diabetes. This is the reason why using the same dose of cardioactive steroids as if in not diabetic subjects--can cause toxic alterations on the heart in diabetic patients. Insulin regulates not only the expression of some membrane proteins but it can initiate the translocation of the Na(+)-pump and GLUT4 from the intracellular membrane compartments to the plasma membrane in muscle, heart and adipose tissue. Therefore the uptake of K+ and glucose into these tissues will increase significantly under the acute influence of insulin. Untreated diabetic patients generally show hyperkalemia. Forceful treatment with insulin of these subjects often causes severe hypokalemia as a consequence of sudden translocation of the Na(+)-pump. Different Ca(2+)-transport systems are also impaired in diabetes. These changes may result significantly higher free Ca2+ concentration in the cytoplasma of cardiomyocytes. This is one of the most important reason for the Ca2+ overloading and ultimately for heart death. According to authors opinion, beside the dangerous metabolic disorders, general membrane damage and extended disturbances in membrane functions are also very characteristic for diabetes. The acknowledgement of these alterations are very important for the exact planning of the up to date treatment of diabetes.
|Translated title of the contribution||Diabetes mellitus as a general membrane disease and its consequences|
|Number of pages||8|
|Publication status||Published - Aug 19 2001|
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