By H.P.T. Ammon, H.U. Häring, M. Kellerer, H. Laube, L. Mosthaf, E.J. Verspohl and M.A. Wahl (Eds.)
Quantity 27, the 1st thematic quantity within the sequence, offers an outline of current wisdom with reference to the pharmacological and scientific elements of antidiabetic medicines. It goals to stimulate additional attention of attainable recommendations within the improvement of recent antidiabetic medications.
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Haben Sie Fragen zu Arzneimittelauswahl und Therapieführung? Die thirteen. Auflage des Taschenbuchs der Arzneibehandlung bietet zuverlässige Informationen zur genauen Beurteilung der therapeutischen Wirkung der 1. 500 meistverwendeten Arzneimittel. In 24 krankheitsbezogenen Kapiteln werden die Prinzipien der Arzneitherapie auf der foundation von Pathogenese und Symptomatik dargestellt (Teil I).
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Extra resources for Antidiabetic Agents: Recent Advances in their Molecular and Clinical Pharmacology
8). , 1988, 1989). , 1989) and specificity for ligand binding. , 1989). The 12 amino acids at the C-terminus of the a-subunit also appear to play MECHANISMS OF INSULIN ACTION 31 a role in insulin binding, since the presence of these amino acids (insulin receptor isoform B) results in a decrease in insulin affinity. The coupling of the a-subunit to the extracellular part of the/3-subunit occurs through disulphide bonds. There is some evidence from tryptic cleavage experiments (Frias and Waugh, 1989) that the amino acids involved in the disulphide coupling are located in positions 435,468 or 524 in the a-chain.
The incidence of Type-I diabetes (insulitis) varies considerably in its geographic distribution among countries and has increased dramatically, up to 3 times during the past 3 decades in Finland. The highest rates of occurrence are found predominantly in the northern hemisphere. Finland has a leading position with 28 cases/100 000 per year. 8/100 000). This again suggests a predominant effect of environmental factors in the genesis of Type-I diabetes. The incidence rate of Type-I diabetes may also vary considerably over a narrow geographic range.
There are many adjustments to the therapeutic regimen which an individual with IDDM can make in order to avoid changes in glucose homoeostasis during or after exercise. Thus, individualized recommendations for exact treatment modification in association with exercise are necessary. Exercise-induced glycogen depletion, with an increase in glucose storage and insulin-stimulated glucose disposal, both of which may add to postexercise hypoglycaemia in Type-I diabetes, is associated with increased peripheral sensitivity to insulin.