By Bernard Testa, Urs A. Meyer
Quantity 27, the 1st thematic quantity within the sequence, presents an summary of current wisdom in regards to the pharmacological and scientific elements of antidiabetic medications. It goals to stimulate extra attention of attainable innovations within the improvement of recent antidiabetic medications.
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Additional info for Antidiabetic Agents: Recent Advances in their Molecular and Clinical Pharmacology, Volume 27
Some patients may retain a few functioning B-cells with some endogenous insulin production in the long term, thus having better blood glucose control and being less prone to diabetic complications. 3 NATURAL HISTORY AND PROGNOSIS The natural history of the disease is determined by the onset and extent of chronic diabetic complications. Microangiopathic changes are diabetesspecific, causing retinopathy, nephropathy and alterations in the peripheral and autonomous nervous system. Macroangiopathy, which is more typical for Type-II diabetes, leads predominantly to cardiovascular complications with coronary heart disease, myocardial infarction and peripheral vascular occlusion.
1987). , 1991b). , 1991b). It is believed that this association leads to activation of PI 3-kinase which results in phosphorylation of phosphatidylinositol molecules (Cantley et al. , 1991). , 1993). Although some functional properties of IRS-1 have been defined, we can presume that not all of the functions of IRS-1 have been discovered. The role of IRS-1 is probably not restricted to its function as a docking protein for PI 3-kinase; it might rather play a multifunctional role as a signalling element for growth-promoting and metabolic effects.
2 AUTOACTIVATION OF THE RECEPTOR KINASE BY TYROSINE PHOSPHORYLATION: THE A U T O P H O S P H O R Y L A T I O N CASCADE It appears that after kinase activation a signal amplification occurs through autophosphorylation. , 1988b). Autophosphorylation proceeds through a sequential mechanism in which Tyr-l146 and either Q Ins Ins @ Ins3 ;> | 33 MECHANISMS OF INSULIN ACTION ,,s311C,,, K,nasq C Ins Tyr Tyr 1 (9 1 Ins0 C Ins ,,, / p- _p Tyr- p-Tyr _ -p Postkinase signal transducers \ Postkinase signal transducers FIG.