Insulin interactions

When insulin interacts with its receptor, vesicles move to surface and fuse with the plasma membrane, increasing the number of glucose transporters in the plasma membrane. 

Consequently, we now have a fairly clear idea of how insulin binds to a specific receptor and exerts its effects on target cells. Knowledge of exactly how insulin interacts with target tissues is important since defects in receptor binding and problems in the sub-... 

Profrock, A., Schnefel, S., and Schulz, I. (1991). Receptors for insulin interact with G,-proteins and for epidermal growth factor withh G,- and G,-proteins in rat pancreatic acinar cells. Biochem. Biophys. Res. Common. 775 380-386. 

Insulin interacts with its cell surface receptor via key amino acid residues located along the N- and C-termini of the A chain of insulin and along the carboxy terminus of the B chain of insulin (Table 32.6). The binding of insulin occurs to amino acid residues located within the N- and C-terminal regions of the a subunit of the receptor, which includes a cysteine-rich region (5). Binding and activation of the insulin receptor results in a cascade of biochemical events previously described. 

Emdin SO, Dodson GG, Cutfield JM, Cutfield SM. Role of zinc in insulin biosynthesis some possible zinc insulin interactions in the pancreatic beta cell. Diabetologia 1980 19 174-182. 

Hollenberg, M. D., and Cuatrecasas, P., 1975, Insulin Interaction with membrane receptors and relationship to cyclic purine nucleotides and cell growth. Fed. Proc. 34 1556. 

Metabolic Functions. Chromium (ITT) potentiates the action of insulin and may be considered a cofactor for insulin (137,138). In in vitro tests of epididymal fat tissue of chromium-deficient rats, Cr(III) increases the uptake of glucose only in the presence of insulin (137). The interaction of Cr(III) and insulin also is demonstrated by experimental results indicating an effect of Cr(III) in translocation of sugars into ceUs at the first step of sugar metaboHsm. Chromium is thought to form a complex with insulin and insulin receptors (136). 

P-Adrenoceptors have been subdivided into P - and P2-adrenoceptors. A third subset called nontypical P-adrenoceptors or P -adrenoceptors have been described but are stiU the subject of debate. In terms of the interactions with various subsets of P-adrenoceptors, some antagonists are nonselective in that they antagonize the effects of activation of both P - and P2-adrenoceptors, whereas others are selective for either P - or P2-adrenoceptors. P - and P2-adrenoceptors coexist in almost all organs but generally, one type predominates. The focus herein is on the clinically relevant P -adrenoceptor-mediated effects on heart and on P2-adrenoceptor-mediated effects on smooth muscles of blood vessels and bronchioles, the insulin-secreting tissue of the pancreas, and skeletal muscle glycogenolysis for side effects profile (36). 

Lectures and symposia are used to orally give information to a group of practitioners or patients. These methods can be used to address broad topics (e.g., the MCO s process for developing practice guidelines) or narrow topics (e.g., use of the MCO s practice guideline for insulin-dependent diabetics). An advantage of lectures, compared to written communication, is that two-way interaction can occur. Allowing people to ask questions and discuss issues can help clarify information and can facilitate their use of the information. 

Bouaboula M, Perrachon S, Milligan L, Canat X, Rinaldi-Carmona M, Portier M, Barth F, Calandra B, Pecceu F, Lupker J, Maffrand JP, Le Fur G, Casellas P. A selective inverse agonist for central cannabinoid receptor inhibits mitogen-activated protein kinase activation stimulated by insulin or insulin-like growth factor 1. Evidence for a new model of receptor/ligand interactions. J Biol Chem 1997 272 22330-22339. 

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