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Abstract Zinc i.~ an es,~ential trocf’ metal that is directly involved in the physiology of i~ulin. There are ~evera/ reasons to suspect that abnormal zinc metabolism could play a role in the pathogenesis of diabete.~ mellitus. and some of its complications (Kinlaw et al., l983). Insulin is stored in the pancreatic beta-cell as a hexameric crystal containing a variable number of zinc molecules (Scott and Fisher, l938). This crystal is released into the portal venous system at the time of beta-cell degranulation. Variation of the zinc-toinsulin ratio within this crystal has been shown to alter its antigenic properties (Arquilla et al., l978b). In addition to its structural role in the storage form of insulin, zinc is also capable of modulating insulin action. Arquilla et al. (l978a), demonstrated that hepatic binding of insulin is enhanced by zinc. Stimulation o( Upogene8is in the adipocyte ha.<> aim been described, with synergism between insulin and zinc (Coulston and Dandonna, 1980). Aim of this studY is to in\’estigate :inc deficiency in type 11 diabetes mt!l/itJ.J.::, ana to .”’uggest a hypothesis regarding its mechanism |