Insulin wild-type

A similar approach is fruitful for investigating insulin mutants that may be under consideration as replacements for wild-type insulin in human therapy. For lispro insulin (in which positions P28 and K29 in human insulin are reversed), and for several other insulin mutants, PLIMSTEX clearly can distinguish the self-association properties and binding constants of lispro and r-human insulins [33]. 

More specifically, fo integrate data from PC2- and PCl/3-deficient mouse studies with recent data that demonstrate a candidate role for cathepsin L in neuropeptide production, results of neuropeptides studied in PC 2- and PC 1/3-deficient mice are summarized here. In PC2 knockout mice, many neuropeptides were partially reduced, with the exception of a-MSH that was nearly obliterated. PC2-deficient mice show increases in the POMC-derived peptide hormones ACTH and 3-endorphin (1-31), which identifies fhem as subsfrafes for PC2 (40). Among fhe POMC-derived peptide hormones, only a-MSH was nearly complefely absenf in the PC2 knockout (40). NPY was unchanged in the brain but was decreased in ileum and was increased in adrenal (41). Somatostatin was increased in the brain and was unchanged in the intestine (Met)enkephalin was partially decreased in the brain but was not altered in adrenal and intestinal tissues. (41). No changes in VIP, galanin, or CRF were observed in PC2-deficient mice. Insulin in the pancreas was reduced by 75% compared with wild-type controls, and... 

In PCI/3-deficient mice, reduction of GnRH by about 80% was observed as well as decreases in GLP-1 and GLP-2 (46). Reduction in processing of proinsulin to insulin was observed in PCI/3-deficient mice (47). Interestingly, no change in vasopressin occurred, and little change in POMC-derived peptide hormones were observed in the PCl/3-deficient mice compared with wild-type controls (48). 

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