. . . . . . . . . . . "p(MGI:Il1b) -> a(SCHEM:\"Serum Glucagon\")" . "Approximately 61,000 statements." . "Copyright (c) 2011-2012, Selventa. All rights reserved." . "BEL Framework Large Corpus Document" . . "1.4" . "IL-1 was reported to be involved in the feeding suppression caused by leptin, which is released from adipocytes and suppresses food intake through actions in the hypothalamus. IL-1 promotes the release of corticotropin releasing factor (CRF; references 18, 19), melanocortins, and other neuropeptides (4). CRF suppresses feeding behavior when administered intracerebroventricularly. IL-1B selectively destroys the insulin-producing B cells, but not the {alpha} cells, in vitro. This cytotoxic effect of IL-1 is suggested to be mediated by the induction of inducible nitric oxide synthase or prostaglandins On the other hand, it was reported that IL-1 acts as a hypoglycemic agent not only in normal animals but also in alloxan-induced diabetic and genetically diabetic mice (32) and increases insulin and glucagon levels, suggesting that IL-1 has antidiabetic effects (33)" . . "Selventa" . . . . "2014-07-03T14:30:16.605+02:00"^^ . . .