sub:provenance {
  beldoc: dce:description "Approximately 61,000 statements." ;
    dce:rights "Copyright (c) 2011-2012, Selventa. All rights reserved." ;
    dce:title "BEL Framework Large Corpus Document" ;
    pav:authoredBy sub:_4 ;
    pav:version "1.4" .
  sub:_3 prov:value "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)" ;
    prov:wasQuotedFrom pubmed:12975454 .
  sub:_4 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:12975454 ;
    prov:wasDerivedFrom beldoc: , sub:_3 .
}