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:_3 ;
    pav:version "1.4" .
  sub:_2 prov:value "Despite these striking increases in adipocyte number, average adipocyte size was not significantly different in any of the groups, and the observed increases in adipose pad weights reflect the adipocyte hyperplasia that occurs with the loss of one or more of these CDKIs. The important role for p27 and p21, separately and together, in regulating adipocyte number and adipose mass indicates that these CDKIs are potential targets for E2 or other hormonal signals that may result in alterations in final adipocyte number. In addition, other recent reports have demonstrated the critical role of proteins such as sirtuin 1 in regulating adipogenesis (68), and work to establish whether estrogen effects on adipocyte number are mediated through p27 and p21 or other target proteins that play critical roles in adipogenesis is ongoing.  Table 1. Estrogen Effects on Adipose Tissue Direct Effects Lipogenesis (down) Lipoprotein lipase mRNA and protein expression (29) - (up) Hormone sensitive lipase activity (31) (up) Epinephrine-induced - (32) Site-specifically attenuates subcutaneous tissue - (34) Adipogenesis (up) Adipocyte precursor proliferation (57) (down) Expression of adipocyte differentiation factors (49, 60, 61) Central Effects CNS/hypothalamic effects (down) Feed consumption (25) (down) Leptin secretion (36) (up) Activity and energy expenditure (25, 26) Lipid profile and hepatic effects Absence of estrogen causes hepatic steatosis and altered lipid homeostasis" ;
    prov:wasQuotedFrom pubmed:15564439 .
  sub:_3 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:15564439 ;
    prov:wasDerivedFrom beldoc: , sub:_2 .
}