title: Cell type-specific expression and coregulation of murine resistin and resistin-like molecule-alpha in adipose tissue.
abstract: Adipocytes are the exclusive or predominant source of several secreted proteins that exert profound effects on systemic carbohydrate and lipid metabolism. Resistin, a 10-kDa adipose tissue specific secretory protein, has recently been implicated in exerting a negative effect on systemic insulin sensitivity. It is, however, not known how resistin mediates this insulin-desensitizing effect or what regulatory mechanisms control resistin expression. Resistin-like molecule-alpha (RELMalpha), a homolog of resistin originally identified by its upregulation in asthmatic lung, is another secreted protein expressed in adipose tissue. The regulation of RELMalpha in adipose tissue and its relationship to resistin expression has not been addressed so far. Here, we demonstrate that the expression of resistin and RELMalpha are similarly regulated in adipose tissue despite the fact that RELMalpha is exclusively expressed in the stromal vascular fraction of adipose tissue and not in adipocytes. Interestingly, this coregulation is limited to adipose tissue as the expression of RELMalpha in lung is independent of metabolic regulation. Additionally, we show that resistin and RELMalpha levels are not subject to regulation by proinflammatory stimuli. Finally, acute hyperglycemia leads to up-regulation of resistin and RELMalpha transcription in various adipose depots.
authors.affiliation: Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
authors.forename: Michael W
authors.initials: MW
authors.lastname: Rajala
authors.forename: Ying
authors.initials: Y
authors.lastname: Lin
authors.forename: Mollie
authors.initials: M
authors.lastname: Ranalletta
authors.forename: Xiao Man
authors.initials: XM
authors.lastname: Yang
authors.forename: Hao
authors.initials: H
authors.lastname: Qian
authors.forename: Ron
authors.initials: R
authors.lastname: Gingerich
authors.forename: Nir
authors.initials: N
authors.lastname: Barzilai
authors.forename: Philipp E
authors.initials: PE
authors.lastname: Scherer
mesh_terms: D016475:3T3 Cells; D017667:Adipocytes / Q000378:metabolism; D000273:Adipose Tissue / Q000098:blood supply / Q000166:cytology / Q000378:metabolism*; D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation; D006729:Hormones, Ectopic / Q000235:genetics* / Q000378:metabolism*; D006943:Hyperglycemia / Q000235:genetics / Q000378:metabolism; D007249:Inflammation / Q000235:genetics / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D008820:Mice, Obese; D020932:Nerve Growth Factor; D011506:Proteins / Q000235:genetics* / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D052243:Resistin; D014018:Tissue Distribution
chemical_list: D006729:Hormones, Ectopic; D036341:Intercellular Signaling Peptides and Proteins; D011506:Proteins; D012333:RNA, Messenger; D052243:Resistin; C499623:Retn protein, mouse; C499622:Retn protein, rat; C413576:Retnla protein, mouse; C486575:Retnla protein, rat; D020932:Nerve Growth Factor