C1q/tumor necrosis factor-related protein 11 (CTRP11), a novel adipose stroma-derived regulator of adipogenesis
Wei Z., Seldin MM., Natarajan N., Djemal DC., Peterson JM., Wong GW.
Animal Study, published in J Biol Chem (2013) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- J Biol Chem (2013)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 23449976
- PMCID
- PMC3624406
- DOI
- 10.1074/jbc.m113.458711
- Citations
- 60
Abstract (original English)
C1q/TNF-related proteins (CTRPs) are a family of secreted regulators of glucose and lipid metabolism. Here, we describe CTRP11, a novel and phylogenetically conserved member of the C1q family. Our studies revealed that white and brown adipose are major tissues that express CTRP11, and its expression is acutely regulated by changes in metabolic state. Within white adipose tissue, CTRP11 is primarily expressed by stromal vascular cells. As a secreted multimeric protein, CTRP11 forms disulfide-linked oligomers. Although the conserved N-terminal Cys-28 and Cys-32 are dispensable for the assembly of higher-order oligomeric structures, they are unexpectedly involved in modulating protein secretion. When co-expressed, CTRP11 forms heteromeric complexes with closely related CTRP10, CTRP13, and CRF (CTRP14) via the C-terminal globular domains, combinatorial associations that potentially generate functionally distinct complexes. Functional studies revealed a role for CTRP11 in regulating adipogenesis. Ectopic expression of CTRP11 or exposure to recombinant protein inhibited differentiation of 3T3-L1 adipocytes. The expression of peroxisome proliferator-activated receptor-γ and CAAT/enhancer binding protein-α, which drive the adipogenic gene program, was markedly suppressed by CTRP11. Impaired adipogenesis was caused by a CTRP11-mediated decrease in p42/44-MAPK signaling and inhibition of
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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