Level D· Scientific groundwork from lab and animal studiesLaboratory StudyPubMed

Nitric oxide and downstream second messenger cGMP and cAMP enhance adipogenesis in primary human preadipocytes.

Hemmrich K., Gummersbach C., Paul NE., Goy D., Suschek CV., Kröncke KD.

Laboratory Study, published in Cytotherapy (2010) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

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
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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
Laboratory Study
Journal
Cytotherapy (2010)
Country
England
Reported sample size
—
Source database
PubMed
PMID
20370354
DOI
10.3109/14653241003695042

Abstract (original English)

Obesity is correlated with chronic low-grade inflammation. Thus the induction of inflammation could be used to stimulate adipose tissue formation in tissue-engineering approaches. As nitric oxide (NO) is a key regulator of inflammation, we investigated the effect of NO and its downstream signaling molecule guanosine 3',5'-cyclic monophosphate (cGMP) as well as adenosine 3',5'-cyclic monophosphate (cAMP) on preadipocytes in vitro. Preadipocytes were isolated from human subcutaneous adipose tissue, cultured until confluence, and differentiated. The NO donor diethylenetriamine (DETA)/NO (30-150 microm) was added during proliferation and differentiation. Additionally, cGMP/cAMP analogs 8-bromoguanosine 3',5'-cyclic monophosphate (8-Br-cGMP), 8-(4-chlorophenylthio)-guanosine 3',5'-cyclic monophosphate (8-pCPT-cGMP) and 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP), and the adenylyl cyclase activator forskolin, specific guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) and adenylyl cyclase inhibitor 2'-5'-dideoxyadenosine (ddA), were applied. Proliferation and differentiation were evaluated. DETA/NO in combination with the standard differentiation procedure significantly enhanced maturation of precursor cells to adipocytes. Proliferation, in contrast, was inhibited in the presence of NO. The application of cGMP and cAMP, respectively, increased pr

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.

How we grade evidence
Adenylyl Cyclase InhibitorsAdipocytesAdipogenesisAdultCell ProliferationCells, CulturedColforsinCyclic AMPCyclic GMPDDT

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