Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMedOpen access

CD24 is required for regulating gene expression, but not glucose uptake, during adipogenesis.

Smith NC., Swaminathan V., Pallegar NK., Cordova C., Buchanan SC., Christian SL.

Animal Study on Stroke Research, published in Adipocyte (2018) — 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
Read the A–D evidence level guide

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
Adipocyte (2018)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
30231671
PMCID
PMC6768182
DOI
10.1080/21623945.2018.1525251
Citations
3

Abstract (original English)

Adipose tissue dysfunction in obesity and lipodystrophy results in major health complications such as heart disease and stroke, and is associated with an increased risk of some cancers. We have previously found that the cell surface receptor CD24 regulates adipogenesis as measured by lipid accumulation and gene expression in mature adipocytes. How CD24 regulates these processes remains unknown. To begin answering this question, we first determined that CD24 does not affect glucose uptake in differentiating adipocytes in vitro. We then examined changes in global gene expression via DNA microarray in 3T3-L1 adipocytes with siRNA-mediated knock-down of CD24 expression. We found that CD24 expression is necessary for upregulation of up to 134 genes. We validated the CD24-mediated regulation of 4 of these genes during in vitro adipogenesis of 3T3-L1 and primary cells isolated from the inguinal white adipose tissue depots of CD24 knockout mice. Surprisingly, we found that only 1 of these genes was also regulated by CD24 in cells from the epididymal depot. Overall, these data suggest that CD24 is necessary for select gene expression in a depot-specific manner during adipogenesis in vitro. These findings could help elucidate the mechanisms regulating lipid accumulation in adipocytes thereby aiding in the development of novel treatment strategies for obesity and lipodystophy.

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
3T3-L1 CellsAdipocytesAdipogenesisAdipose Tissue, WhiteAnimalsCD24 AntigenCells, CulturedGene Expression RegulationGlucoseLipid Metabolism

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