Involvement of acetyl-CoA-producing enzymes in the deterioration of the functional potential of adipose-derived multipotent cells from subjects with metabolic syndrome.
Oliva-Olivera W., Lhamyani S., Coín-Aragüez L., Alcaide-Torres J., Cardona F., El Bekay R.
Prospective Study on Hip, published in Metabolism (2018) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- 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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- Study type
- Prospective Study
- Journal
- Metabolism (2018)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 30172756
- DOI
- 10.1016/j.metabol.2018.08.004
Abstract (original English)
The expansion capacity of white adipose tissue influences the distribution of fat depots in the body, the visceral accumulation of which is linked to metabolic syndrome, regardless of the degree of obesity of the subjects. Alterations in the adipose tissue-derived mesenchymal stem cells (ASCs) may contribute to the adipose tissue remodeling associated with metabolic syndrome and impact the regional distribution of adipose tissue by generating inherently dysfunctional adipocytes. Here we examine the expression levels of acetyl-CoA-producing enzymes and their relationship with the lipogenic, antioxidant and oxidative potential of adipocytes generated from visceral ASCs (adipo-visASCs) and subcutaneous ASCs (adipo-subASCs) from subjects with different metabolic profiles. Paired samples of visceral and subcutaneous adipose tissue were processed to isolate the respective ASCs from normal-weight (Nw) subjects and obese patients with metabolic syndrome (METS) and without METS (NonMETS). qPCR was used to quantify the expression levels of the genes studied in both adipo-ASCs from the patient groups and those generated after silencing by small interfering RNA of acetyl-CoA-producing enzymes. The accumulation of lipids was quantified by absorbance. No significant differences in cell yield or CD34 + CD31 - CD45 - ASC percentage were observed between the different patient groups. Unlike adi
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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