A novel approach towards obesity: The use of a bacterial product, gassericin A, in 3T3-L1 cells.
Taghizad F., Kazerani HR., Dehghani H., Asoodeh A., Yaghubi D.
Clinical Trial, published in Obes Res Clin Pract (2021) — summary generated from the PubMed abstract.
Several human studies show positive signals, while research methods and sample sizes continue to develop.
- 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
- Clinical Trial
- Journal
- Obes Res Clin Pract (2021)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 34474970
- DOI
- 10.1016/j.orcp.2021.08.005
Abstract (original English)
The problem of obesity and its related complications are adversely affecting human society. We studied the effects of gassericin A, a bacteriocin produced by the intestinal bacteria, on adipocyte differentiation and development. Gassericin A was purified from Lactobacillus gasseri LA39 and was added to the culture medium of 3T3-L1 cells in two phases: Phase 1, 3T3-L1 cells were incubated with gassericin A while being induced to adipocytes (days 1-7); phase 2, the cells were incubated with the bacteriocin after being induced to adipocytes (days 8-12). The resultant changes in the pattern of expression of some of the important genes involved in adipogenesis were evaluated by RT-qPCR. The viability of cells and their numbers were also studied. In phase 1 of the study, the levels of transcripts for stearoyl CoA desaturase (SCD-1), zinc finger protein 423 (zfp-423), and glucose transporter 4 (GLUT4) genes were significantly reduced, while that of 422ap2 gene showed a significant increment (p < 0.05). In phase 2, the zfp-423 gene showed a reduction of expression and the 422ap2 gene showed an increase in expression (p < 0.05). The other genes including UCP-1 and TNF-α did not show any significant changes in neither of the groups. Gassericin A did not affect the morphology or viability of the cells, however, the numbers of cells had nearly doubled in the treatment groups. It seems that
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Several human studies show positive signals, while research methods and sample sizes continue to develop.
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