The role of tauroursodeoxycholic acid on adipogenesis of human adipose-derived stem cells by modulation of ER stress.
Cha BH., Kim JS., Ahn JC., Kim HC., Kim BS., Han DK.
Animal Study, published in Biomaterials (2014) — 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
- Biomaterials (2014)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 24424209
- DOI
- 10.1016/j.biomaterials.2013.12.067
- Citations
- 39
Abstract (original English)
Obesity has become a serious public health problem in the developed world. Increased mass of adipose tissue in the obese is due to an increase in both the size (hypertrophy) and number (hyperplasia) of adipocytes. The chemical chaperone tauroursodeoxycholic acid (TUDCA) not only decreases endoplasmic reticulum (ER) stress, but also plays a role as a leptin-sensitizing agent for preadipocytes in mice and humans. In this study, we examine whether TUDCA has an effect on adipogenesis from human adipose-derived stem cells (hASCs). Therefore, the effect of TUDCA on ER stress, lipid accumulation, and adipogenic differentiation from hASCs was investigated using histological staining, reverse-transcriptase polymerase chain reaction (RT-PCR), and western blotting in vitro. It was found that TUDCA treatment of hASCs significantly decreases the representative ER stress marker (glucose-regulated protein 78 kDa (GRP78)), adipogenic markers (peroxisome proliferator-activated receptor gamma (PPARγ) and glycerol-3-phosphate dehydrogenase 1 (GPDH)), and lipid accumulation. Furthermore, we confirmed that TUDCA treatment of hASCs significantly decreased in vivo adipogenic tissue formation and ER stress comparing with PBS treatment of hASCs. The results indicate that TUDCA plays a critical role in adipogenesis from hASCs by modulating ER stress and, therefore, has potential pharmacologic and therap
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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