Proteasome activity correlates with male BMI and contributes to the differentiation of adipocyte in hADSC.
Sakamoto K., Sato Y., Sei M., Ewis AA., Nakahori Y.
Laboratory Study with a reported sample of 61, published in Endocrine (2010) — 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
- Laboratory Study
- Journal
- Endocrine (2010)
- Country
- United States
- Reported sample size
- 61
- Source database
- PubMed
- PMID
- 20960262
- DOI
- 10.1007/s12020-009-9298-4
Abstract (original English)
We have previously reported that 26S proteasome subunit mRNA expressions correlate with male body mass index (BMI). In this study, to investigate whether proteasome activities are correlated with BMI, we recruited 61 healthy young Japanese male subjects, measured proteasome activities in their plasma, and correlated them with their BMI and various metabolic factors. We found that among three different proteasome activities, chymotrypsin-like activity in plasma was positively correlated with BMI in healthy Japanese male subjects. Furthermore, we analyzed proteasome activity in vitro during the differentiation of human adipose-derived stem cell (hADSC) into mature adipocytes. In the early stage of differentiation, proteasome activity was at its highest level, and proteasome inhibitor could inhibit hADSC adipocyte differentiation. Our findings suggest that proteasome is an important controlling factor for the development of obesity and adipogenesis.
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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