Water-soluble extract of Pacific Krill prevents triglyceride accumulation in adipocytes by suppressing PPARγ and C/EBPα expression.
Yamada H., Ueda T., Yano A.
Animal Study, published in PLoS One (2011) — 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
- PLoS One (2011)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 21760932
- DOI
- 10.1371/journal.pone.0021952
Abstract (original English)
Pacific Krill (Euphausia pacifica) are small, red crustaceans, similar to shrimp, that flourish in the North Pacific and are eaten in Japan. We investigated the effect of a water-soluble extract of Pacific Krill on adipocytes and discovered that this extract suppressed triglyceride accumulation in adipocytes. Furthermore, the water-soluble extract of Pacific Krill suppressed the expression of two master regulators of adipocyte differentiation, peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT enhancer binding protein alpha (C/EBPα). C/EBPβ promotes PPARγ and C/EBPα expression, but the water-soluble extract of Pacific Krill did not inhibit the expression of C/EBPβ or C/EBPβ-mediated transcriptional activation. The Pacific Krill extract was more effective than a PPARγ antagonist in suppressing PPARγ and C/EBPα expression. These results indicated that the water-soluble extract of Pacific Krill was not simply a PPARγ antagonist, but that it prevented triglyceride accumulation in adipocytes by suppression of PPARγ and C/EBPα via a pathway that is independent of C/EBPβ.
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 evidenceBrowse all related research
Filter the research library by this study's title keywords, author, or publication year.