β -Lapachone Regulates Obesity through Modulating Thermogenesis in Brown Adipose Tissue and Adipocytes: Role of AMPK Signaling Pathway.
Kwak HJ., Jeong MY., Um JY., Park J.
Animal Study, published in Am J Chin Med (2019) — 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
- Am J Chin Med (2019)
- Country
- Singapore
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 31094212
- DOI
- 10.1142/S0192415X19500423
Abstract (original English)
Activation of brown adipose tissue (BAT) has been proposed as a promising target against obesity due to its increased capacity for thermogenesis. In this study, we explored the effect of β -Lapachone ( β L), a compound obtained from the bark of the lapacho tree, against obesity. In vivo administration of β L into either high fat diet (HFD)-induced obese C57BL6 mice and genetically obese Lepr - ∕ - mice prevented body weight gain, which was associated with tissue weight loss of white adipose tissue (WAT). In addition, β L elevated thermogenic proteins including uncoupling protein 1 (UCP1) and mitochondrial count in BAT and human adipose tissue-derived mesenchymal stem cells (hAMSCs). β L also induced AMP-activated protein kinase (AMPK) phosphorylation, subsequent upregulation of acetyl-CoA carboxylase (ACC) and UCP1, and these effects were diminished by AMPK inhibitor compound C, suggesting that AMPK underlies the effects of β L. Mitogen-activated protein kinase pathways participated in the thermogenesis of β L, specifically p38, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase 1/2 (ERK1/2) were activated by β L treatment in hAMSCs. Additionally, inhibitors of p38/JNK/ERK1/2 abrogated the activity of β L. Taken together, β L exerts anti-obese effects by inducing thermogenesis mediated by AMPK signaling pathway, suggesting that β L may have a potential ther
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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