Oligomeric peptides LLRLTDL and GYALPCDCL alleviate obesity through HO-1/Nrf2-dependent pathways in high-fat diet-induced mice.
Marasinghe CK., Dayarathne LA., Suryaningtyas IT., Jasmadi, Je JY.
Animal Study on Chronic Inflammation, published in J Nutr Biochem (2026) — 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
- J Nutr Biochem (2026)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41921669
- DOI
- 10.1016/j.jnutbio.2026.110360
Abstract (original English)
The potential antiobesity, anti-inflammatory, and antioxidative stress properties of ark shell-derived LLRLTDL (Bu1) and GYALPCDCL (Bu2) peptides were comprehensively investigated. In bone marrow-derived mesenchymal stem cells, both peptides demonstrated significant antiadipogenic effects by downregulating key adipogenic transcription factors, including peroxisome proliferator-activated receptor gamma, CCAAT/enhancer-binding protein alpha, and sterol regulatory element-binding protein 1 and their downstream adipocyte-specific genes, including adipocyte fatty acid-binding protein 2, fatty acid synthase, and lipoprotein lipase. Mechanistically, Bu1 and Bu2 promoted lipolysis through the activation of AMP-activated protein kinase and hormone-sensitive lipase. These peptides also exhibited potent antioxidative stress activity by suppressing reactive oxygen species generation and activating the heme oxygenase-1/Nrf2 signaling pathway, as confirmed through heme oxygenase-1 small interfering RNA silencing. In addition, Bu1 and Bu2 demonstrated robust anti-inflammatory effects by reducing proinflammatory cytokine production and inhibiting mitogen-activated protein kinase signaling pathways. These findings were corroborated in a high-fat diet-induced mouse model, where oral administration of Bu1 and Bu2 resulted in significant reductions in body weight, weight gain, and adipose tissue a
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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