Collagen-specific molecular chaperone Hsp47 in inguinal white adipose tissue promotes high-fat diet-induced inflammatory gene expression in male mice
Ito S., Kamei R., Kasai A., Nagata K.
Animal Study on Systemic / IV, published in Sci Rep (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
- Sci Rep (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41862663
- PMCID
- PMC13144313
- DOI
- 10.1038/s41598-026-45003-4
Abstract (original English)
A chronic high-fat diet (HFD) leads to obesity through a process involving adipocyte hypertrophy, hyperplasia, induction of pro-inflammatory gene expression, and ultimately fibrosis that impairs systemic health. Adipocytes are surrounded by an extracellular matrix (ECM) containing collagen. The interaction between adipocytes and the ECM regulates adipocyte turnover under both physiological and HFD conditions. Previous studies have shown that the collagen-specific molecular chaperone Hsp47 (SerpinH1) increases with overfeeding and decreases with short-term fasting. Hsp47 affects adipocyte size through collagen-integrin interactions. However, the long-term contribution of Hsp47 under chronic HFD conditions remains unclear, particularly whether there are depot-specific differences between subcutaneous inguinal white adipose tissue (ingWAT) and visceral epididymal white adipose tissue (epiWAT). In this study, mice fed an HFD for 12 weeks exhibited increased Hsp47 mRNA and protein specifically in adipose tissue. Adipocyte-specific Hsp47 knockout (aKO) mice exhibited reduced adipocyte size and decreased fibrosis markers and pro-inflammatory gene expression, specifically in ingWAT, with minimal impact in epiWAT. Serum analysis revealed that the metabolic deterioration induced by an HFD was alleviated in Hsp47 aKO mice. These results suggest that increased Hsp47 in ingWAT during an HFD
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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