Adipose microsomal triglyceride transfer protein deficiency protects against hepatic steatosis by upregulating PPARα activity
Rajan S., Verano M., Palaia T., Prakashmurthy C., Chung J., Islam S.
Laboratory Study with a reported sample of 3, published in JHEP Rep (2025) — 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
- JHEP Rep (2025)
- Reported sample size
- 3
- Source database
- Europe PMC
- PMID
- 41321937
- PMCID
- PMC12657731
- DOI
- 10.1016/j.jhepr.2025.101549
Abstract (original English)
Background & aim Metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing health issue. Identifying factors that prevent hepatic lipid accumulation could inform new MASLD prevention or treatment strategies. We previously demonstrated that adipocyte microsomal triglyceride transfer protein (MTP) regulates intracellular lipolysis by inhibiting adipose triglyceride lipase activity. The aim of this study was to investigate the impact of adipose MTP deficiency on MASLD. Methods We used previously described adipose-specific MTP knockout (A- Mttp -/- ) mice. Fat mobilization from adipose to liver was assessed using: (1) lipidomic profiling of plasma, epididymal fat, and liver, and (2) treatment of wild-type hepatocytes with conditioned media from MTP-deficient adipocytes. Fatty acid (FA) oxidation was evaluated using 14 C-oleate. Transcriptome analysis, quantitative reverse-transcription PCR and western blotting were performed to determine gene expression. PPARα activity was assessed using a reporter assay. Results A- Mttp -/- mice on an obesogenic diet exhibited moderately elevated plasma triglyceride levels and less hepatic steatosis compared to wild-type mice (n = 3-4 per group; two-way repeated measures ANOVA p = 0.0076). Elevated plasma triglyceride levels in A- Mttp -/- mice were attributable to increased hepatic triglyceride synthesis and production of trig
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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