Loss of myeloid lipoprotein lipase exacerbates adipose tissue fibrosis with collagen VI deposition and hyperlipidemia in leptin-deficient obese mice
Takahashi M., Yamamuro D., Wakabayashi T., Takei A., Takei S., Nagashima S.
Animal Study, published in J Biol Chem (2022) — 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 Biol Chem (2022)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 35926714
- PMCID
- PMC9440390
- DOI
- 10.1016/j.jbc.2022.102322
- Citations
- 3
Abstract (original English)
During obesity, tissue macrophages increase in number and become proinflammatory, thereby contributing to metabolic dysfunction. Lipoprotein lipase (LPL), which hydrolyzes triglyceride in lipoproteins, is secreted by macrophages. However, the role of macrophage-derived LPL in adipose tissue remodeling and lipoprotein metabolism is largely unknown. To clarify these issues, we crossed leptin-deficient Lep ob/ob mice with mice lacking the Lpl gene in myeloid cells (Lpl m-/m- ) to generate Lpl m-/m- ;Lep ob/ob mice. We found the weight of perigonadal white adipose tissue (WAT) was increased in Lpl m-/m- ;Lep ob/ob mice compared with Lep ob/ob mice due to substantial accumulation of both adipose tissue macrophages and collagen that surrounded necrotic adipocytes. In the fibrotic epidydimal WAT of Lpl m-/m- ;Lep ob/ob mice, we observed an increase in collagen VI and high mobility group box 1, while α-smooth muscle cell actin, a marker of myofibroblasts, was almost undetectable, suggesting that the adipocytes were the major source of the collagens. Furthermore, the adipose tissue macrophages from Lpl m-/m- ;Lep ob/ob mice showed increased expression of genes related to fibrosis and inflammation. In addition, we determined Lpl m-/m- ;Lep ob/ob mice were more hypertriglyceridemic than Lep ob/ob mice. Lpl m-/m- ;Lep ob/ob mice also showed slower weight gain than Lep ob/ob mice, which was
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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