Nutritionally Derived Metabolic Cues Typical of the Obese Microenvironment Increase Cholesterol Efflux Capacity of Adipose Tissue Macrophages
O'Reilly ME., Kajani S., Ralston JC., Lenighan YM., Roche HM., McGillicuddy FC.
Animal Study, published in Mol Nutr Food Res (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
- Mol Nutr Food Res (2019)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 30411491
- PMCID
- PMC6492173
- DOI
- 10.1002/mnfr.201800713
- Citations
- 14
Abstract (original English)
Background Cholesterol retention within plasma membranes of macrophages is associated with increased inflammatory signaling. Cholesterol efflux via the transporters ABCA1, ABCG1, and SR-BI to high-density lipoprotein (HDL) particles is a critical mechanism to maintain cellular cholesterol homeostasis. Little is known about the impact of the obese microenvironment on cholesterol efflux capacity (CEC) of macrophages. In this study, the CEC of obese-derived primary adipose-tissue macrophages (ATM) is evaluated and the in vivo microenvironment is modeled in vitro to determine mechanisms underlying modulated CEC. Materials and methods F4/80 + ATM are labeled with 3 H-cholesterol ex vivo, and CEC and ABCA1/ABCG1 protein levels are determined. Total, ABCA1-dependent, and ABCA1-independent CECs are determined in J774 macrophages polarized to M1 (LPS&IFNγ), M2 (IL-4&IL-13), or metabolic phenotypes (glucose, insulin, and palmitic acid). Results Obese ATM exhibit enhanced CEC and ABCA1 and ABCG1 expression compared to lean ATM. In contrast, ABCA1-CEC is suppressed from M1 polarized macrophages compared to untreated in vitro, by activation of the JAK/STAT pathway. Incubation of macrophages in vitro in high glucose augments cAMP-induced ABCA1 protein expression and ABCA1-CEC. Conclusions These novel findings demonstrate remarkable plasticity of macrophages to respond to their environment wi
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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