Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMedOpen access

Macrophage beta2-adrenergic receptor is dispensable for the adipose tissue inflammation and function.

Petkevicius K., Bidault G., Virtue S., Newland SA., Dale M., Dugourd A.

Animal Study on Type 2 Diabetes, Chronic Inflammation, published in Mol Metab (2021) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

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
Read the A–D evidence level guide

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 Metab (2021)
Country
Germany
Reported sample size
—
Source database
PubMed
PMID
33774223
PMCID
PMC8086137
DOI
10.1016/j.molmet.2021.101220
Citations
20

Abstract (original English)

Objective Neuroimmune interactions between the sympathetic nervous system (SNS) and macrophages are required for the homeostasis of multiple tissues, including the adipose tissue. It has been proposed that the SNS maintains adipose tissue macrophages (ATMs) in an anti-inflammatory state via direct norepinephrine (NE) signaling to macrophages. This study aimed to investigate the physiological importance of this paradigm by utilizing a mouse model in which the adrenergic signaling from the SNS to macrophages, but not to other adipose tissue cells, was disrupted. Methods We generated a macrophage-specific B2AR knockout mouse (Adrb2 ΔLyz2 ) by crossing Adrb2 fl/fl and Lyz2 Cre/+ mice. We have previously shown that macrophages isolated from Adrb2 ΔLyz2 animals do not respond to NE stimulation in vitro. Herein we performed a metabolic phenotyping of Adrb2 ΔLyz2 mice on either chow or high-fat diet (HFD). We also assessed the adipose tissue function of Adrb2 ΔLyz2 animals during fasting and cold exposure. Finally, we transplanted Adrb2 ΔLyz2 bone marrow to low-density lipoprotein receptor (LDLR) knockout mice and investigated the development of atherosclerosis during Western diet feeding. Results We demonstrated that SNS-associated ATMs have a transcriptional profile indicative of activated beta-2 adrenergic receptor (B2AR), the main adrenergic receptor isoform in myeloid cells. Howev

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.

How we grade evidence
AdipocytesAdipose Tissue, WhiteAnimalsAtherosclerosisBone Marrow TransplantationCells, CulturedDiet, High-FatDiet, WesternDisease Models, AnimalFemale

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