Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

The nuclear retinoid-related orphan receptor RORα controls circadian thermogenic programming in white fat depots

Monnier C., Auclair M., Le Cam G., Garcia MP., Antoine B.

Animal Study, published in Physiol Rep (2018) — 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
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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
Physiol Rep (2018)
Reported sample size
—
Source database
Europe PMC
PMID
29673115
PMCID
PMC5907938
DOI
10.14814/phy2.13678
Citations
17

Abstract (original English)

The RORα-deficient staggerer (sg/sg) mouse is lean and resistant to diet-induced obesity. Its thermogenic activity was shown to be increased not only in brown adipose tissue (BAT), but also in subcutaneous white adipose tissue (WAT) where UCP1 content was enhanced, however, without Prdm16 coexpression. Our observation of partial multilocular lipid morphology of WAT in sg/sg mice both in the inguinal and perigonadal sites led us to focus on the phenotype of both fat depots. Because RORα is a nuclear factor acting in the clock machinery, we looked at the circadian expression profile of genes involved in thermogenesis and browning in WAT and BAT depots of sg/sg and WT mice, through real-time quantitative PCR and western blotting. This 24-h period approach revealed both a rhythmic expression of thermogenic genes in WAT and an increased browning of all the WAT depots tested in sg/sg mice that indeed involved the canonical browning process (through induction of Pgc-1α and Prdm16). This was associated with an enhanced isoproterenol-induced oxygen consumption rate of WAT explants from sg/sg mice, which was reproducible in WT explants by treatment with a RORα inverse agonist SR 3335, that induced a parallel increase in the UCP1 protein. Inhibitors of browning differentiation, such as TLE3 and RIP140, could be new targets of RORα that would be rather implicated in the whitening of adipoc

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
AdipocytesAnimalsMice, KnockoutMiceEnergy MetabolismThermogenesisCircadian RhythmAdipose Tissue, WhiteNuclear Receptor Subfamily 1, Group F, Member 1

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