Level C· Early human research exploring benefitsCohort StudyEurope PMCOpen access

Oncostatin M suppresses browning of white adipocytes via gp130-STAT3 signaling

van Krieken PP., Odermatt TS., Borsigova M., Blüher M., Wueest S., Konrad D.

Cohort Study with a reported sample of 66, published in Mol Metab (2021) — summary generated from the PubMed abstract.

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Level C· Early human research exploring benefitsEvidence level of this study

Early human evidence such as case series or small samples is exploring possible benefits.

  • 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
Cohort Study
Journal
Mol Metab (2021)
Reported sample size
66
Source database
Europe PMC
PMID
34547509
PMCID
PMC8502775
DOI
10.1016/j.molmet.2021.101341
Citations
9

Abstract (original English)

Objective Obesity is associated with low-grade adipose tissue inflammation and locally elevated levels of several glycoprotein 130 (gp130) cytokines. The conversion of white into brown-like adipocytes (browning) may increase energy expenditure and revert the positive energy balance that underlies obesity. Although different gp130 cytokines and their downstream targets were shown to regulate expression of the key browning marker uncoupling protein 1 (Ucp1), it remains largely unknown how this contributes to the development and maintenance of obesity. Herein, we aim to study the role of gp130 cytokine signaling in white adipose tissue (WAT) browning in the obese state. Methods Protein and gene expression levels of UCP1 and other thermogenic markers were assessed in a subcutaneous adipocyte cell line, adipose tissue depots from control or adipocyte-specific gp130 knockout (gp130 Δadipo ) mice fed either chow or a high-fat diet (HFD), or subcutaneous WAT biopsies from a human cohort of lean and obese subjects. WAT browning was modeled in vitro by exposing mature adipocytes to isoproterenol after stimulation with gp130 cytokines. ERK and JAK-STAT signaling were blocked using the inhibitors U0126 and Tofacitinib, respectively. Results Inguinal WAT of HFD-fed gp130 Δadipo mice exhibited significantly elevated levels of UCP1 and other browning markers such as Cidea and Pgc-1α. In vitro

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

How we grade evidence
Cells, Cultured3T3-L1 CellsAnimalsHumansMiceMaleSTAT3 Transcription FactorCytokine Receptor gp130Oncostatin MAdipocytes, White

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