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Related Concept Videos

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Related Experiment Video

Updated: Apr 8, 2026

Author Spotlight: Semi-Automated Isolation of the Stromal Vascular Fraction from Murine White Adipose Tissue Using a Tissue Dissociator
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Mesoderm-specific transcript (MEST) is a negative regulator of human adipocyte differentiation.

M Karbiener1, C Glantschnig2,3,4, D F Pisani5,6,7

  • 1Department of Phoniatrics, ENT University Hospital, Medical University Graz, Graz, Austria.

International Journal of Obesity (2005)
|June 30, 2015
PubMed
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Mesoderm-specific transcript (MEST) inhibits human fat cell formation, unlike in mice. Lowering MEST boosts adipogenesis by activating key metabolic pathways and transcription factors, offering new insights into obesity.

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Area of Science:

  • Metabolic research
  • Adipose tissue biology
  • Obesity pathogenesis

Background:

  • Obesity-related diseases are linked to molecular changes in white adipose tissue (WAT).
  • Excessive adipocyte expansion can be counteracted by increasing adipocyte recruitment (adipogenesis).
  • Mesoderm-specific transcript (MEST) correlates with adiposity and adipocyte size in mice.

Purpose of the Study:

  • To characterize MEST expression and function in human white adipose tissue and adipogenesis.
  • To investigate the role of MEST in human adipocyte differentiation.

Main Methods:

  • Analysis of human WAT samples.
  • In vitro adipogenesis model using human multipotent adipose-derived stem cells.
  • MEST gene knockdown and overexpression experiments.
  • Measurement of MEST mRNA and protein levels.
  • Analysis of key signaling pathways (PPAR, CREB, ATF1) and metabolic processes.

Main Results:

  • MEST levels increase during human adipocyte differentiation and are higher in obese individuals, correlating with adipocyte volume.
  • MEST knockdown enhances human adipogenesis, promoting PPAR signaling, glycolysis, and fatty acid biosynthesis.
  • MEST overexpression impairs adipogenesis.
  • MEST silencing replaces the need for IBMX in inducing adipogenesis.
  • MEST knockdown significantly increases phosphorylation of CREB and ATF1.

Conclusions:

  • MEST acts as an inhibitor of human adipogenesis, contrasting with findings in murine models.
  • A novel link between MEST and the CREB/ATF1 pathway in metabolic regulation is established.
  • These findings have potential relevance for understanding and treating obesity-associated diseases.