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Related Experiment Video

Updated: Mar 30, 2026

Quantitative Determination of De Novo Fatty Acid Synthesis in Brown Adipose Tissue Using Deuterium Oxide
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Sugar Makes Fat by Talking to SCAP.

Wei Shao1, Peter J Espenshade1

  • 1Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

Cancer Cell
|November 12, 2015
PubMed
Summary

High blood glucose fuels fat production by activating sterol regulatory element-binding protein (SREBP) transcription factors. This study reveals glucose stabilizes SCAP, a key SREBP pathway regulator, in tumors.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Elevated blood glucose is linked to increased lipogenesis (fat synthesis).
  • Tumors demonstrate heightened glucose uptake and lipogenesis, yet the underlying mechanisms remain unclear.
  • Sterol regulatory element-binding proteins (SREBP) are key transcription factors regulating lipogenesis.

Purpose of the Study:

  • To elucidate the mechanisms by which glucose regulates lipogenesis in cancer.
  • To investigate the role of SREBP transcription factors and their regulators in tumor-associated lipogenesis.

Main Methods:

  • Analysis of SREBP pathway activation in cancer cells.
  • Investigation of the interaction between glucose, SCAP, and SREBP.
  • Cellular and molecular biology techniques to assess lipogenesis.

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Last Updated: Mar 30, 2026

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Main Results:

  • Glucose directly activates SREBP transcription factors, promoting lipogenesis.
  • The study identifies SCAP (SREBP cleavage-activating protein) as a critical mediator.
  • Glucose stabilizes SCAP, thereby enhancing SREBP activity and lipogenesis.

Conclusions:

  • Glucose-induced stabilization of SCAP is a key mechanism driving lipogenesis in tumors.
  • Targeting the glucose-SCAP-SREBP axis may offer novel therapeutic strategies for cancer.
  • Understanding this pathway provides insights into metabolic reprogramming in cancer.