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Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
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Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro

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Mammalian target of rapamycin complex 1 suppresses lipolysis, stimulates lipogenesis, and promotes fat storage

Partha Chakrabarti1, Taylor English, Jun Shi

  • 1Boston University School of Medicine, Boston, Massachusetts, USA.

Diabetes
|January 14, 2010
PubMed
Abstract

Insights

Target of rapamycin complex 1 (TORC1) promotes fat storage by inhibiting lipolysis and boosting lipogenesis in mammalian cells. This pathway is crucial for regulating triglyceride metabolism and lipid accumulation.

Area of Science:

  • Cellular metabolism
  • Molecular biology
  • Lipid biochemistry

Background:

  • Target of rapamycin complex 1 (TORC1) is a central regulator of cellular metabolism in response to nutrients and hormones.
  • The specific role of TORC1 in controlling triglyceride storage and metabolism is not well understood.

Purpose of the Study:

  • To investigate the effect of mammalian TORC1 (mTORC1) signaling on key enzymes and processes involved in triglyceride metabolism.
  • To elucidate the role of mTORC1 in regulating lipolysis, lipogenesis, and lipid storage in mammalian cells.

Main Methods:

  • Analysis of adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) expression.
  • Assessment of lipolysis and lipogenesis rates.
  • Investigation of lipid storage in various mammalian cell types (3T3-L1 adipocytes, C2C12 myoblasts, mouse embryonic fibroblasts) under mTORC1 modulation (activation via Rheb, inhibition via rapamycin/raptor knockdown, TSC2 gene ablation).

Main Results:

  • mTORC1 activation suppressed ATGL and HSL expression, reduced lipolysis, and increased de novo lipogenesis, leading to triglyceride accumulation in 3T3-L1 adipocytes.
  • mTORC1 inhibition by rapamycin or raptor knockdown stimulated lipolysis, primarily through ATGL upregulation.
  • Similar effects were observed in C2C12 myoblasts and mouse embryonic fibroblasts, where ATGL overexpression counteracted the lipogenic effects of TSC2 knockout.

Conclusions:

  • mTORC1 signaling promotes fat storage in mammalian cells.
  • This promotion occurs via the suppression of lipolysis and the stimulation of de novo lipogenesis.

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