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Area of Science:

  • Cellular Metabolism
  • Lipid Metabolism
  • Mitochondrial Function

Background:

  • Basal lipolysis and re-esterification are ongoing processes in adipocytes.
  • The role of coupled lipolysis and re-esterification under basal conditions is not fully understood.
  • Re-esterification may protect against lipotoxicity during stimulated lipolysis.

Purpose of the Study:

  • To investigate the role of diacylglycerol acyltransferases (DGAT1 and DGAT2) in regulating fatty acid oxidation.
  • To determine the effect of inhibiting DGAT1 and DGAT2 on adipocyte energetics and mitochondrial function.

Main Methods:

  • Used in vitro differentiated brown and white adipocytes.
  • Employed pharmacological inhibitors of DGAT1 and DGAT2, alone and in combination.
  • Assessed cellular energetics, lipolysis flux, lipidomics, mitochondrial properties, and fuel utilization.

Main Results:

  • DGAT1 and DGAT2-mediated re-esterification modulates fatty acid oxidation.
  • Combined inhibition of DGAT1 and DGAT2 (D1+2i) increased oxygen consumption via enhanced mitochondrial respiration.
  • D1+2i promoted mitochondrial fatty acid import and activated AMP Kinase, facilitating fatty acyl-CoA entry into mitochondria.

Conclusions:

  • Re-esterification regulates mitochondrial fatty acid utilization.
  • A novel mechanism of fatty acid oxidation regulation involving crosstalk with FA re-esterification was uncovered.