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Eynaudi A, Díaz-Castro F, Bórquez JC, et al. Differential Effects of Oleic and Palmitic Acids on Lipid Droplet-Mitochondria Interaction in the Hepatic Cell Line HepG2. Front Nutr. 2021;8:775382doi: 10.3389/fnut.2021.775382.
Eynaudi, A., Díaz-Castro, F., Bórquez, J. C., Bravo-Sagua, R., Parra, V., & Troncoso, R. (2021). Differential Effects of Oleic and Palmitic Acids on Lipid Droplet-Mitochondria Interaction in the Hepatic Cell Line HepG2. Frontiers in nutrition, 8775382. https://doi.org/10.3389/fnut.2021.775382
Eynaudi, Andrea, et al. "Differential Effects of Oleic and Palmitic Acids on Lipid Droplet-Mitochondria Interaction in the Hepatic Cell Line HepG2." Frontiers in nutrition vol. 8 (2021): 775382. doi: https://doi.org/10.3389/fnut.2021.775382
Eynaudi A, Díaz-Castro F, Bórquez JC, Bravo-Sagua R, Parra V, Troncoso R. Differential Effects of Oleic and Palmitic Acids on Lipid Droplet-Mitochondria Interaction in the Hepatic Cell Line HepG2. Front Nutr. 2021 Nov 12;8:775382. doi: 10.3389/fnut.2021.775382. eCollection 2021. PMID: 34869541; PMCID: PMC8632770.
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Front Nutr. 2021 Nov 12;8:775382. doi: 10.3389/fnut.2021.775382. eCollection 2021.

Differential Effects of Oleic and Palmitic Acids on Lipid Droplet-Mitochondria Interaction in the Hepatic Cell Line HepG2.

Frontiers in nutrition

Andrea Eynaudi, Francisco Díaz-Castro, Juan Carlos Bórquez, Roberto Bravo-Sagua, Valentina Parra, Rodrigo Troncoso

Affiliations

  1. Laboratorio de Investigación en Nutrición y Actividad Física (LABINAF), Instituto de Nutrición y Tecnología de los Alimentos (INTA), Universidad de Chile, Santiago, Chile.
  2. Laboratorio de Obesidad y Metabolismo Energético (OMEGA), Instituto de Nutrición y Tecnología de los Alimentos (INTA), Universidad de Chile, Santiago, Chile.
  3. Advanced Center for Chronic Diseases (ACCDiS), Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile.
  4. Red de Investigación en Envejecimiento Saludable, Consorcio de Universidades del Estado de Chile, Santiago, Chile.
  5. Red Para el Estudio de Enfermedades Cardiopulmonares de Alta Letalidad (REECPAL), Universidad de Chile, Santiago, Chile.

PMID: 34869541 PMCID: PMC8632770 DOI: 10.3389/fnut.2021.775382

Abstract

Fatty acid overload, either of the saturated palmitic acid (PA) or the unsaturated oleic acid (OA), causes triglyceride accumulation into specialized organelles termed lipid droplets (LD). However, only PA overload leads to liver damage mediated by mitochondrial dysfunction. Whether these divergent outcomes stem from differential effects of PA and OA on LD and mitochondria joint dynamics remains to be uncovered. Here, we contrast how both fatty acids impact the morphology and interaction between both organelles and mitochondrial bioenergetics in HepG2 cells. Using confocal microscopy, we showed that short-term (2-24 h) OA overload promotes more and bigger LD accumulation than PA. Oxygen polarography indicated that both treatments stimulated mitochondrial respiration; however, OA favored an overall build-up of the mitochondrial potential, and PA evoked mitochondrial fragmentation, concomitant with an ATP-oriented metabolism. Even though PA-induced a lesser increase in LD-mitochondria proximity than OA, those LD associated with highly active mitochondria suggest that they interact mainly to fuel fatty acid oxidation and ATP synthesis (that is, metabolically "active" LD). On the contrary, OA overload seemingly stimulated LD-mitochondria interaction mainly for LD growth (thus metabolically "passive" LDs). In sum, these differences point out that OA readily accumulates in LD, likely reducing their toxicity, while PA preferably stimulates mitochondrial oxidative metabolism, which may contribute to liver damage progression.

Copyright © 2021 Eynaudi, Díaz-Castro, Bórquez, Bravo-Sagua, Parra and Troncoso.

Keywords: fatty acids; hepatocytes; lipid droplets; mitochondria; oxygen consumption

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

References

  1. Cell Metab. 2017 Mar 7;25(3):686-697 - PubMed
  2. Circ Res. 2018 Mar 16;122(6):e20-e33 - PubMed
  3. EMBO Rep. 2017 Jul;18(7):1123-1138 - PubMed
  4. Life Sci. 2018 Jun 15;203:291-304 - PubMed
  5. Biochim Biophys Acta. 2015 May;1853(5):918-28 - PubMed
  6. Mol Endocrinol. 2015 Oct;29(10):1414-25 - PubMed
  7. J Bioenerg Biomembr. 2011 Feb;43(1):47-51 - PubMed
  8. J Physiol. 2016 Feb 1;594(3):509-25 - PubMed
  9. Ann Nutr Metab. 2009;55(1-3):5-7 - PubMed
  10. J Mol Cell Cardiol. 2015 Sep;86:62-74 - PubMed
  11. Diabetes. 2014 Jan;63(1):75-88 - PubMed
  12. EMBO J. 2011 Oct 07;30(21):4371-86 - PubMed
  13. J Lipid Res. 2013 Apr;54(4):953-65 - PubMed
  14. EMBO Rep. 2017 Jul;18(7):1039-1040 - PubMed
  15. Proc Natl Acad Sci U S A. 2003 Mar 18;100(6):3077-82 - PubMed
  16. Trends Endocrinol Metab. 2015 Mar;26(3):144-52 - PubMed
  17. Nat Commun. 2015 May 27;6:7176 - PubMed
  18. Nat Cell Biol. 2018 Jul;20(7):755-765 - PubMed
  19. EMBO J. 2017 Jun 1;36(11):1543-1558 - PubMed
  20. J Physiol. 2019 Mar;597(6):1565-1584 - PubMed
  21. Hepatology. 2019 Jun;69(6):2672-2682 - PubMed
  22. Front Physiol. 2021 Jun 15;12:670753 - PubMed
  23. Sci Rep. 2016 Nov 03;6:36394 - PubMed
  24. Cell Metab. 2018 Apr 3;27(4):869-885.e6 - PubMed
  25. Front Physiol. 2014 Jul 31;5:282 - PubMed
  26. Nat Rev Mol Cell Biol. 2019 Mar;20(3):137-155 - PubMed
  27. Expert Rev Gastroenterol Hepatol. 2019 Sep;13(9):849-866 - PubMed
  28. Semin Cell Dev Biol. 2020 Dec;108:33-46 - PubMed
  29. Lancet. 2005 Oct 1;366(9492):1197-209 - PubMed
  30. Diabetes. 2001 Aug;50(8):1771-7 - PubMed
  31. Int Rev Cell Mol Biol. 2018;337:83-110 - PubMed
  32. Trends Cell Biol. 2021 May;31(5):345-358 - PubMed
  33. Dev Cell. 2015 Mar 23;32(6):678-92 - PubMed
  34. J Gastroenterol Hepatol. 2009 May;24(5):830-40 - PubMed
  35. Physiol Res. 2015;64(Suppl 5):S627-36 - PubMed
  36. Biochim Biophys Acta. 2013 Aug;1832(8):1334-44 - PubMed
  37. Adv Exp Med Biol. 2012;748:13-40 - PubMed
  38. Mol Cell. 2019 Dec 5;76(5):811-825.e14 - PubMed
  39. Biochem J. 2011 Apr 15;435(2):297-312 - PubMed
  40. Cell Metab. 2019 Apr 2;29(4):827-835 - PubMed
  41. World J Gastroenterol. 2008 Jan 14;14(2):193-9 - PubMed
  42. Biochem Pharmacol. 2014 Oct 1;91(3):323-36 - PubMed
  43. J Physiol. 2016 Jun 1;594(11):3061-77 - PubMed
  44. Cell Death Differ. 2019 Jul;26(7):1195-1212 - PubMed
  45. EMBO J. 2018 Jun 15;37(12): - PubMed
  46. Cell Death Differ. 2017 Dec;24(12):1999-2012 - PubMed
  47. Exp Cell Res. 2017 May 15;354(2):85-94 - PubMed
  48. Mol Nutr Food Res. 2021 Jan;65(1):e1900942 - PubMed
  49. Am J Physiol Regul Integr Comp Physiol. 2007 Mar;292(3):R1271-8 - PubMed
  50. J Lipid Res. 2011 Dec;52(12):2159-2168 - PubMed
  51. Diabetes. 2019 Mar;68(3):543-555 - PubMed
  52. J Microsc. 1993 Mar;169(3):375-382 - PubMed

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