Bresciani Martins de Andrade 2014 Abstract MiP2014

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Mitochondrial function in white adipose tissue: palmitoleic acid (C16:1n7) treatment enhances white adipocyte oxygen consumption.
Link:
Bresciani Martins de Andrade P
Mitochondr Physiol Network 19.13 - MiP2014

Cruz MM, Bolsoni-Lopes A, Curi R, Pithon-Curi TC, Alonso-Vale MI, Bresciani Martins de Andrade P (2014)

Event: MiP2014

White adipose tissue (WAT) has a crucial role in the development of obesity and related diseases, and the relevance of WAT mitochondrial function has been highlighted in the literature during the last decade [1,2,4]. Mitochondrial parameters, such as reactive oxygen species, biogenesis, fatty acid oxidation, respiration and uncoupling have been implicated in white adipocyte proliferation, adipogenesis, transdifferentiation, lipolysis and lipogenesis [1,2,4]. Therefore, WAT mitochondria function regulation is a promising target for the development of therapies tackling insulin resistance, obesity and related diseases. Palmitoleic acid is a monounsaturated n-7 fatty acid (16:1n7), produced and released by adipocytes, that has been shown to enhance whole body glucose disposal, to attenuate high-fat-fed mice hepatic steatosis, to protect pancreatic beta-cells from palmitic acid-induced death and to improve circulating lipid profile in both rodents and humans [3]. Our group has recently found strong evidence that palmitoleic acid is an important positive modulator of white adipocyte lipolysis and the content of the major lipases ATGL and HSL through a PPAR alpha-dependent mechanism in vitro and in vivo. Acute and chronic palmitoleic treatment led to enhanced lipolysis and inhibited lipogenesis [3]. To study the correlation of the previously described effects of palmitoleic acid in WAT with mitochondrial function, we performed oxygen consumption experiments using the Oroboros Oxygraph-2k. Our results show that both acute and chronic treatments with palmitoleic acid enhanced basal oxygen consumption in 3T3-L1 adipocytes by 7.6% and 12.8%, respectively. Experiments were carried out to test whether lipolysis and respiration enhancement by palmitoleic acid are linked to improved mitochondrial fatty acid oxidation and/or uncoupling.


O2k-Network Lab: BR Sao Paulo Bresciani Martins de Andrade P


Labels: MiParea: Respiration  Pathology: Diabetes, Obesity 


Tissue;cell: Fat  Preparation: Intact cells 

Regulation: Fatty acid 

Pathway:HRR: Oxygraph-2k  Event: A4, Oral  MiP2014 

Affiliation

1-Dep Biol Sc, Inst Environm Sc, Chem Pharmac, Federal Univ São Paulo, Diadema; 2-Dep Physiol Biophysics, Inst Biomed Sc, Univ Sao Paulo; 3-Inst Physical Activ Sc and Sport, Cruzeiro do Sul Univ Sao Paulo; Brazil. - paulabre@yahoo.com

References and acknowledgements

Supported by: FAPESP, CAPES. Acknowledgement: Prof. Alicia Kowaltowski and group (Univ Sao Paulo, Brazil).

  1. De Pauw A, Tejerina S, Raes M, Keijer J, Arnould T (2009) Mitochondrial (dys)function in adipocyte (de)differentiation and systemic metabolic alterations. Am J Pathol 175: 927-39.
  2. Forner F, Kumar C, Luber CA, Fromme T, Klingenspor M, Mann M (2009) Proteome differences between brown and white fat mitochondria reveal specialized metabolic functions. Cell Metab 4: 324-35.
  3. Bolsoni-Lopes A, Festuccia WT, Farias TS, Chimin P, Torres-Leal FL, Derogis PB, de Andrade PB, Miyamoto S, Lima FB, Curi R, Alonso-Vale MI (2013) Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPARalpha-dependent manner. Am J Physiol Endocrinol Metab 305: E1093-102.
  4. Shen W, Liu K, Tian C, Yang L, Li X, Ren J, Packer L, Cotman CW, Liu J (2008) R-α- Lipoic acid and acetyl-L-carnitine complementarily promote mitochondrial biogenesis in murine 3T3-L1 adipocytes. Diabetologia 51: 165–74.