Bresciani Martins de Andrade 2014 Abstract MiP2014
|Mitochondrial function in white adipose tissue: palmitoleic acid (C16:1n7) treatment enhances white adipocyte oxygen consumption.|
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 . 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 . 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: F HRR: Oxygraph-2k Event: A4, Oral MiP2014
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. - email@example.com
References and acknowledgements
Supported by: FAPESP, CAPES. Acknowledgement: Prof. Alicia Kowaltowski and group (Univ Sao Paulo, Brazil).
- 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.
- 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.
- 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.
- 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.