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. - firstname.lastname@example.org
References and acknowledgements
Supported by: FAPESP, CAPES. Acknowledgement: Prof. Alicia Kowaltowski and group (Univ Sao Paulo, Brazil).
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