Difference between revisions of "Alonso-Vale 2015 FASEB J"

Latest revision as of 14:50, 23 January 2019

Alonso-Vale MI, Cruz M, Bolsoni-Lopes A, de Sá R, Bresciani Martins de Andrade P (2015) Palmitoleic acid (C16:1n7) treatment enhances fatty acid oxidation and oxygen consumption in white adipocytes. FASEB J 29:884.25.

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Alonso-Vale MI, Cruz M, Bolsoni-Lopes A, de Sa R, Bresciani Martins de Andrade P (2015) FASEB J

Abstract: 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 16:1n7 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. To study the correlation of the previously described effects of 16:1n7 in white adipose tissue with mitochondrial function, we performed oxygen consumption experiments using the Oroboros Oxygraph-2k. Our results show that both acute and chronic treatments with 16:1n7 enhanced basal oxygen consumption in 3T3-L1 adipocytes by 7.6% and 12.8%, respectively. Experiments were also carried out to test whether lipolysis and respiration enhancement by palmitoleic acid are linked to improved mitochondrial fatty acid oxidation (FAO) and/or uncoupling. We observed an increase (~30%) in FAO by the adipocytes treated with C16:1n7. Taken together, our data suggest that the palmitoleic acid, by concerted action of stimulated lipolysis, mitochondrial FAO and oxygen consumption may contribute to enhance white adipocytes energy expenditure.

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

Labels: MiParea: Respiration

Organism: Mouse Tissue;cell: Fat Preparation: Intact cells

Regulation: Fatty acid Coupling state: ROUTINE

HRR: Oxygraph-2k

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 |year=2015
 |journal=FASEB J
-|abstract=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 16:1n7 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''. To study the correlation of the previously described effects of 16:1n7 in white adipose tissue with mitochondrial function, we performed oxygen consumption experiments using the OROBOROS Oxygraph-2k. Our results show that both acute and chronic treatments with 16:1n7 enhanced basal oxygen consumption in 3T3-L1 adipocytes by 7.6% and 12.8%, respectively. Experiments were also carried out to test whether lipolysis and respiration enhancement by palmitoleic acid are linked to improved mitochondrial fatty acid oxidation (FAO) and/or uncoupling. We observed an increase (~30%) in FAO by the adipocytes treated with C16:1n7. Taken together, our data suggest that the palmitoleic acid, by concerted action of stimulated lipolysis, mitochondrial FAO and oxygen consumption may contribute to enhance white adipocytes energy expenditure.
+|abstract=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 16:1n7 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''. To study the correlation of the previously described effects of 16:1n7 in white adipose tissue with mitochondrial function, we performed oxygen consumption experiments using the Oroboros Oxygraph-2k. Our results show that both acute and chronic treatments with 16:1n7 enhanced basal oxygen consumption in 3T3-L1 adipocytes by 7.6% and 12.8%, respectively. Experiments were also carried out to test whether lipolysis and respiration enhancement by palmitoleic acid are linked to improved mitochondrial fatty acid oxidation (FAO) and/or uncoupling. We observed an increase (~30%) in FAO by the adipocytes treated with C16:1n7. Taken together, our data suggest that the palmitoleic acid, by concerted action of stimulated lipolysis, mitochondrial FAO and oxygen consumption may contribute to enhance white adipocytes energy expenditure.
 |mipnetlab=BR Sao Paulo Bresciani Martins de Andrade P
 }}