We are analyzing https://link.springer.com/article/10.1007/bf03174067.

Title:
Effects of eicosapentaenoic acid (EPA) on adiponectin gene expression and secretion in primary cultured rat adipocytes | Journal of Physiology and Biochemistry
Description:
Adiponectin, a hormone produced by adipocytes, is involved in glucose metabolism and insulin sensitivity. The production of this adipokine is impaired in obesity and insulin resistance. Eicosapentaenoic acid (EPA) is a dietary n-3 polyunsaturated fatty acid that improves insulin sensitivity in several models of obesity and diabetes, which has been suggested to be related to adiponectin induction. An increase in adiponectin production has been also associated with an up-regulation of the transcriptional factor PPARγ. The aim of this trial was to evaluate the direct effects of EPA on adiponectin gene expression and protein secretion in isolated rat adipocytes as well as to explore the potential mechanisms involved. A comparative study with troglitazone, a PPARγ agonist, was also performed. For these purposes, primary rat adipocytes were cultured with EPA (100 and 200 μM) and with troglitazone (10 μM) for 96 hours. Both EPA and troglitazone improved glucose utilization by adipocytes. As expected, troglitazone enhanced adiponectin secretion and increased PPARγ gene expression. However, EPA significantly decreased adiponectin gene expression and protein secretion and reduced PPARγ mRNA levels, suggesting that the inhibition of adiponectin by EPA is likely to be secondary to the down-regulation of this adipogenic transcription factor. Moreover, these results suggest that other mechanisms different from the direct stimulation of adiponectin by the fatty acid are underlying the insulin-sensitizing properties observed after EPA treatment in vivo.
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Topics {✒️}

sobre la expresión el ácido eicosapentaenoico month download article/chapter agonista de pparγ adipogenic transcription factor transcriptional factor pparγ insulin-sensitizing properties observed situaciones de obesidad primary rat adipocytes con troglitazona por otra parte van de casteele mejora la sensibilidad isolated rat adipocytes full article pdf adiponectin gene expression privacy choices/manage cookies se ha sugerido se ha observado la sensibilidad improves insulin sensitivity article lorente-cebrián june 2006 volume 62 european economic area scope submit manuscript pparγ agonist estos hallazgos sugieren pparγ agonists check access instant access conditions privacy policy related subjects fatty acid article journal insulin resistance accepting optional cookies vitro mechanistic approach article log journal finder publish epa treatment author correspondence insulin sensitivity pérez-echarri potential mechanisms involved article cite pérez-matute se realizó lipid res adiponectin induction adipocytes

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         description:Adiponectin, a hormone produced by adipocytes, is involved in glucose metabolism and insulin sensitivity. The production of this adipokine is impaired in obesity and insulin resistance. Eicosapentaenoic acid (EPA) is a dietary n-3 polyunsaturated fatty acid that improves insulin sensitivity in several models of obesity and diabetes, which has been suggested to be related to adiponectin induction. An increase in adiponectin production has been also associated with an up-regulation of the transcriptional factor PPARγ. The aim of this trial was to evaluate the direct effects of EPA on adiponectin gene expression and protein secretion in isolated rat adipocytes as well as to explore the potential mechanisms involved. A comparative study with troglitazone, a PPARγ agonist, was also performed. For these purposes, primary rat adipocytes were cultured with EPA (100 and 200 μM) and with troglitazone (10 μM) for 96 hours. Both EPA and troglitazone improved glucose utilization by adipocytes. As expected, troglitazone enhanced adiponectin secretion and increased PPARγ gene expression. However, EPA significantly decreased adiponectin gene expression and protein secretion and reduced PPARγ mRNA levels, suggesting that the inhibition of adiponectin by EPA is likely to be secondary to the down-regulation of this adipogenic transcription factor. Moreover, these results suggest that other mechanisms different from the direct stimulation of adiponectin by the fatty acid are underlying the insulin-sensitizing properties observed after EPA treatment in vivo.
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      headline:Effects of eicosapentaenoic acid (EPA) on adiponectin gene expression and secretion in primary cultured rat adipocytes
      description:Adiponectin, a hormone produced by adipocytes, is involved in glucose metabolism and insulin sensitivity. The production of this adipokine is impaired in obesity and insulin resistance. Eicosapentaenoic acid (EPA) is a dietary n-3 polyunsaturated fatty acid that improves insulin sensitivity in several models of obesity and diabetes, which has been suggested to be related to adiponectin induction. An increase in adiponectin production has been also associated with an up-regulation of the transcriptional factor PPARγ. The aim of this trial was to evaluate the direct effects of EPA on adiponectin gene expression and protein secretion in isolated rat adipocytes as well as to explore the potential mechanisms involved. A comparative study with troglitazone, a PPARγ agonist, was also performed. For these purposes, primary rat adipocytes were cultured with EPA (100 and 200 μM) and with troglitazone (10 μM) for 96 hours. Both EPA and troglitazone improved glucose utilization by adipocytes. As expected, troglitazone enhanced adiponectin secretion and increased PPARγ gene expression. However, EPA significantly decreased adiponectin gene expression and protein secretion and reduced PPARγ mRNA levels, suggesting that the inhibition of adiponectin by EPA is likely to be secondary to the down-regulation of this adipogenic transcription factor. Moreover, these results suggest that other mechanisms different from the direct stimulation of adiponectin by the fatty acid are underlying the insulin-sensitizing properties observed after EPA treatment in vivo.
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         Adiponectin
         PPARγ
         Troglitazone
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         Adipocitos
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