Research article

Short-term and rapid effects of lysophosphatidic acid on human adipose cell lipolytic and glucose uptake activities

  • Received: 22 February 2016 Accepted: 12 May 2016 Published: 16 May 2016
  • Lysophosphatidic acid (LPA) is a bioactive phospholipid that activates cell proliferation, differentiation and migration via the activation of its membrane-bound receptors (LPAR 1 to 6) expressed in various tissues and organs. Adipose tissue produces LPA, which, in turn, increases preadipocyte proliferation, mainly through the stimulation of LPA1R. However, while LPA plasma levels increase with obesity, only few studies have investigated the acute autocrine properties of LPA on mature adipocytes. We therefore assessed the lipolytic and antilipolytic effects of LPA on human adipocytes. Here, we show that, in human subcutaneous adipocytes, LPA (0.1–10 µM) did not mimic insulin effects in human adipocytes, i.e. lipolysis inhibition and glucose uptake activation. By contrast, supramicromolar doses of the phospholipid slightly activated lipolysis, and the effect of 100 µM LPA was additive to the β-adrenergic stimulation of lipolysis by isoprenaline. Moreover, LPA did not alter the activity of primary amine oxidase, an enzyme highly expressed in human adipose cells. Our observations indicate that, although rapid and direct, LPA impact on triglyceride storage in mature adipocytes is less pronounced than its ability to stimulate proliferation in preadipocytes.

    Citation: Christian Carpéné, Jean Galitzky, Jean Sébastien Saulnier-Blache. Short-term and rapid effects of lysophosphatidic acid on human adipose cell lipolytic and glucose uptake activities[J]. AIMS Molecular Science, 2016, 3(2): 222-237. doi: 10.3934/molsci.2016.2.222

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  • Lysophosphatidic acid (LPA) is a bioactive phospholipid that activates cell proliferation, differentiation and migration via the activation of its membrane-bound receptors (LPAR 1 to 6) expressed in various tissues and organs. Adipose tissue produces LPA, which, in turn, increases preadipocyte proliferation, mainly through the stimulation of LPA1R. However, while LPA plasma levels increase with obesity, only few studies have investigated the acute autocrine properties of LPA on mature adipocytes. We therefore assessed the lipolytic and antilipolytic effects of LPA on human adipocytes. Here, we show that, in human subcutaneous adipocytes, LPA (0.1–10 µM) did not mimic insulin effects in human adipocytes, i.e. lipolysis inhibition and glucose uptake activation. By contrast, supramicromolar doses of the phospholipid slightly activated lipolysis, and the effect of 100 µM LPA was additive to the β-adrenergic stimulation of lipolysis by isoprenaline. Moreover, LPA did not alter the activity of primary amine oxidase, an enzyme highly expressed in human adipose cells. Our observations indicate that, although rapid and direct, LPA impact on triglyceride storage in mature adipocytes is less pronounced than its ability to stimulate proliferation in preadipocytes.


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