Endothelial Cells From Visceral Adipose Tissue Disrupt Adipocyte Functions in a Three-Dimensional Setting: Partial Rescue by Angiopoietin-1

  1. Danièle Lacasa1,2,3,4
  1. 1INSERM, UMRS 872 Nutriomique, Paris, France
  2. 2Pierre et Marie Curie–Paris 6 University, Cordeliers Research Center, UMRS 872, Paris, France
  3. 3Paris Descartes University, UMRS 872, Paris, France
  4. 4Cardiometabolism and Nutrition Institute, Pitié Salpetrière Hospital, Paris, France
  5. 5General Surgery, Digestive, Metabolic, and Laparoscopic, Public Assistance Hospitals of Paris, Ambroise Paré Hospital, Versailles Saint-Quentin University, Boulogne-Billancourt, France
  1. Corresponding authors:
    Vanessa Pellegrinelli, vanessa.pellegrinelli{at}, and Danièle Lacasa, daniele.lacasa{at}


During obesity, chronic inflammation of human white adipose tissue (WAT) is associated with metabolic and vascular alterations. Endothelial cells from visceral WAT (VAT-ECs) exhibit a proinflammatory and senescent phenotype and could alter adipocyte functions. We aimed to determine the contribution of VAT-ECs to adipocyte dysfunction related to inflammation and to rescue these alterations by anti-inflammatory strategies. We developed an original three-dimensional setting allowing maintenance of unilocular adipocyte functions. Coculture experiments demonstrated that VAT-ECs provoked a decrease in the lipolytic activity, adipokine secretion, and insulin sensitivity of adipocytes from obese subjects, as well as an increased production of several inflammatory molecules. Interleukin (IL)-6 and IL-1β were identified as potential actors in these adipocyte alterations. The inflammatory burst was not observed in cocultured cells from lean subjects. Interestingly, pericytes, in functional interactions with ECs, exhibited a proinflammatory phenotype with diminished angiopoietin-1 (Ang-1) secretion in WAT from obese subjects. Using the anti-inflammatory Ang-1, we corrected some deleterious effects of WAT-ECs on adipocytes, improving lipolytic activity and insulin sensitivity and reducing the secretion of proinflammatory molecules. In conclusion, we identified a negative impact of VAT-ECs on adipocyte functions during human obesity. Therapeutic options targeting EC inflammation could prevent adipocyte alterations that contribute to obesity comorbidities.


  • Received April 5, 2013.
  • Accepted October 3, 2013.

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