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Metabolic disease: Differential drug response in lean and obese patients explained

Date:
April 3, 2010
Source:
Journal of Clinical Investigation
Summary:
One thing that predisposes individuals who are obese to type 2 diabetes is the persistent, low-level inflammation that results, in part, from dysregulation of the function of white fat tissue in the abdominal cavity between the internal organs (visceral white fat tissue). New insight into the signaling pathways that contribute to visceral white fat tissue dysregulation has now been provided by researchers who determined that the PPAR-gamma signaling pathway operates differently in the visceral white fat tissue of lean and obese mice and humans.
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One thing that predisposes individuals who are obese to type 2 diabetes is the persistent, low-level inflammation that results, in part, from dysregulation of the function of white fat tissue in the abdominal cavity between the internal organs (visceral white fat tissue).

New insight into the signaling pathways that contribute to visceral white fat tissue dysregulation has now been provided by Philippe Lefebvre and colleagues, at INSERM, UMR1011, France, who determined that the PPAR-gamma signaling pathway operates differently in the visceral white fat tissue of lean and obese mice and humans. Specifically, it shows increased sensitivity to activation by the anti-diabetic drug rosiglitazone in obese mice and humans.

These data therefore provide a mechanistic explanation why rosiglitazone acts differently in lean and obese patients.

The research appears in the Journal of Clinical Investigation.


Story Source:

The above post is reprinted from materials provided by Journal of Clinical Investigation. Note: Materials may be edited for content and length.


Journal Reference:

  1. Bruno Lefebvre, Yacir Benomar, Aurore Guédin, Audrey Langlois, Nathalie Hennuyer, Julie Dumont, Emmanuel Bouchaert, Catherine Dacquet, Luc Pénicaud, Louis Casteilla, Francois Pattou, Alain Ktorza, Bart Staels, and Philippe Lefebvre. Proteasomal degradation of retinoid X receptor α reprograms transcriptional activity of PPARγ in obese mice and humans. Journal of Clinical Investigation, 2010; DOI: 10.1172/JCI38606

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Journal of Clinical Investigation. "Metabolic disease: Differential drug response in lean and obese patients explained." ScienceDaily. ScienceDaily, 3 April 2010. <www.sciencedaily.com/releases/2010/04/100401220646.htm>.
Journal of Clinical Investigation. (2010, April 3). Metabolic disease: Differential drug response in lean and obese patients explained. ScienceDaily. Retrieved August 2, 2015 from www.sciencedaily.com/releases/2010/04/100401220646.htm
Journal of Clinical Investigation. "Metabolic disease: Differential drug response in lean and obese patients explained." ScienceDaily. www.sciencedaily.com/releases/2010/04/100401220646.htm (accessed August 2, 2015).

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