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Xbp1s, a transcriptional factor that is activated in response to endoplasmic reticulum (ER) stress, is elevated in subcutaneous fat tissue from obese human subjects. This suggests that Xbp1s induction is a possible link between ER stress and obesity.

Under fasting conditions, when there are high levels of lipolysis, pyrimidine biosynthesis in adipocytes is elevated. As a result, plasma uridine concentrations double. Even though only moderate in terms of the magnitude of the change, the doubling of uridine concentrations has major implications for temperature regulation and energy expenditure.

Deng et al. find that although the expression of Xbp1s in adipocytes is induced by a number of lipolytic stimuli, lipolysis per se is not dependent on Xbp1s. Conversely, adipocyte overexpression of Xbp1s leads to profound loss of fat mass, and this loss is associated with elevation of uridine in adipose tissue and blood circulation. The authors demonstrate that Xbp1s triggered fat mass loss relies on pyrimidine biosynthesis. Also, their data suggest a direct regulatory role of ER stress in pyrimidine metabolism. Based on these observations, they propose that the stimulation of the adipocyte uridine synthesis pathway is a potential therapeutic target area for the treatment of obesity.

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In this section authors briefly report on their work recently published in Molecular Metabolism.

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Landon Wood, Darleen Sandoval
University of Michigan, Ann Arbor, USA
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