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The other sweet face of XBP-1

Nature Medicine volume 17, pages 246–248 (2011)Cite this article

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X-box–binding protein-1 (XBP-1) increases insulin sensitivity by activating endoplasmic reticulum capacity during feeding to control glucose homeostasis, a function severely impaired in obesity. But XBP-1 can also increase glucose tolerance in obese and diabetic mice by blocking gluconeogenesis, independent of its effect on insulin sensitivity, opening new avenues for type 2 diabetes therapies (pages 356–365).

Obesity is a major risk factor for many diseases, such as type 2 diabetes and cardiovascular disease. The endoplasmic reticulum (ER), a luminal network for protein synthesis, maturation, folding and transport, can undergo stress when there are perturbations in its homeostasis, for example, an increased demand for protein synthesis. The consequent unfolded protein response (UPR) aims to preserve homeostasis and cellular integrity1.

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Figure 1: A dual mechanistic role for XBP-1 in improving glucose homeostasis.

Katie Vicari

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Authors and Affiliations

  1. Kohjiro Ueki and Takashi Kadowaki are in the Department of Diabetes and Metabolic Disease, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.,

    Kohjiro Ueki & Takashi Kadowaki

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  1. Kohjiro Ueki
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  2. Takashi Kadowaki
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Correspondence to Kohjiro Ueki.

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Ueki, K., Kadowaki, T. The other sweet face of XBP-1. Nat Med 17, 246–248 (2011). https://doi.org/10.1038/nm0311-246

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