Science  26 Oct 2007:
Vol. 318, Issue 5850, pp. 565
DOI: 10.1126/science.318.5850.565b

In a paper titled “Visfatin: a protein secreted by visceral fat that mimics the effects of insulin” (1), we identified a protein that is secreted by visceral fat of humans and mice and named it “visfatin.” The same protein had been identified previously by other laboratories as “pre-B cell—colony enhancing factor,” a cytokine that is expressed by lymphocytes (2) and that displays nicotinamide phosphoribosyltransferase activity (3). In the Science Report, we investigated visfatin-s metabolic effects and the biochemical mechanism by which it might exert these effects. We showed that visfatin induces adipocyte differentiation in vitro and that plasma levels of visfatin correlate with visceral fat mass in humans. We also showed that male mice with only one functional copy of the visfatin gene have modest elevations in plasma glucose and that adenovirus-mediated delivery of the visfatin gene to c57BL/6J or KKAy mice resulted in a lowering of plasma glucose and insulin levels. Finally, we reported that visfatin binds to and activates the insulin receptor and we speculated that its activity as an insulin mimetic might explain its metabolic effects.

The visfatin work performed in our laboratory was recently investigated by the Committee for Research Integrity (CRI) of Osaka University Graduate School of Medicine. On the basis of the CRI report, which focused largely on our biochemical experiments examining visfatin-s interaction with the insulin receptor, the Faculty Council of Osaka University Medical School recommended that we retract the entire paper. At the suggestion of the Editor of Science, we have agreed to retract the paper, even though we continue to stand by our conclusions. We note that over a dozen subsequent publications have shown that plasma visfatin levels in humans correlate with various metabolic states, including obesity, visceral fat mass, and diabetes [for example, (46)]. We note also that another laboratory recently reported that visfatin has insulin mimetic effects in cultured osteoblasts (7). We acknowledge that, since publication of the Science Report, we have found that not all preparations of visfatin bind to and activate the insulin receptor. Thus far, we have found four different lots of purified recombinant visfatin protein that have both adipogenic and insulin mimetic activities. We still have the preparations of visfatin that show insulin mimetic activity, although the amount is limited, and we are willing to send them to other investigators for independent validation. We are continuing to investigate the significance of this molecule.

We regret any inconvenience caused by this retraction to researchers and readers. The corresponding author is responsible for the retraction.


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