Diabetes paper retracted for “misgrouping errors” that remain under investigation

A group of researchers at the University of Minnesota have retracted a paper in Diabetes for image problems, but exactly what happened is still under investigation.

Here’s the notice:

Zhang W, Zhang X, Wang H, Guo X, Li H, Wang Y, Xu X, Tan L, Mashek MT, Zhang C, Chen Y, Mashek DG, Foretz M, Zhu C, Zhou H, Liu X, Viollet B, Wu C, Huo Y. AMP-activated protein kinase α1 protects against diet-induced insulin resistance and obesity. Diabetes 2012;61:3114–3125

The authors have formally requested to retract the above-titled article, which was published in the December 2012 print issue of Diabetes. The authors cite concerns that Figures 2F, 4G, and 6G included misgrouping errors that were not identified before the time of submission or publication. The authors apologize to the readers of Diabetes for any inconvenience this may have caused.

Here’s the original abstract:

AMP-activated protein kinase (AMPK) is an essential sensor of cellular energy status. Defects in the α2 catalytic subunit of AMPK (AMPKα1) are associated with metabolic syndrome. The current study investigated the role AMPKα1 in the pathogenesis of obesity and inflammation using male AMPKα1-deficent (AMPKα1(-/-)) mice and their wild-type (WT) littermates. After being fed a high-fat diet (HFD), global AMPKα1(-/-) mice gained more body weight and greater adiposity and exhibited systemic insulin resistance and metabolic dysfunction with increased severity in their adipose tissues compared with their WT littermates. Interestingly, upon HFD feeding, irradiated WT mice that received the bone marrow of AMPKα1(-/-) mice showed increased insulin resistance but not obesity, whereas irradiated AMPKα1(-/-) mice with WT bone marrow had a phenotype of metabolic dysregulation that was similar to that of global AMPKα1(-/-) mice. AMPKα1 deficiency in macrophages markedly increased the macrophage proinflammatory status. In addition, AMPKα1 knockdown enhanced adipocyte lipid accumulation and exacerbated the inflammatory response and insulin resistance. Together, these data show that AMPKα1 protects mice from diet-induced obesity and insulin resistance, demonstrating that AMPKα1 is a promising therapeutic target in the treatment of the metabolic syndrome.

The American Diabetes Association, which publishes Diabetes, tells us the matter is still under investigation:

A reader notified the authors and the editor of Diabetes. When preparing the images, Western blots were grouped from different mice and multiple membranes. It appears that some of the blots among the three cited panels are identical. Even though ADA agreed to the author’s request to quickly publish a retraction, the matter is still being investigated.

The paper has been cited by three other publications, one of which is the retraction notice, according to Thomson Scientific’s Web of Knowledge.

We’ve asked last author Yuqing Huo — who seems to have recently moved to Georgia Regents University — for more details. He told us last week that he was traveling but would get back to us soon, so we’ll update with anything we learn.