Comment on: Schuit et al. β-Cell–Specific Gene Repression: A Mechanism to Protect Against Inappropriate or Maladjusted Insulin Secretion? Diabetes 2012;61:969–975
Year: 2012
Type: letter
Abstract: We write in connection to the recent reviewarticle by Schuit et al. (1) on gene repressionin the b-cell. Although most review articlesdisplay a natural (and forgivable) bias toward the authors ’ own contributions and point of view, we feel that this article goes well beyond the norm. Firstly, the section entitled “How islet-specifically re-pressed genes were identified ” is largely restricted to the authors ’ own work. This significantly distorts the true historical narrative. It fails to mention, in particular, that the founder members (LDHA and MCT1/SLC16A1) of what were later dubbed the “disallowed ” group were, in fact, first identified in a systematic comparison of the met-abolic enzymology of fluorescence-activated cell sorting– purified b-cells versus a range of insulinoma cells and a limited number of primary mouse tissues (notably liver and islet non–b-cells) in a collaboration between G.A.R. and Claes Wollheim reported in 1994 (2). A further article by Matschinksy and colleagues (3), which also demon-strated low levels of lactate dehydrogenase in a relatively well-differentiated b-cell line, also goes uncited, as well as a much earlier paper by Hellman et al. (4) suggesting lac-tate dehydrogenase activity may be unusually low in the islet. An additional, and greater concern, is that the review by Schuit et al. (1) fails to cite the first bioinformatics analysis to provide a list of “disallowed ” genes in the b-cell (5), referring instead only to the later article from the authors’ own group (6). Similarities and differences between the gene lists generated by these two articles are therefore not discussed. Strikingly, both analyses indicate that LDHA and MCT1 are probably the most strongly (selectively) repressed b-cell genes (5,6), further emphasizing the im-portance of our original findings (2). ACKNOWLEDGMENTS No potential conflicts of interest relevant to this article were reported.
Source: Diabetes
DOI: 10.2337/db12-0775
Authors: Guy A. Rutter, Timothy J. Pullen
Institution: Imperial College London
Language: English
Subfield: Surgery
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Funders: Wellcome Trust, Medical Research Council
OpenAlex ID: W2149120311
