Much has been made of the “civil war” between type 1 and type 2 diabetics. To be honest, it seems silly to me, so I won’t dwell long on it; but it does interest me that so many type 1 diabetics seem to be left out in the cold, unattended and alone. To me, given the number of people who have type 1 diabetes, it seems we get way more than our fair share of attention, press, and dollars. (This is just my unresearched, fairly biased opinion. For more information, you might start with the NIH funding allocations or the claims of the Fair Foundation.)
That said, all my love to the people and organizations who contribute to autoimmune disease research. And here I want to point out a particular group that doesn’t intend to be associated with type 1 diabetes at all, but that I have noticed seems to have a particular interest in the science of type 1 diabetes: the Proceedings of the National Academy of Sciences (PNAS). Over the past year or so, they have had several major papers– and even a feature article– specifically related to type 1 diabetes. I don’t know why, but I speculate it has something to do with the fact that type 1 diabetes exists in some particular intersection of immune research, stem cell research, and nanotech research that is right inside PNAS’s hometown. But, in 2010 alone–
– May-yun Wang, Lijun Chen, Gregory O. Clark, Young Lee, Robert D. Stevens, Olga R. Ilkayeva, Brett R. Wenner, James R. Bain, Maureen J. Charron, Christopher B. Newgard, and Roger H. Unger. From the Cover: Feature Article: Leptin therapy in insulin-deficient type I diabetes. PNAS 2010 107 (11) 4813-4819
– Brian D. Stadinski, Li Zhang, Frances Crawford, Philippa Marrack, George S. Eisenbarth, and John W. Kappler. Diabetogenic T cells recognize insulin bound to IAg7 in an unexpected, weakly binding register. PNAS 2010 107 (24) 10978-10983
– Sarika Gupta, Tandrika Chattopadhyay, Mahendra Pal Singh, and Avadhesha Surolia. Supramolecular insulin assembly II for a sustained treatment of type 1 diabetes mellitus. PNAS 2010 107 (30) 13246-13251
– Zaida Alipio, Wenbin Liao, Elizabeth J. Roemer, Milton Waner, Louis M. Fink, David C. Ward, and Yupo Ma. Reversal of hyperglycemia in diabetic mouse models using induced-pluripotent stem (iPS)-derived pancreatic ?-like cells. PNAS 2010 107 (30) 13426-13431
– Roger H. Unger and Lelio Orci. Paracrinology of islets and the paracrinopathy of diabetes. PNAS 2010 107 (37) 16009-16012
– Teppei Fujikawa, Jen-Chieh Chuang, Ichiro Sakata, Giorgio Ramadori, and Roberto Coppari. Leptin therapy improves insulin-deficient type 1 diabetes by CNS-dependent mechanisms in mice. PNAS 2010 107 (40) 17391-17396
– Brian J. Smith, Kun Huang, Geoffrey Kong, Shu Jin Chan, Satoe Nakagawa, John G. Menting, Shi-Quan Hu, Jonathan Whittaker, Donald F. Steiner, Panayotis G. Katsoyannis, Colin W. Ward, Michael A. Weiss, and Michael C. Lawrence. Structural resolution of a tandem hormone-binding element in the insulin receptor and its implications for design of peptide agonists. PNAS 2010 107 (15) 6771-6776
– Dina Fomina-Yadlin, Stefan Kubicek, Deepika Walpita, Vlado Dan?ik, Jacob Hecksher-Sørensen, Joshua A. Bittker, Tanaz Sharifnia, Alykhan Shamji, Paul A. Clemons, Bridget K. Wagner, and Stuart L. Schreiber. Small-molecule inducers of insulin expression in pancreatic alpha-cells. PNAS 2010 107 (34) 15099-15104
– Hideaki Shibata, Yun Jung Heo, Teru Okitsu, Yukiko Matsunaga, Tetsuro Kawanishi, and Shoji Takeuchi. Injectable hydrogel microbeads for fluorescence-based in vivo continuous glucose monitoring. PNAS 2010 107 (42) 17894-17898
Those are just the ones I happened to come across, and I even left out a whole bunch that focused on the molecular mechanisms of insulin and glucose homeostasis, since those aren’t really type 1 specific. And, granted, PNAS has had no shortage of articles focused on type 2 diabetes, but, regardless, we type-onies seem to be doing decently on the research front.
So, I conclude:
1. Forget any civil war. The two types of diabetes share many goals, so any boon to a type 2 I take as a boon to type 1s as well.
2. And for that matter, thanks, type 2s! Without you, I would have a disease whose name was unknown and whose friends were few, and I would much rather be your step-sister than an orphan.
3. Speaking of orphans, don’t forget that there are very many diseases out there with no articles in any Posts, and no attention whatsoever. Let’s learn what we can.
4. Finally, thanks PNAS! The more you publish about diabetes, the more people will pursue treatments and cures.