I am a new resident in Pediatrics at Kaplan Hospital inRehovot, Israel. Recently, we had a child with new onset type 1 diabetes, which required less and less insulin. It seems like the “honeymoon” phenomena. I, along with the Pediatric Endocrinologist, wondered what the mechanism is for this effect? I searched for papers on this issue, but haven’t found one with a suggested model.

What you describe seems like a typical ‘honeymoon’ response in a case of type1A or autoimmune diabetes. Rather simplistically, this is usually ascribed to partial, but transitory, recovery of the remaining beta cells as insulin demands are assumed by an exogenous hormone. It is not the whole story, however, as there is evidence from serum C peptide studies at this time that insulin resistance is also a factor. Insulin resistance in type 1 diabetes is a relevant article.

Of considerable interest also are very recent observations in animal models that, even as insulin dependance develops, there are new insulin producing cells developing around the pancreatic ducts. Some part of the ‘honeymoon’ phenomenon may then be due to insulin production by these cells before they, too, are destroyed by the autoimmune process. The prescence of these cells nonetheless suggests that insulin independence might still be preserved by the combination of immunomodulation, with anti CD3 for example, combined with the introduction of one of the trancription factors for islet cell growth. Another much less likely possibility is that you are observing the more permanent restoration of insulin sufficiency that is seen in some 50% of cases with type1B or antibody negative diabetes.

DOB