In their recent Gastroenterology journal article, Jackson et al report on the role of functional autoantibodies in the development of gastrointestinal dysfunction. The Flinders Medical Centre group investigated the effects of autoantibodies on the colonic migrating motor complex (MMC) in isolated mouse colon.  This co-ordinated pattern of colonic activity which contributes to overall intestinal transit was disrupted by IgG from 8 of 16 patients with type 1 diabetes but not by control IgG. Passive transfer of diabetic IgG to mice also disrupted MMCs, showing access to the antigen in vivo. The acute effect of the autoantibody was mimicked by the L-type calcium channel activator Bay K8644. Both Bay K8644 and the autoantibody competitively inhibited the effect on MMC contraction of the L-type calcium channel inhibitor, nicardipine. 

These data suggest that an autoantibody produced by patients with type 1 diabetes may be responsible for gastrointestinal dysfunction in these patients and that the autoantibody acts through the activation of smooth muscle L-type calcium channels and may lead to the development of new approaches to this complication of diabetes.