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( Sybille D Reichardt ),( Martin Oppermann ),( Holger M Reichardt ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Glucocorticoids (GCs) are widely used in the clinic to treat autoimmune and atopic diseases but they also cause many side-effects. Here we characterized a yet unknown activity of GCs in the stomach, namely the induction of gastroparesis by oral application of dexamethasone. Using conditional knock-out mice we initially ruled out that enterocytes or macrophages were responsible for the observed effect. This finding suggested that the stomach itself was the primary target of GC action. Against our expectations, however, impaired gastric emptying was also unrelated to the enhanced HCl production after dexamethasone administration. In contrast, we found that oral GC therapy up-regulated arginase 2 in the stomach. Importantly, this effect should lead to the depletion of L-arginine and thereby impede production of nitric oxide, which is required for gastric motility. In support of this notion, supplementing the drinking water with L arginine prevented the induction of gastroparesis by dexamethasone in mice. Our fi ndings suggest that combining L-arginine with orally applied GCs might reduce treatment-related gastrointestinal complications. Furthermore, our data provide a plausible explanation for the well-known anti-emetic effect of GCs. In the future it will be intriguing to explore whether the observed phenomenon can be confi rmed in patients under high-dose GC therapy as well.
( Henrike J Fischer ),( Jens Van Den Brandt ),( Holger M Reichardt ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
T cells are an important line of defense against infections. Following antigen recognition they become activated and start to express the insulin receptor (InsR), which helps to cover the cells`s increased energy demand. Here we report that full activation of T cells could not be achieved when the InsR was ablated in transgenic knock-down rats. This was refi ected by a delayed up-regulation of CD25, a reduced secretion of pro-infiammatory cytokines and a diminished proliferation of CD4+ T cells. Interestingly, the observed effects were unrelated to differences in gene expression but rather seemed to be caused by alterations at the post-transcriptional level. CD8+ T cells, which are central to the clearance of viral infections, were also affected by the absence of the InsR. In particular their cytotoxic activity against foreign antigen was signifi cantly reduced. Preliminary experiments further suggested that adaptive immune responses in vivo were dampened when the InsR was absent in T cells. Collectively, our fi ndings indicate that insulin signaling fosters T cell activation. We would therefore expect that various T cell functions are compromised in patients with type 2 diabetes mellitus, which might explain why they are at greater risk of infections.