Effects of Exercise and Inhibition of Dipeptidyl Peptidase-4 on Insulin Secretion in Subjects With Type 1 Diabetes
Status:
Completed
Trial end date:
2016-08-05
Target enrollment:
Participant gender:
Summary
Increasing evidence suggests pancreatic islet beta-cell regeneration occurs throughout the
course of the disease in patients with type 1 diabetes. Therefore, decreased beta-cell mass
in type 1 diabetes may be improved through inhibition of beta-cell destruction and
stimulation of proliferation, even after prolonged duration of disease.
Physical activity improves insulin secretion via unknown underlying mechanisms. We recently
observed that Interleukin-6 induces glucagon like Peptide (GLP)-1 production and release from
the islet alpha-cell and the intestinal L-cell. Furthermore, exercise induces release of
Interleukin-6 from skeletal muscle resulting in elevated circulating Interleukin-6 levels.
Therefore we hypothesize that exercise-induced Interleukin-6 promotes glucagon like peptide-1
secretion from the islet α-cell and the intestinal L-cell, thereby providing a mechanism how
physical activity can help maintain and improve beta-cell function in patients with type 1
diabetes. This mechanism can be enhanced by concomitant dipeptidyl peptidase-IV inhibition.
Physical activity is also known to enhance insulin sensitivity and to attenuate the immune
system activity.
Therefore by combining physical activity and dipeptidyl peptidase-IV inhibition we aim to
allow for beta-cell regeneration in a interventional randomized open-label study.