Activation of the GLP-1 Receptor Signalling Pathway: A Relevant Strategy to Repair a Deficient Beta-Cell Mass
Figure 2
DPPIV inhibitors activate beta-cells regeneration in vivo. The aim was to investigate in the rat model of neonatal beta-cell regeneration (nSTZ model), the capacity of in vivo treatment by DPPIV inhibitors (LAF237 or S38013) to promote beta-cell regeneration. To this end, nSTZ rats were submitted to DPPIV administration from postnatal day 2 to day 6 only, and their beta-cell masses were tested on day 7. Ex-4 was taken as a beta-cell growth stimulator comparator. In the 7-day-old untreated nSTZ group, total beta-cell mass per pancreas was only 22% of the value in the untreated normal group (). In the nSTZ/LAF237 group, the total beta-cell mass increase (by 46%) did not reach statistical significance. In the nSTZ/S38013 group, the total beta-cell mass increase (by 68%) reached statistical significance (*). Beta-cell mass in the nSTZ/Ex-4 group was twice increased (**). In the 7-day-old untreated nSTZ group, basal plasma glucose value was significantly increased by 70% () as compared to that of untreated normal group. By contrast, in the nSTZ/LAF237, nSTZ/S38013, and nSTZ/Ex-4 groups, basal plasma glucose levels were significantly decreased ( or ) at the end of treatment as compared with those in the untreated nSTZ group and reached values no longer significantly different from those in untreated normal pups.
