Salivary gland dysfunction is a common complication of diabetes. Decreased saliva production and changes in saliva composition may cause oral diseases. Reactive oxygen species (ROS) generation in the salivary glands results in the loss of acinar cells and decreased saliva secretion. Glucagon-like peptide 1 (GLP-1) is the incretin hormone that regulates blood glucose level and can suppress ROS production and inflammation through its antioxidant effects. Dipeptidyl peptidase-4 (DPP-4) is an enzyme that breaks down GLP-1. In this study, we evaluated the pathological role of DPP-4 and GLP-1 on salivary gland dysfunction in type 2 diabetic db/db mice. We observed reduced salivary secretion and histopathological alteration of salivary glands in the db/db mice. The increased DPP-4 and decreased GLP-1 levels in the salivary glands were also detected in the db/db mice. Furthermore, the db/db mice had increased apoptosis and oxidative injury in salivary glands. There was an accumulation of advanced glycation end products and mucus in the salivary glands of the db/db mice. In conclusion, these results showed the possible involvement of DPP-4 and GLP-1, leading to increased ROS-induced apoptosis in diabetes-related salivary gland dysfunction. DPP-4 and GLP-1 may be a pharmacological target for patients with diabetes-related salivary gland dysfunction.

In present study, we investigated the antidiabetic effect of Momordica charantia(as well known “bitter melon”). This study was conducted to determine antidiabetic mechanism of Bitter Melon Extract (BME). We measured blood glucose, insulin, glucagon level in a Sprague-Dawley rat model of high-fat diet/streptozotocin(HFD/STZ)-induced diabetes. Five experimental groups were used: normal, HFD/STZ, BME 62.5 mg/kg HFD/STZ, BME 125 mg/kg HFD/STZ and BME 250 mg/kg HFD/STZ. BME was orally administered to the rats every other day for 9 weeks. Results showed that fasting blood glucose levels were significantly lower in the BME 125 mg/kg(150.17 ± 20.22 mg/dL) and 250 mg/kg(124.17 ± 22.17 mg/dL) groups than in the vehicle group(188.83 ± 26.63 mg/dL)(p<0.05). In addition, glucagon levels were lower in the three BME treatment groups than in the vehicle group(p<0.05). Oral glucose tolerance tests revealed that the BME 250 mg/kg group had significantly(p<0.05) reduced 120-minute blood glucose levels and areas under the curve. Our results suggest that BME induces antidiabetic effects via the reduction of glucagon and blood glucose levels.