1624-P: Hudev-PRE, a Combination of Plant Extracts, Improves Glucose Homeostasis in Both High-Fat Diet C57Bl/6J and Ob/Ob Mice

Despite advances in the understanding of the pathogenesis of type 2 diabetes (T2D), new therapeutic & nutritional solutions are needed to delay its emergence and prevent the development of its associated complications. Here, we tested the effect of HUDEV-PRE, an original mixture of plant extracts, on glucose homeostasis in in two different mouse models of T2D. In a first experiment, 8 weeks old C57Bl/6J males were fed with high-fat diet during 8 weeks to induce insulin resistance. In a second set-up, we used 6 weeks old Ob/Ob males. In both experiments, mice received a double daily oral administration of vehicle, metformin (150mg/kg) or HUDEV-PRE for 30 days. Food intake, body weight change, random fed plasma glucose, cholesterol and triglyceride levels were measured once weekly. Finally, oral glucose tolerance tests (GTT) were performed after 7 and 21 days of treatment. In both models, HUDEV-PRE did not alter food intake and body weight. Interestingly, a rapid, sustainable and significant reduction of random fed blood glucose levels was observed in HFD fed C57Bl/6J and Ob/Ob mice receiving metformin or HUDEV-PRE administration. In HFD fed C57Bl/6J mice, GTT revealed no significant effects at day 7 but a strong improvement of glucose tolerance in mice treated for 21 days with metformin or HUDEV-PRE compared to control vehicle treated mice. In Ob/Ob mice, we observed similar results and the glucose tolerance was even improved after only 7 days of treatment. Finally, at day 21, we also measured a significant reduction of fasting plasma insulin levels and HOMA-IR in both mouse models treated with HUDEV-PRE. Together, our data demonstrate that HUDEV-PRE rapidly improve glucose homeostasis in two mouse models of T2D. Although additional studies are warranted to decipher the mechanisms of action, these findings indicate that HUDEV-PRE could represent a nutritional supplement of interest to delay the onset of insulin resistance and T2D in patients at metabolic risk.