Résumé
Purpose@#The prevalence of diabetes mellitus (DM) continues to increase worldwide, and blood glucose control may reduce mortality from diabetic complications and healthcare costs. Mulberry twig (MT) has been used as a herbal medicine in Asia, and its antidiabetic efficacy has recently been reported, but research in this area is still limited. This study examined the antidiabetic effects of water extracts of MT in diabetic animals. @*Methods@#Six weeks old male ICR mice were divided randomly into three groups; normal control (NC, n = 10), DM control (DC, n = 10), and MT (n = 10). Streptozotocin (STZ, 50 mg/ kg/day) was injected intraperitoneally into mice in the DC and MT groups for 5 consecutive days. After 10 days of the last STZ injection, the mice in the MT group were administered orally with MT water extracts (5 g/kg body weight) for 16 days. @*Results@#The MT water extracts ameliorated the swelling of the liver in the diabetic mice and reduced the elevated levels of fasting blood and plasma glucose, total cholesterol (T-CHO), low density lipoprotein-CHO, and the ratio of high density lipotrotein (HDL)-CHO/T-CHO. The liver triglyceride (TG) and glycogen contents were also significantly lower in the MT group mice than in the DC group. The small intestine disaccharidase activity was analyzed to understand the therapeutic effects and the mechanism of MT water extracts in diabetic animals. MT group mice showed reduced lactase and sucrase activity in the proximal part of the small intestine. On the other hand, body weight, plasma insulin, TG, HDL-CHO, and hepatic T-CHO levels were similar in the DC and MT groups. @*Conclusion@#These results suggest that MT water extracts have antidiabetic effects and can be developed as a functional source to reduce the postprandial blood glucose or to prevent DM incidence.
Résumé
BACKGROUND/OBJECTIVE: The incidence of colorectal cancer (CRC) has been attributed to higher intake of fat and protein. However, reports on the relationship between protein intake and CRC are inconsistent, possibly due to the complexity of diet composition. In this study, we addressed a question whether alteration of protein intake is independently associated with colonic inflammation and colon carcinogenesis. MATERIALS/METHODS: Balb/c mice were randomly divided into 4 experimental groups: 20% protein (control, 20P, 20% casein/kg diet), 10% protein (10P, 10% casein/kg diet), 30% protein (30P, 30% casein/kg diet), and 50% protein (50P, 50% casein/kg diet) diet groups and were subjected to azoxymethane-dextran sodium sulfate induced colon carcinogenesis. RESULTS: As the protein content of the diet increased, clinical signs of colitis including loss of body weight, rectal bleeding, change in stool consistency, and shortening of the colon were worsened. This was associated with a significant decrease in the survival rate of the mice, an increase in proinflammatory protein expression in the colon, and an increase in mucosal cell proliferation. Further, colon tumor multiplicity was dramatically increased in the 30P (318%) and 50P (438%) groups compared with the control (20P) group. CONCLUSIONS: These results suggest that a high protein diet stimulates colon tumor formation by increasing colonic inflammation and proliferation.