Determination of the transient period of the EIS complex and investigation of the suppression of blood glucose levels by L-arabinose in healthy adults.

PURPOSE: L-Arabinose uncompetitively inhibits intestinal sucrase by forming an enzyme-inhibitor-substrate (EIS) complex. The transient period of the EIS complex affects the time span of inhibition. We determined the apparent transient period of the EIS complex of sucrase, L-arabinose, and sucrose both in vitro and in humans. METHODS: Intestinal acetone powder (a source of sucrase), L-arabinose, and sucrose were mixed and injected into a dialysis membrane that was placed in a sucrose solution. The production rate of D-glucose and the release rate of L-arabinose from sucrase were determined. We also investigated the suppression of blood glucose levels by L-arabinose in 21 healthy volunteers. Sucrose (40 g) was ingested with or without L-arabinose (2 g), then blood glucose values were measured, which returned to steady-state conditions within 2 h. Volunteers were then given 90 g of commercial adzuki bean jelly containing 40 g sucrose as the sucrose load, and blood glucose values were measured again. RESULTS: Addition of L-arabinose reduced the production rate of D -glucose compared to the rates measured in the absence of L-arabinose for several hours in vitro. L-Arabinose was released at a lower rate in the presence of sucrose than in its absence. Blood glucose values measured 2 h after sucrose was given with L -arabinose were significantly lower than those measured when L-arabinose was not given (Δ change in maximum value: with L-arabinose, 53.8 ± 19.7 mg/dL; without L-arabinose, 65.0 ± 17.7 mg/dL). CONCLUSION: The EIS complex of sucrase-L -arabinose-sucrose was maintained for several hours both in vitro and in humans.

Promoting Effects of Sucrose-rich Diet on N-Nitrosobis (2-oxopropyl) amine-induced Pancreatic Carcinogenesis in Hamsters.

It has been reported that there is an association between pancreatic cancer and obesity, impaired glucose metabolism and diabetes based on excess dietary fat and sugar intakes. A number of studies have suggested that a high-fat diet increases development of carcinomas in various organs and possible risk factors for pancreatic cancer. However, how an excess sugar intake promotes pancreatic carcinogenesis is still unknown. In the present study, we investigated the influence of an excess sugar intake on pancreatic carcinogenesis by administration of a sucrose-rich diet in which starch was replaced by sucrose in order to contain the same calories and other nutrients. Two similar experiments were performed. Six-week-old male Syrian golden hamsters were given N-nitrosobis (2-oxopropyl) amine (BOP) at a dose of 50 and 20 mg/kg body weight as a carcinogen in Week 0 and 1, respectively. In Week 2, the animals were divided into control and experimental groups. In experiment 1, 15 animals received a control diet or sucrose-rich diet in which 100% of the starch was replaced by sucrose, respectively. Since five animals fed on the sucrose-rich diet died by Week 12, the diet was changed to a sucrose-rich diet in which 50% of the starch was replaced by sucrose. In experiment 2, 15 animals received a control diet or sucrose-rich diet in which 50 or 20% of the starch was replaced by sucrose, respectively. All animals were sacrificed 25 weeks after the start of the experiment, and histological examination of the pancreas was performed. No significant difference was seen in the body weight at the end of the experiment. There were no significant differences in the glycosylated hemoglobin (HbA1c) and serum triglyceride, total cholesterol and HDL-cholesterol levels between the control and sucrose-rich diet groups in experiments 1 and 2. The incidence and number of carcinomas increased in hamsters fed the sucrose-rich diet compared with the control diet in experiments 1 and 2. These results suggest that an excess sucrose intake may promote the development of pancreatic cancer in hamsters.