Subject headings diabetes mellitus; maltose; gymnemic acid; alpha-glucosidases; intestinal mucosa; rats; nutrition Luo H, Wang LF, Imoto T, Hiji Y. Inhibitory effect and mechanism of acarbose combined with gymnemic acid on maltose absorption in rat intestine. World J Gastroenterol, 2001;7(1):9-15 Abstract AIM To compare the combinative and individual effect of acarbose and gymnemic acid (GA) on maltose absorption and hydrolysis in small intestine to determine whether nutrient control in diabetic care can be improved by combination of them. METHODS The absorption and hydrolysis of maltose were studied by cyclic perfusion of intestinal loops in situ and motility of the intestine was recorded with the intestinal ring in vitro using Wistar rats. RESULTS The total inhibitory rate of maltose absorption was improved by the combination of GA (0.1g/L -1.0g/L) and acarbose (0.1mmol/L -2.0mmol/L) throughout their effective duration (P <0.05, U test of Mann-Whitney), although the improvement only could be seen at a low dosage during the first hour. With the combination, inhibitory duration of acarbose on maltose absorption was prolonged to 3 h and the inhibitory effect onset of GA was fastened to 15 min. GA suppressed the intestinal mobility with a good correlation (r = 0.98) to the inhibitory effect of GA on maltose absorption and the inhibitory effect of 2 mmol/L (high dose) acarbose on maltose hydrolysis was dual modulated by 1 g/L GA in vivo indicating that the combined effects involved the functional alteration of intestinal barriers. CONCLUSION There are augmented effects of acarbose and GA,which involve pre-cellular and paracellular barriers. Diabetic care can be improved by employing the combination.

Tumor necrosis factor alpha (TNF-alpha) responses of alveolar macrophages (AMs) and peritoneal macrophages (PMs) were studied in rats after intravenous injection of lipopolysaccharide (LPS). High levels of plasma TNF-alpha, increased pulmonary myeloperoxidase activity, and leukopenia occurred within 2 h after LPS injection. Alveolar spaces exhibited a strict compartment property, as manifested by only slightly increased LPS and TNF-alpha levels in alveolar lavage fluid and an unchanged capacity of AMs to produce TNF-alpha. By contrast, the peritoneal cavity had greatly increased local LPS and TNF-alpha levels and a diminished PMs TNF-alpha response to LPS. The amount of LPS in the alveolar spaces was less than 0.2% of the level in peritoneal fluid. These results indicate that activation of resident macrophages is dependent on the amounts of local LPS and, in addition, suggest that resident AMs neither participate in the plasma TNF-alpha response nor contribute to neutrophil sequestration in the lung during the early stages of endotoxemia.