Postprandial hyperglycaemia is thought to increase inflammation in leucocytes. In the present study, we examined whether sucrose loading in rats with moderate postprandial hyperglycaemia induces the expression of cytokines in peripheral leucocytes and whether these inductions are suppressed by inhibiting postprandial hyperglycaemia with the a-glucosidase inhibitor miglitol. One group of streptozotocin-treated rats and agematched saline-treated rats were orally administered sucrose only, and another group of streptozotocin-treated rats was administered sucrose with miglitol, at a single daily dose for 4 d, under 4 h fasting conditions. Blood glucose levels at 0, 0·25, 0·5, 1, 2 and 3 h and cytokine mRNA in peripheral leucocytes at 0 and 3 h after sucrose loading on days 1 and 4 from the start of sucrose loading were determined. Streptozotocin-treated rats showed moderate postprandial hyperglycaemia (. 2000 mg/l) at 0·25 -1 h after sucrose loading on days 1 and 4. Postprandial hyperglycaemia was not observed in the miglitol-treated rats loaded with sucrose. Gene expression levels of IL-1b and TNF-a were higher in the streptozotocin-treated rats at fasting on day 1 than in saline-treated rats. Fasting IL-1b and TNF-a gene expression on day 1 were not only increased at 3 h on the same day of sucrose loading, but was also increased at the fasting period on day 4. These inductions on day 4 by intermittent sucrose administration were inhibited by miglitol. The present results suggest that miglitol decreases postprandial hyperglycaemia and intermittent sucrose-induced expression of the IL-1b and TNF-a genes in rat peripheral leucocytes.
2 integrins (CD11s/CD18) promote the attachment of leukocytes to vascular endothelial cells. We performed in this study sucrose loading to rats with moderate postprandial hyperglycemia with/without once-daily dosing of the -glucosidase inhibitor, miglitol, for 4 days under 4-h fasting conditions. The streptozotocin (STZ)-treated rats showed moderate postprandial hyperglycemia on days 1 and 4. The gene expression was higher for CD11a with fasting and 3-h postprandial on day 1, and with fasting on day 4, for CD11b with fasting on day 1 and 3-h postprandial on day 4, and for CD18 with fasting on days 1 and 4 in peripheral leukocytes from the STZ-treated rats than in peripheral leukocytes from the saline-treated rats. Miglitol reduced postprandial hyperglycemia and the gene expression of CD11a with fasting and of CD11b 3-h postprandial on day 4. These results indicate that inhibiting postprandial hyperglycemia reduced the mRNA expression of 2 integrins in peripheral leukocytes of moderately postprandial hyperglycemic rats.
Postprandial hyperglycemia is thought to cause inflammation in many tissues. In this study, we examined whether the gene expression of inflammatory cytokines in peripheral leukocytes are altered by chromic and/or acute postprandial hyperglycemia. Seven‐week‐old male Sprague‐Dawley rats received a high‐fat (64 energy%) diet for 77 days to induce an insulin resistance. Blood was collected from tail vein, and the total RNA extracted from peripheral leukocytes was subjected to microarrays and real‐time RT‐PCR. In another experiment, rats treated with streptozotocin (35 mg/kg BW) received an oral dose of sucrose (2 g/kg BW) in the presence or absence of α‐glucosidase inhibitor, miglitol, and the gene expressions of peripheral leukocytes were analyzed thereafter. Microarray analysis of the genes in peripheral leukocytes showed that rats with chronic postprandial hyperglycemia had greater expressions of the genes coding inflammatory cytokines (IL‐1β, S100 a8/a9) and those related to host defense. Oral sucrose loading in rats with glucose intolerance led to a 2‐fold increase in IL‐1β and TNF‐α mRNA levels in peripheral leukocytes within 3h, which was abolished by addition of miglitol to the sucrose solution. These results suggest that both chromic and acute postprandial hyperglycemia enhances the gene expression of inflammatory cytokines in peripheral leukocytes.
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