The alpha-glucosidase inhibitor miglitol suppresses postprandial hyperglycaemia and interleukin-1beta and tumour necrosis factor-alpha gene expression in rat peripheral leucocytes induced by intermittent sucrose loading.
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 alpha-glucosidase inhibitor miglitol. One group of streptozotocin-treated rats and age-matched 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-1beta and TNF-alpha were higher in the streptozotocin-treated rats at fasting on day 1 than in saline-treated rats. Fasting IL-1beta and TNF-alpha 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-1beta and TNF-alpha genes in rat peripheral leucocytes.
Tanaka
Yutaro
Y
Laboratory of Nutritional Physiology, Graduate School of Nutritional and Environmental Sciences and the Global COE Program, The University of Shizuoka, Shizuoka 422-8526, Japan.
Mochizuki
Kazuki
K
Fukaya
Nanae
N
Shimada
Masaya
M
Goda
Toshinao
T
D017485:1-Deoxynojirimycin / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000818:Animals; D003921:Diabetes Mellitus, Experimental; D019422:Dietary Sucrose / Q000008:administration & dosage; D015870:Gene Expression / Q000187:drug effects; D065089:Glycoside Hydrolase Inhibitors; D006943:Hyperglycemia / Q000188:drug therapy* / Q000276:immunology; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000201:enzymology / Q000276:immunology*; D008297:Male; D023421:Models, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D013549:Sweetening Agents / Q000008:administration & dosage; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
D019422:Dietary Sucrose; D065089:Glycoside Hydrolase Inhibitors; D053583:Interleukin-1beta; D013549:Sweetening Agents; D014409:Tumor Necrosis Factor-alpha; C045621:miglitol; D017485:1-Deoxynojirimycin