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Chronic and acute postprandial hyperglycemia enhances the gene expressions of inflammatory cytokines in the peripheral leukocytes in rats
Author(s) -
Goda Toshinao,
Fujimoto Saki,
Tanaka Yutaro,
Fukaya Nanae,
Shimada Masaya,
Mochizuki Kazuki
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.597.7
Subject(s) - postprandial , medicine , endocrinology , proinflammatory cytokine , peripheral , inflammation , gene expression , insulin , biology , gene , biochemistry
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.