| Literature DB >> 17651698 |
Toshinari Takamura1, Masao Honda, Yoshio Sakai, Hitoshi Ando, Akiko Shimizu, Tsuguhito Ota, Masaru Sakurai, Hirofumi Misu, Seiichiro Kurita, Naoto Matsuzawa-Nagata, Masahiro Uchikata, Seiji Nakamura, Ryo Matoba, Motohiko Tanino, Ken-ichi Matsubara, Shuichi Kaneko.
Abstract
We hypothesized that systemically circulating peripheral blood mononuclear cells (PBMCs) reflect the pathophysiology of type 2 diabetes. PBMCs were obtained from 18 patients with type 2 diabetes and 16 non-diabetic subjects. The expression of genes in the PBMCs was analyzed by using a DNA chip followed by statistical analysis for specific gene sets for biological categories. The only gene set coordinately up-regulated by the existence of diabetes and down-regulated by glycemic control consisted of 48 genes involved in the c-Jun N-terminal kinase (JNK) pathway. In contrast, the only gene set coordinately down-regulated by the existence of diabetes, but not altered by glycemic control consisted of 92 genes involved in the mitochondrial oxidative phosphorylation (OXPHOS) pathway. Our findings suggest that genes involved in the JNK and OXPHOS pathways of PBMCs may be surrogate transcriptional markers for hyperglycemia-induced oxidative stress and morbidity of type 2 diabetes, respectively.Entities:
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Year: 2007 PMID: 17651698 DOI: 10.1016/j.bbrc.2007.07.006
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575