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ID 51468
FullText URL
Author
Kurose, Yuko
Kanzaki, Motoko
Teshigawara, Sanae Kaken ID
Murakami, Kazutoshi ORCID Kaken ID publons
Inoue, Kentaro
Terami, Takahiro
Katayama, Akihiro
Watanabe, Mayu
Higuchi, Chigusa
Miyatake, Nobuyuki
Abstract
Background: Galectin-9 (Gal-9) induces apoptosis in activated T helper 1 (T(H)1) cells as a ligand for T cell immunoglobulin mucin-3 (Tim-3). Gal-9 also inhibits the G1 phase cell cycle arrest and hypertrophy in db/db mice, the hallmark of early diabetic nephropathy, by reversing the high glucose-induced up-regulation of cyclin dependent kinase inhibitors such as p27(Kip1) and p21(Cip1). Methods: We investigated the serum levels of Gal-9 in the patients with type 2 diabetes and various stages of chronic kidney disease (CKD) (n = 182). Results: Serum Gal-9 levels in the patients with type 2 diabetes were 131.9 +/- 105.4 pg/ml and Log(10)Gal-9 levels significantly and positively correlated with age (r = 0.227, p = 0.002), creatinine (r = 0.175, p = 0.018), urea nitrogen (r = 0.162, p = 0.028) and osmotic pressure (r = 0.187, p = 0.014) and negatively correlated with estimated glomerular filtration rate (eGFR) (r = -0.188, p = 0.011). Log(10)Gal-9 levels increased along with the progression of GFR categories of G1 to G4, and they were statistically significant by Jonckheere-Terpstra test (p = 0.012). Log(10)Gal-9 levels remained similar levels in albuminuria stages of A1 to A3. Conclusion: The elevation of serum Gal-9 in the patients with type 2 diabetes is closely linked to GFR and they may be related to the alteration of the immune response and inflammation of the patients with type 2 diabetes and CKD.
Keywords
Type 2 diabetes
Glomerular filtration
Inflammation
Kidney disease
Nephropathy
Published Date
2013-01-22
Publication Title
BMC Nephrology
Volume
volume14
Publisher
Biomed Central Ltd
ISSN
1471-2369
Content Type
Journal Article
Official Url
http://dx.doi.org/10.1186/1471-2369-14-23
Related Url
http://ousar.lib.okayama-u.ac.jp/metadata/51451
language
英語
File Version
publisher
Refereed
True
DOI
Web of Science KeyUT