Reduced serum level of leukocyte cell-derived chemotaxin 2 is associated with the presence of diabetic retinopathy.
BACKGROUND
Vascular endothelial growth factor (VEGF) signaling is an important pathway in the development of diabetic retinopathy (DR). A recent report showed that leukocyte cell-derived chemotaxin 2 (LECT2) suppresses the VEGF signaling in endothelial cells. However, the clinical relevance of LECT2 in DR is unknown. This study aimed to investigate serum LECT2 levels and the presence of DR.


METHODS
The study included 230 people with type 2 diabetes mellitus (DM), 95 with DR and 135 without DR. Serum LECT2 levels were measured using an enzyme-linked immunosorbent assay. Data were evaluated using Spearman's rank correlation, univariate and multivariate logistic regression.


RESULTS
Serum LECT2 levels were significantly lower in participants with DM having DR than in those not having DR (35.6±14.9ng/ml vs. 44.5±17.6ng/ml, P<0.001). Spearman's rank correlation analysis revealed a significant association between serum LECT2 levels and the presence of DR (P<0.001). Multiple regression analysis revealed that serum LECT2 levels were independently related to DR (P<0.001).


CONCLUSIONS
These findings indicated that serum LECT2 level is negatively associated with the presence of DR and suggest that low circulating LECT2 level is a risk factor for DR.
Department of Diabetic Complications, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo 162-8655, Japan.
Akinori
A
Okumura
Department of Diabetic Complications, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo 162-8655, Japan.
Hiroyuki
H
Unoki-Kubota
Department of Ophthalmology, Center Hospital, National Center for Global Health and Medicine, Tokyo 162-8655, Japan.
Natsuyo
N
Yoshida-Hata
Department of Diabetes, Endocrinology, and Metabolism, Center Hospital, National Center for Global Health and Medicine, Tokyo 162-8655, Japan.
Ritsuko
R
Yamamoto-Honda
Department of Diabetes and Endocrinology, JR Tokyo General Hospital, Tokyo 151-8528, Japan.
Shigeo
S
Yamashita
First Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama 930-0194, Japan.
Minoru
M
Iwata
First Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama 930-0194, Japan.
Kazuyuki
K
Tobe
Department of Diabetes, Endocrinology, and Metabolism, Center Hospital, National Center for Global Health and Medicine, Tokyo 162-8655, Japan.
Hiroshi
H
Kajio
Department of Diabetes, Endocrinology, and Metabolism, Center Hospital, National Center for Global Health and Medicine, Tokyo 162-8655, Japan; Department of Endocrinology and Diabetes, Saitama Medical University, Saitama 350-0495, Japan.
Mitsuhiko
M
Noda
Department of Ophthalmology, Center Hospital, National Center for Global Health and Medicine, Tokyo 162-8655, Japan.
Naomichi
N
Katai
Department of Chemotherapy and Mycosis, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Satoshi
S
Yamagoe
Department of Diabetic Complications, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo 162-8655, Japan. Electronic address: kaburagi@ri.ncgm.go.jp.
Yasushi
Y
Kaburagi
D000328:Adult; D000368:Aged; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D003930:Diabetic Retinopathy / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood*; D008297:Male; D008875:Middle Aged
D036341:Intercellular Signaling Peptides and Proteins; C103468:LECT2 protein, human
Diabetic retinopathy; Leukocyte cell-derived chemotaxin 2; Type 2 diabetes mellitus