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He R.,Shanghai Institute for Diabetes | Shen J.,Shanghai Institute for Diabetes | Liu F.,Shanghai Institute for Diabetes | Zeng H.,Shanghai Institute for Diabetes | And 6 more authors.
Diabetic Medicine | Year: 2014

Aims: To investigate the relationship between vitamin D deficiency and diabetic retinopathy. Methods: In total, 1520 patients with Type 2 diabetes were recruited and divided into three groups according to their fundus oculi results: no diabetic retinopathy (n = 625, 41.12%); non-sight-threatening diabetic retinopathy (n = 562, 36.97%); and sight-threatening diabetic retinopathy (n = 333, 21.91%). Vitamin D deficiency was defined as a serum circulating 25-hydroxyvitamin D level < 20 ng/ml. Clinical characteristics and biochemical parameters were detected and compared. Results: The patients with sight-threatening diabetic retinopathy had significantly lower serum 25-hydroxyvitamin D concentrations and higher prevalence of vitamin D deficiency than other two groups (all P < 0.05). In addition, there was a downward trend in average 25-hydroxyvitamin D level with the increased stages of diabetic retinopathy (P < 0.01). The prevalence of diabetic retinopathy and sight-threatening diabetic retinopathy in patients with vitamin D deficiency was also higher than in those without vitamin D deficiency (both P < 0.01). After adjusting for all potential confounders, vitamin D deficiency was still associated with increased risk of diabetic retinopathy (odds ratio 1.93) and sight-threatening diabetic retinopathy (odds ratio 2.42) (both P < 0.01). Logistical regression analysis further revealed that vitamin D deficiency was an independent risk factor for diabetic retinopathy (β = 0.66) and sight-threatening diabetic retinopathy (β = 0.93) (both P < 0.01). ROC analysis indicated that a serum 25-hydroxyvitamin D level < 15.57 ng/ml suggested the occurrence of sight-threatening diabetic retinopathy (odds ratio 2.38, P < 0.01). Conclusions: Vitamin D deficiency is an independent risk factor for diabetic retinopathy and sight-threatening diabetic retinopathy. The prevalence of sight-threatening diabetic retinopathy doubles when the serum 25-hydroxyvitamin D level is < 15.57 ng/ml. © 2014 Diabetes UK. Source


Zhang D.,Shanghai Institute for Diabetes | Hou W.,Shanghai Institute for Diabetes | Liu F.,Shanghai JiaoTong University | Yin J.,Shanghai Institute for Diabetes | And 6 more authors.
Diabetes Technology and Therapeutics | Year: 2015

Background: This study was designed to clarify the influence of metformin on serum carbohydrate antigen 199 (CA199) levels and its associated factors in Chinese type 2 diabetes mellitus (T2DM) patients. Subjects and Methods: In total, 1,253 T2DM patients were enrolled, including a non-metformin group (n=616), a short-term metformin group (at least 1 week to 2 years; n=325), and a long-term metformin group (≥2 years; n=312). Their clinical and biochemical characteristics were collected and compared. After 1 year, the biochemical parameters were re-examined in 296 patients. Sex hormones were determined, and associations between CA199 and other variables were assessed. Results: At baseline, the incidence of abnormal CA199 levels was 14.7%, 8.9%, and 4.7% in the non-metformin, short-term metformin, and long-term metformin groups, respectively. CA199 levels in females were significantly higher than in males (P<0.01) and decreased significantly with the time of taking metformin (25.60±13.68 U/mL in non-metformin controls vs. 17.62±10.87 U/mL in the short-term group vs. 10.54±8.14 U/mL in the long-term group; P=0.000). The correlation and multiple stepwise regression analysis revealed that glycosylated hemoglobin, metformin, gender, total cholesterol, and follicle-stimulating hormone were independent impact factors on CA199 concentrations (all P<0.05). Binary logistic regression revealed that the risk of abnormal CA199 concentrations of the total population with short-term metformin or long-term metformin treatment decreased 11% (odds ratio=0.89; P=0.001) and 30% (odds ratio=0.70; P=0.000), respectively, at baseline. After a 1-year follow-up, the incidence of high CA199 level decreased in both the short-term and the long-term metformin group compared with that of controls (P<0.05). The extent of CA199 decrease in the long-term metformin group was the greatest (-17% vs. -4.9% in the short-term group vs. 3% in controls, P=0.000), and the group's risk of high blood CA199 level was reduced 67% (odds ratio=0.33; P=0.023). The reduction in women was more apparent than that in men (-18% vs. -5%, P=0.000). Conclusions: Metformin therapy reduced the CA199 level in Chinese T2DM patients, and its greatest decrease occurred in women with longer therapeutic time. © Copyright 2015, Mary Ann Liebert, Inc. 2015. Source


Li Q.,Shanghai JiaoTong University | Li Q.,Shanghai Institute for Diabetes | Liu F.,Shanghai JiaoTong University | Liu F.,Shanghai Institute for Diabetes | And 8 more authors.
Acta Pharmacologica Sinica | Year: 2010

Aim: To investigate the potential relationship between the SLC22A2 gene polymorphism and blood lactate concentration in Shanghai Hans suffering from type 2 diabetes mellitus (T2DM). Methods: The SLC22A2 single nucleotide polymorphism (SNP) 808G/T was genotyped in 400 T2DM patients, including a metformin-treated group (n=200) and a non-metformin-treated group (n=200). Fasting plasma lactic acid levels were measured with an enzyme-electrode assay. Biochemical indexes, including plasma alanine aminotransferase (ALT), creatinine (Cr), and glycolated hemoglobin (HbA1c), were also measured. Results: The fasting plasma lactate concentration in the metformin-treated group was significantly higher than that in the non-metformin-treated group (1.29±0.45 mmol/L vs 1.18±0.44 mmol/L, P=0.015). Additionally, the ratio of patients with hyperlactacidemia was 8% (16/200) for the metformin-treated group and 5.5% (11/200) for the non-metformin-treated group, with no lactic acidosis found in either group. The frequency of the SLC22A2 808G/T T allele was 12.9%. Patients with the mutant genotype (TT) had a higher blood lactate concentration in the metformin-treated group than those in the non-metformin-treated group (t=2.492, P=0.013). This trend was not observed in the GG and GT genotypes when compared with metformin-treated and non-metformin-treated groups. Patients with the mutant genotype (TT) in the metformin-treated group also had a higher incidence of hyperlactacidemia compared with the GG genotype (40.0% vs 6.9%, P=0.050) in the metformin-treated group and the GG (6.0%, P=0.042) or GT (4.3%, P=0.043) genotypes in the non-metformin-treated group. In the metformin-treated group, there were significant gender differences in lactate concentrations in the TT (2.18±0.15 vs 1.04±0.27 mmol/L, P=0.008) and GG genotypes (1.40±0.51 vs 1.19±0.35 mmol/L, P=0.004). The lactate levels of women with the TT genotype were the highest in the metformin-treated group, but differences in lactate levels among the genotypes were not observed in the non-metformin-treated group. Conclusion: There is an 808G/T polymorphism in the SLC22A2 gene in Chinese Hans with T2DM. The 808G>T variance in the SLC22A2 gene can affect the plasma lactate level and the incidence of hyperlactacidemia in T2DM patients undergoing metformin therapy. Additionally, the female patients carrying the TT genotype are prone to lactatemia. © 2010 CPS and SIMM All rights reserved. Source

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