Objective To investigate the additive effects of uncoupling protein 2(UCP2) gene 3′-untranslated region(3′-UTR) 45-base pair insertion/deletion( I/D) variation and peroxisome proliferator activated receptor( PPAR)γ2 gene Pro12Ala variation on type 2 diabetes(T2DM) in Chinese Han popula-tion.Methods The UCP2 gene 3′-UTR I/D variation and PPARγ2 gene Pro12Ala variation were exam-ined by polymerase chain reaction-restriction fragment length polymorphism ( PCR-RFLP) in 490 type 2 dia-betes subjects and in 585 control subjects .The additive effects of the two gene mutations were analyzed . Results ⑴The frequency of PPARγ2 gene Pro12Ala variation in type 2 diabetes was not significantly dif-ferent from that in control subjects.(χ2 =0.058, P =0.809).In T2DM group, A12 allele carriers had larger waist circumference than Pro12Pro genotype carriers;Glucose stimulated insulin secretion by oral glu-cose tolerance test (OGTT) was significantly lower in carriers of the Ala12Ala or Pro12Ala genotype com-pared with Pro12Pro genotype.( Z =2.222, P =0.026; Z =2.051, P =0.040; Z =2.079, P =0.038 ) .⑵There wasn't significant difference among 3 genotypes with 3′-UTR I/D variation in UCP2 gene (χ2 =2.311 , P =0.315 ) .In control group , Glucose stimulated insulin secretion by oral glucose tolerance test ( OGTT) was significantly higher in carriers of the I/D or I/I genotype compared with D/D genotype ( Z =1.997 , P =0.046 ) .⑶The genotype carriers with Pro/Ala +Del/Del were the greatest relation to T2DM (OR=1.22, 95%CI 1.078~1.386).Conclusion Though the UCP2 gene mutation alone or the PPARγ2 gene mutation alone is not associated with T 2DM, the possible additive effects of the two micro genes increase the occurring of T 2DM.

Objective To investigate the association of CA repeats polymorphism in the promoter region of human IGF-I gene with type 2 diabetes in narthen Han nationality. Methods Gender-age matched subjects with type 2 diabetes and normal glucose tolerance (NGT) were enrolled for this study, 147 subjects in type 2 diabetes group and 159 subjects in NGT group. Genomic DNA was extracted by standard methods. PCR, Genescan,Genotyper, and direct sequencing were conducted to screen CA repeats polymorphism in the promoter region of the human IGF-I gene. Results No significant association was observed between any ( CA), repeat genotype and type 2 diabetes. A lowered serum uric acid was seen in genotypes that included alleles with larger than (CA) 20 repeats [(4.18 ± 1.25 vs 4.63 ± 1.36) mg/dl, P = 0.03]. Conclusion Alleles with larger than (CA) 20 repeats may be a protective factor for type 2 diabetes.

Objective To explore the association of NH2-terminal pro-B-type natriuretic peptide ( NT-proBNP) with the risk of type 2 diabetes.Methods One hundred and twenty-six impaired glucose regulation( IGR) participants from Diabetic Identification Center of Tianjin Metabolic Diseases Hospital were included.NT-proBNP was measured in plasma samples collected from participants at baseline condition.Results At baseline, NT-proBNP was inversely associated with body mass index, waist circumference, fasting glucose, insulin and low-density lipoprotein-cholesterol( LDL-C) levels.During a follow-up of 2 years, 51 participants reported a new diagnosis of diabetes from OGTT.Baseline quartiles of NT-proBNP were inversely associated with diabetes risk, even after multivariable adjustment.Theadjustedrelativerisksfordiabeteswere1.0(reference),0.83(95%CI0.74-0.96),0.78(95%CI 0.68-0.90), 0.74 (95%CI 0.64-0.87) for the 1st, 2nd, 3rd, and 4th quartiles of baseline NT-proBNP, respectively ( P<0.01 ) .Conclus ion In IGRpopulation , lowlevels of NT-proBNP were associated with a significantly increased risk of type 2 diabetes.

so higher in diabetic patients 4 h after the meal (all P<0. 05). Positive correlation existed between serum triglycerides and white blood cell counting, neutrophils, and high-sensitivity C-reactive protein(r were between 0.268 and 0.548, all P<0.05).

Objective This study observed the clinical curative effects of aldose reductase inhibitor epalrestat in treat-ment of diabetic sensory neuropathy. Methods Thirty-four diabetic sensory neuropathy patients were selected. The nerve electrophysiological data were collected before and after treating with epalrestat. Results The ratios of nerve con-ductive velocity in peroneal nerve sensory showed slowing down than normal before and after the treatment, which were respectively 61% and 32%; The ratios of the nerve conductive velocity in tibial nerve sensory nerve segment 1 showed slowing down before and after the treatment,which were respectively 97% and 65%; The nerve conductive velocity of the peroneal sensory nerve after treatment was significantly faster than that before treatment, the nerve conductive ve-locity of the the tibial nerve sensory nerve motion segments in 1 after treatment was significantly faster than that before treatment. Conclusion Epalrestat is one of the effective methods in the treatment of diabetic peripheral neuropathy.

BACKGROUNDCopious evidence from epidemiological and laboratory studies has revealed that sleep status is associated with glucose intolerance, insulin resistance, thus increasing the risk of developing type 2 diabetes. The aim of this study was to reveal the interaction of sleep quality and sleep quantity on glycemic control in patients with type 2 diabetes mellitus.

METHODSFrom May 2013 to May 2014, a total of 551 type 2 diabetes patients in Tianjin Metabolic Diseases Hospital were enrolled. Blood samples were taken to measure glycosylated hemoglobin (HbA1c), and all the patients completed the Chinese version of the Pittsburgh Sleep Quality Index (PSQI) questionnaire to evaluate their sleep status. "Good sleep quality" was defined as PQSI <5, "average sleep quality" was defined as PQSI 6-8, and "poor sleep quality" was defined as PQSI >8. Poor glycemic control was defined as HbA1c ≥7%. Sleep quantity was categorized as <6, 6-8, and >8 hours/night. Short sleep time was defined as sleep duration <6 hours/night.

RESULTSIn the poor glycemic control group, the rate of patients who had insufficient sleep was much higher than that in the other group (χ(2) = 11.16, P = 0.037). The rate of poor sleep quality in poor glycemic control group was much greater than that in the average control group (χ(2) = 9.79, P = 0.007). After adjusted by gender, age, body mass index, and disease duration, the adjusted PSQI score's OR was 1.048 (95% CI 1.007-1.092, P = 0.023) for HbA1c level. The sleep duration's OR was 0.464 (95% CI 0.236-0.912, P = 0.026) for HbA1c level. One-way analysis of variance showed that the poor sleep quality group had the highest homeostasis model assessment-insulin resistance (P < 0.01).

CONCLUSIONSInadequate sleep, in both quality and quantity, should be regarded as a plausible risk factor for glycemic control in type 2 diabetes. Poor sleep might bring much more serious insulin resistance and could be the reason for bad glycemic control. A good night's sleep should be seen as a critical health component tool in the prevention and treatment of type 2 diabetes. It is important for clinicians to target the root causes of short sleep duration and/or poor sleep quality.

Adult ; Aged ; Aged, 80 and over ; Blood Glucose ; metabolism ; physiology ; Cross-Sectional Studies ; Diabetes Mellitus, Type 2 ; blood ; physiopathology ; Female ; Humans ; Male ; Middle Aged ; Sleep ; physiology ; Young Adult