model assessment (HOMA). Homeostasis model assess the insulin resistance (HOMA-IR) is
calculated using the formula: =fasting insulin concentration (in mU/L) × fasting plasma glucose
concentration (in mmol/L)/22.5, and homeostasis model assessment beta cell function
(HOMA-B) is calculated using the formula: =20 × fasting insulin concentration/ (fasting
plasma glucose concentration - 3.5)[14]. Intravenous arginine stimulation tests were performed
under fasting conditions and the acute insulin response to arginine (AIR, in mU/L) was
calculated as the mean insulin value of 2, 4, and 6 min samples minus fasting insulin
concentration to evaluate the potential function of beta cells, and acute insulin secretion after
adjusted for plasma glucose was calculated as well[14].
typing
Genomic DNA was extracted from peripheral blood leucocytes in whole blood samples. SNP
was identified by PCR amplification followed by DNA sequencing.PCR amplification was
carried out on the GeneAmp PCR system 9700 (Applied Biosystems, Foster City, CA, USA),
and DNA sequencing was carried out using 3100 Genetic Analyzer (Applied Biosystem, Foster
City, CA, USA).
tical analysis
The allele frequencies determined by gene calculating and the Hardy–Weinberg equilibrium
tests were performed[15]. Parameters (expressed as means ± SEM) presented in Table1 was
determined for normal distribution by the Shapiro-Wilk test. Differences between parameters
with normal distribution were tested using the multiple linear regression (adjusted for sex, age,
BMI, genotype and hospitals), and differences between parameters with abnormal distribution
were tested by the Kruskal-Wallis Test. The parameters tested include (i) baseline value, (ii)
value at 24 weeks after repaglinide therapy, and (iii) Δ value between (i) and (ii). All of these
analyses were performed using SAS for Windows (version 6.12; SAS Institute, Cary, NC). A
two-tailed P value < 0.05 was considered statistically significant. Mixed effect model analysis
was performed using SPSS for Windows (version 13.0; SPSS Inc., Chicago, IL, USA) to test
int
论文范文http://www.chuibin.com/ eraction effect between genotype and repaglinide treatment. Parameters of each individual本文来自优.文,论-文·网原文请找腾讯32491-14
at pre and post 24-week repaglinide treatment were considered as repeated measure factor.
Compound symmetry was chosen as covariance structure. Covariates were sex, age, BMI, and
centers.
lts
Of total 104 patients recruited, 100 (66 men, 34 women) completed the 24-week study. Two
patients were excluded because of glycated hemoglobin 8% at two consecutive times, and
two were dropped out. The GG, GT, TT genotype distribution among the patients was 40, 50,
and 10, respectively. The alleles of the G/T variant in rs10494366 were 65 and 35. The minor
allele frequency was 0.350 (T allele) and genotype distribution was in agreement with the
Hardy-Weinberg equilibrium (P = 0.323)[15]. The subjects were divided into three groups
according to NOS1AP genotype.
The baseline value of BMI, HOMA-IR, HOMA-B, and fasting insulin level among GG, GT,
and TT genotypes were significantly different (P = 0.024, 0.030, 0.005, and 0.007, respectively)
(Table 1). The values of these four clinic parameters all increased from GG, GT to TT genotype.
The Δ values of parameters at pre and post treatment between different genotypes were
determined by multiple linear regression or Kruskal-Wallis Test when appropriate; the results
showed that the Δ values of HOMA-IR (P = 0.011) and fasting insulin (P = 0.019) were
statistically significant between the three groups (Table 1). However, the baseline values of
HOMA-IR (P = 0.030) and fasting insulin (P =0.007) were significant different as well. To
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