Relationship Between Serum Leptin,PolymoRphism Of Leptin Gene 2548g/a,leptin Receptor Gene Gln223Arg And Correlation To Obstructive Sleep Apnea Hypopnea Syndrom

Objective:1.Compare the level of serum leptin between Obstructive sleep apnea hypopnea syndrom(OSAHS) patients and control group , discuss the clinical significance.2.To analyze each genotype distribution and allele frequency of leptin gene2548G/A, leptin receptor gene Gln223Arg in OSAHS patients .3.Discuss the relationship between the two sites gene polymorphism and OSAHS susceptibility .Methods:Collect 384 male issued were monitored by polysomnography graph (PSG) in the sleep room of Department of Respiratory Medicine Affiliated Kai-Luan Hospital North China Coal Medical College during January 2010 - December 2010, divided into two groups:OSAHS group(183 cases) and control group (201 cases),including obese OSAHS group (90 cases), non-obese OSAHS group (93 cases), obesity control group (105 patients) and normal control group (96 cases) .All accord with cases inclusion criteria, do not accord with exclusion standard. Research object in using face-to-face questionnaire form before sleep monitoring.By investigators each inquiry questionnaires content Simultaneously screening, including the life and eating habits such as sleep situation, life habit, medical history, family history, cigarette, wine, tea, salt and so on.The issued must be monitored at least 7 hours at night In s-type polysomnography(the changes of AHI every hour and the dynamic change of blood pressure at night). Extracting morning hollow cubits venous 8ml for inspection. Enzymatic oxidation was used to measure the level of triglycerides and total cholesterol in blood serum. Enzyme-linked immunosorbent assay (ELISA) was used to measure the level of leptin in blood serum.To detect the leptin gene 2548G/A and genotypes of Leptin receptor gene Gln223Arg by using Polymerize chain reaction-Restriction fragment length polymorphism (PCR-RLFP). Material processing with EXCEL2003. Statistical analysis is used SPSS13.0 packages. According to genetic numeration method to calculate the allele frequency and inspect Hardy-Weinberg balance alignmenton of two locus genotype by using geneticχ~2testing method. Counting data usedχ~2 inspection.Measurement data were said to mean±standard deviations ( x±s) , using t-test and analysis of variance. Take P < 0.05 for differences are statistically significant.Results:obese OSAHS group and obesity control group weight index increased obviously, significantly higher than non-obese OSAHS group and normal control group, significant difference (P < 0.05). Neck circumference and waist-hip ratio of OSAHS group (obese OSAHS group and non-obese OSAHS group) is higher than that of obesity control group and normal control group(P<0.05).But there was no statistically significant in obese OSAHS group and non-obese OSAHS group(P>0.05).AHI comparative , there was no statistically significant in obesity control group(1.20±1.22/h) and normal control group(1.29±1.43/h), OSAHS group(obese OSAHS group and non-obese OSAHS group) is higher than that of them, especially for obese OSAHS group(44.49±22.86/h),but the lowest blood oxygen saturation (LSO2)on the contrary, obese OSAHS group is 0.61±0.18, obviously lower than other groups, significant difference (P< 0.05).The level of serum leptin in non-obese OSAHS patients(13.37±4.83μg/L)and obesity control patients (12.55±1.90μg/L) are more increased than normal control group(7.1±1.55μ g/L), but there was no difference between them. The level of leptin increased significantly for (18.44±3.26μg/L) after OSAHS merger obesity, compared with the other three groups, significant difference (P< 0.05). There was no interaction between besity and OSAHS (F=0.351,P>0.05) .TG comparative ,it was obviously higher in obese OSAHS group, non-obese OSAHS group and obesity control group than that of in normal control group (P < 0.05). it was higher in obese OSAHS group than that of in non-obese OSAHS group and obesity control group (P < 0.05). The difference was no statistically significant in non-obese OSAHS group and obesity control group(P>0.05). TC comparative, the difference was no statistically significant in each group(P>0.05). The level of serum leptin and AHI, neck circumference , waist-hip ratio and TG into positive correlation(P<0.05),and LSO~2 a negative correlation(P<0.05). After merger obesity( obese OSAHS group), the level of serum leptin and BMI into positive correlation(P<0.05). 2548G/A and Gln223Arg genotype and allele frequency comparative in four groups was no statistically significant (P>0.05). But AA genotype patient(s0.93±0.07或0.89±0.05) in 2548G/A below AG/GG type in waist-hip ratio of comparative(P<0.05). Neck circumference(41.66±2.87cm)of GG genotype patients in Gln223Arg is greater than that of AA/AG patients(P<0.05).Conclusion:1.The level of serum leptin in OSAHS patients is remarkable than that of in control crowd, and independent of obesity factors.It and AHI, neck circumference, waist-hip ratio and TG into positive correlation, and LSO~2 a negative correlation. The level of leptin significantly increased after merging obesity, and BMI into positive correlation.2. There is no relations between The gene polymorphism of two sites in Leptin gene 2548G/A, leptin receptor gene Gln223Arg and the onset of OSAHS. But 2548G/A variations may related with the occur of abdominal obesity, Gln223Arg variation may be involved in regulating OSAHS patients neck fat distribution.