The relationship between serum leptin level and metabolic syndrome among a middle-aged Chinese population / 中华预防医学杂志

<p><b>OBJECTIVE</b>To explore the relationship between serum level of leptin and the components of metabolic syndrome in a group of mid-aged Chinese population.</p><p><b>METHODS</b>345 adults (184 men and 161 women) aged 46 - 53 were enrolled from Fetal Origin of Adult Disease (FOAD) cohort to participate the clinic examination including anthropometry, measurements of blood pressure, fasting and 2 hr plasma levels of glucose and insulin, serum levels of lipid and leptin. HOMA-IR index was calculated to estimate individual insulin resistance. Metabolic syndrome (MS) was diagnosed according to the definition criteria issued by the International Diabetes Federation (IDF) in 2005.</p><p><b>RESULTS</b>The prevalences of central obesity, higher serum level of triglyceride (TG), lower serum level of high-density lipoprotein (HDL-C), IFG, higher blood pressure and MS were 53.0%, 47.5%, 34.2%, 26.7%, 33.9%, 31.9% in this mid-aged population, respectively. Serum geometric mean level of leptin was higher in females than in males. Serum level of leptin increased with the prevalence of MS and components of abnormal metabolism. The serum level of leptin compared with central obesity, higher blood pressure, higher serum level of triglyceride (TG), lower serum level of high-density lipoprotein cholesterol (HDL-C), IFG and MS was significantly higher respectively (P < 0.05) without HDL-C in males. The serum level of leptin increased with the number of components of abnormal metabolism subjects had (P < 0.001).</p><p><b>CONCLUSION</b>The serum level of leptin in this population is significantly associated with MS and components of MS. Hyperleptinemia could be a new component of metabolic syndrome. It might be a target in selection of MS and relative diseases.</p>

Ponderal index at birth predicts metabolic syndrome in mid-aged Chinese / 中华预防医学杂志

<p><b>OBJECTIVE</b>To examine the association between Ponderal index (PI) at birth and metabolic syndrome during middle age.</p><p><b>METHODS</b>Totally, 975 adults (494 men and 481 women) aged 41-52 from the study cohort of Fetal Origin of Adult Disease were recruited in the study for clinic examinations, involving anthropometry and measurements of blood pressure, fasting and 2 hr plasma levels of glucose and insulin, serum lipid profile. Their HOMA-insulin resistance (IR) index was estimated. Metabolic syndrome (MS) was diagnosed according to 1999 WHO definition. Multivariate logistic regression analysis was used to estimate the effect of PI on MS and the interaction between PI at birth and body mass index (BMI) in adulthood.</p><p><b>RESULTS</b>Prevalence of MS was 18.7% in this mid-aged population, 24.8%, 19.4%, 16.3% and 14.0% in those with less than the 25th percentile, the 25th to less than the 50th percentile, the 50th to less than the 75th percentile and more than 75th percentile of PI at birth, respectively, in a decreasing trend (chi2 M-H for trend=9.938 adjusted for gender, P=0.002). Logistic regression analysis showed that both PI at birth and BMI during adulthood could influence their occurrence of MS (beta=-0.125, P=0.002, for PI; and beta=0.430, P=0.000, for BMI). A synergistic effect between PI at birth and BMI in adulthood was observed in this population. Persons who were thin at birth with PI less than the 25th percentile, and became overweight with BMI greater than or equal to 24 kg/m2 later in their life, were at higher risk of suffering from metabolic syndrome (OR=29.1, 95% CI=13.6-62.1), in comparison with those who became overweight during adulthood from a higher PI at birth (OR=16.0, 95% CI=7.9-32.3) and those who were thin at birth and remained a appropriate BMI during their adulthood (OR=2.0, 95% CI=0.7-5.7). Attributable fraction of the interaction to MS was 34.6%.</p><p><b>CONCLUSIONS</b>Thin at birth was a predictor for later occurrence of metabolic syndrome, as well as an effect modifier for the association between of later BMI and metabolic syndrome, i.e., overweight later in his life was most deleterious for a person with growth retardation at birth.</p>

Association of Serum Adiponectin and Metabolic Syndrome in Children with Obesity and Nonalcoholic Fatty Liver Disease / 实用儿科临床杂志

Objective To investigate the relationship between serum adiponectin and metabolic syndrome(MS) in children and adolescents with obesity and nonalcoholic fatty liver disease(NAFLD).Methods Four elementary schools and 4 middle schools were selected from Haidian district in Beijing with representative cluster sampling.Two hundred and eighty obese children(obese group),65 obese children with NAFLD(NAFLD group) and 264 normal weight children(healthy control group) aged 7 to 18 years were recruited from the 8 schools with uncompletely randomized sampling.Data including questionnaire,anthropometric measurements,B type ultrasonographic examination for liver were collected and fasting blood laboratory assay were determined.Variables including triglyceride(TG),adiponectin,alanine aminotransferase(ALT) and aspartate aminotransferase(AST) were skewed distribution and natural logarithmical transformations were performed.Chi-square test for category and multiple binary Logistic regression analysis were used to statistical analysis.Results Body mass index(BMI) and waist circumference(WC) in obese group and NAFLD group were higher than those in healthy control group.All the chi-square tests for trend among the 3 groups were statistically significant(P

Study on the relationship between polymorphism of insulin-receptor gene EXON2-2257 and insulin resistance in Chinese people / 中华流行病学杂志

<p><b>OBJECTIVE</b>To understand the role of insulin-receptor gene in the development of insulin resistance on a population-based study in China.</p><p><b>METHODS</b>Polymerase chain reaction (PCR) was used to amplify the EXON2 of the insulin-receptor gene and all amplified products were analyzed by direct sequencing.</p><p><b>RESULTS</b>Three genotypes of single nucleotide at the site of 2257 in EXON2 of the insulin-receptor gene were identified. In 237 of the 345 cases (68.7%), homozygote genotype of CC phenotype was found with a gene frequency of 0.825; 13 cases (3.77%) showed homozygote genotype of TT phenotype with a gene frequency of 0.175 and the rest 95 cases (27.54%) showed heterozygote genotype of CT phenotype. Data were in agreement with the test of Hardy-Weinberg balance (chi(2) = 0.2898, upsilon = 3 - 2 = 1, 0.5 < P < 0.75). The serum level of triglyceride and the HOMA-IR index, the status of insulin resistance assessed by homeostasis model assessment (HOMA), were lower in the TT or CT genotype group than that in the CC genotype group (P < 0.05). Comparing with CC genotype, the proportion of CT genotype (18.4%) in the insulin resistance group (large than 75th percentile of HOMA-IR) was significantly lower than that in the control group (30.6%) (P = 0.022, OR = 0.493). The proportion of TT genotype (2.3%) in insulin resistance group was lower than that in the control group (4.3%, P = 0.297). logistic analysis revealed that after adjusting possible confounding factors such as taking anti-hypertensive and anti-diabetic medications, serum triglyceride and high density lipoprotein cholesterol (HDL-C), hypertension, BMI, smoking history, the OR value of people in the insulin resistance group with CT genotype was 0.448 (95% CI: 0.214 to 0.940) compared to the group with CC genotype.</p><p><b>CONCLUSION</b>The hybridization CT genotype at the site of 2257 in EXON2 of insulin-receptor gene might have a candidate gene to serve as a protective factor for insulin resistance.</p>

Polymorphisms of exon 17 of insulin-receptor gene in pathogenesis of human disorders with insulin resistance / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the relationship between polymorphisms of insulin-receptor (INSR) gene and insulin resistance in a population-based study in China.</p><p><b>METHODS</b>Polymerase Chain Reaction (PCR) was used to the amplify Exon 17 of INSR gene and all amplified products were analyzed by direct sequencing.</p><p><b>RESULTS</b>Six single-nucleotide polymorphisms (SNPs) were found at the following loci: T to TC at the locus of 10699 (Tyr(984)), G to GC at the locus of 10731 (Glu(994)), Deletion G at the locus of 10798 (Asp(1017)), C to T/TC at the locus of 10923 (His(1058)), C to CA at the locus of 10954 (Leu(1069)), and T to TA at the locus of 10961 (Phe(1071)), which might not change the amino acid sequence. The data were in agreement with the test of Hardy-Weinberg balance (P > 0.05). Among the 345 cases, all clinical indices were higher in males than in females except for HDL cholesterol (P < 0.05). The proportion of insulin resistance in males (64.4%) was higher than that in females (35.6%, OR = 1.83). It implied that the relative risk of developing insulin resistance in males was 1.83 times as high as that in females. The biochemical indices in different loci on Exon 17 showed that the individuals with deletion G on the locus of 10798 had lower TG (P = 0.052) and higher HDL (P = 0.027) than those without deletion G on the same site. Homa-Index was lower in those with deletion G than in those without deletion G (P > 0.05). After sex stratification in analysis, all allele frequencies on the six loci of SNPs of Exon 17 had different distributions between the insulin resistant group and the control group, but P > 0.05.</p><p><b>CONCLUSION</b>SNPs of Exon 17 of INSR gene are unlikely to play a direct role in the pathogenesis of human disorders with insulin resistance.</p>