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Search Results: 1 - 10 of 53333 matches for " Lee-Ming Chuang "
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The A54T polymorphism at the intestinal fatty acid binding protein 2 is associated with insulin resistance in glucose tolerant Caucasians
Ken C Chiu, Lee-Ming Chuang, Carol Yoon
BMC Genetics , 2001, DOI: 10.1186/1471-2156-2-7
Abstract: After genotyping, we identified 24 AA, 27 AT and 4 TT subjects. The TT subjects were combined with the AT subjects during the analysis due to its small sample size. No differences were noted in gender distribution, clinical features, and fasting lipid profile between the two genotypic groups (AA vs. AT/TT). The AT/TT group had a higher fasting plasma insulin concentration and a lower %S than the AA group (p = 0.0444 and p = 0.0461, respectively). However, no differences were noted in plasma glucose concentrations and %B. Univariate analysis revealed that this polymorphism explained 7.3% of the variation in %S. Multivariate analysis revealed that the polymorphism was an independent determinant for %S (p = 0.0434) and with body mass index accounted for 28.7% of the variation in %S. In contrast, this polymorphism had no impact on %B.The A54T polymorphism at the FABP2 locus is a risk factor for insulin resistance in a Caucasian population.The Pima Indians have a very high prevalence for type 2 diabetes mellitus (or non-insulin-dependent diabetes mellitus, NIDDM) with evidence of strong familial aggregation [1]. In this population, insulin resistance is a major risk factor for the development of the disease [2], and maximal insulin action (i.e. glucose disposal rate at pharmacological insulin levels) was found to be determined by a co-dominantly inherited autosomal gene [3]. Initially, Bogardus and colleagues observed an association and linkage between insulin resistance and red cell antigens on chromosome 4q [4]. After the analysis of 128 sib-pairs using quantitative trait sib-pair analysis, they observed a significant linkage between maximal insulin action and the intestinal fatty acid-binding protein 2 (FABP2) gene and the annexin V (ANX5) gene on chromosome 4q [5].It is well recognized that fatty acid metabolism is linked to insulin resistance [6,7]. Intestinal FABP2 contains a single ligand binding site that displays a high affinity for fatty acid [8]. Because it is
The vitamin D receptor polymorphism in the translation initiation codon is a risk factor for insulin resistance in glucose tolerant Caucasians
Ken C Chiu, Lee-Ming Chuang, Carol Yoon
BMC Medical Genetics , 2001, DOI: 10.1186/1471-2350-2-2
Abstract: There were 18 FF, 21 Ff, and 10 ff subjects. Since only 10 ff subjects were identified, they were pooled with the Ff subjects during analyses. The FF and Ff/ff groups had similar glucose levels at each time point before and after a glucose challenge. The Ff/ff group had higher insulin levels than the FF group at fasting (P=0.006), 30 minutes (P=0.009), 60 minutes (P=0.049), and 90 minutes (P=0.042). Furthermore, the Ff/ff group also had a larger insulin area under the curve than the FF group (P=0.009). While no difference was noted in %B, the Ff/ff group had a lower %S than the FF group (0.53 vs. 0.78, P=0.006). A stepwise regression analysis confirmed that the Fok I polymorphism was an independent determinant for %S, accounting for 29.3% of variation in %S when combined with waist-hip ratio.We report that the Fok I polymorphism at the VDR gene locus is associated with insulin sensitivity, but has no influence on beta cell function in healthy Caucasians. Although this polymorphism has been shown to affect the activation of vitamin D-dependent transcription, the molecular basis of the association between this polymorphism and insulin resistance remains to be determined.Although conflicting findings about bone mineral density (BMD) in patients with type 2 diabetes have been reported, there are substantial data which support the notion that type 2 diabetes is associated with increased BMD [1,2,3]. The Rotterdam Study [2], which involved 5,931 subjects, including 243 men and 355 women with type 2 diabetes, provides the most convincing evidence. They found that diabetic men and women had increased BMD independent of age, obesity, the use of estrogen, thiazide, or loop diuretics, impairment in the ability of daily living, and smoking [2]. Furthermore, hyperinsulinemia has been reported to be associated with an increased BMD in diabetic [4] and non-diabetic subjects [5]. From the Rancho Bernardo Study [5], the level of fasting insulin was significantly and positively assoc
Hepatic glucokinase promoter polymorphism is associated with hepatic insulin resistance in Asian Indians.
Ken C Chiu, Lee-Ming Chuang, Carol Yoon, Mohammad F Saad
BMC Genetics , 2000, DOI: 10.1186/1471-2156-1-2
Abstract: We identified 38 GG, 24 GA, and one AA subjects. The AA subject was pooled with the GA subjects during the analysis. No difference was noted in the demographic features between the two genotypic groups (GG vs. GA/AA). Compared to the GG group, the GA/AA group had a lower ISIH (p=0.002), a lower ISIM (p=0.009), a higher %B (p=0.014), and a higher dI/dG (p=0.030). Multivariate analysis revealed that this polymorphism is an independent determinant for ISIH (p=0.019) and along with age, waist-hip ratio, gender, and diastolic blood pressure accounted for 51.5% of the variation of ISIH. However, this polymorphism was a weak, but independent determinant for ISIM (p=0.089) and %B (p=0.083). Furthermore, it had no independent effect on dI/dG (p=0.135).These data suggest that the G-to-A polymorphism in the hepatic GCK promoter is associated with hepatic insulin resistance in Asian Indians.Glucokinase (GCK) was originally proposed to be a glucose sensor and metabolic signal generator in pancreatic beta cells and hepatocytes [1]. The discoveries of a linkage and subsequent identification of mutated GCK genes [2,3] in families with maturity-onset diabetes of the young (MODY) provide the strongest evidence for a crucial role of GCK in the pathogenesis of MODY [1]. However, the structural mutations (missense, nonsense mutation, or mutations affecting the splicing mechanism) of GCK were only found in less than 1% of patients with type 2 diabetes [4]. Thus, the mutated GCKs do not play a key role in the pathogenesis of most forms of diabetes.Nonetheless, some studies suggest that defective liver GCK may play a role in the pathogenesis of insulin resistance and type 2 diabetes [5]. In patients with type 2 diabetes who underwent elective cholecystectomy, hepatic GCK activity was decreased by about 50% in obese diabetic subjects compared to lean controls and obese controls [5]. Hyperglycemia in animals has been shown to decrease hepatic GCK activity, which can be reversed by treatment
Endothelin Type A Receptor Genotype is a Determinant of Quantitative Traits of Metabolic Syndrome in Asian Hypertensive Families: A SAPPHIRe Study
Low-Tone Ho,Yung-Pei Hsu,Lee-Ming Chuang
Frontiers in Endocrinology , 2013, DOI: 10.3389/fendo.2013.00172
Abstract: Co-heritability of hypertension and insulin resistance (IR) within families not only implies genetic susceptibility may be responsible for these complex traits but also suggests a rational that biological candidate genes for hypertension may serve as markers for features of the metabolic syndrome (MetS). Thus we determined whether the T323C polymorphism (rs5333) of endothelin type A (ETA) receptor, a predominant receptor evoking potent vasoconstrictive action of endothelin-1, contributes to susceptibility to IR-associated hypertension in 1694 subjects of Chinese and Japanese origins. Blood pressures (BPs) and biochemistries were measured. Fasting insulin level, insulin-resistance homeostasis model assessment (HOMAIR) score, and area under curve of insulin concentration (AUCINS) were selected for assessing insulin sensitivity. Genotypes were obtained by methods of polymerase chain reaction-restriction fragment length polymorphism. Foremost findings were that minor allele frequency of the T323C polymorphism was noticeable lower in our overall Asian subjects compared to multi-national population reported in gene database; moreover both the genotypic and allelic frequencies of the polymorphism were significantly different between the two ethnic groups we studied. The genotype distributions at TT/TC/CC were 65, 31, 4% in Chinese and 51, 41, 8% in Japanese, respectively (p < 0.0001). Additionally, carriers of the C homozygote revealed characteristics of IR, namely significantly higher levels of fasting insulin, HOMAIR score, and AUCINS at 29.3, 35.3, and 39.3%, respectively, when compared to their counterparts with TT/TC genotypes in Chinese. Meanwhile, the CC genotype was associated with a higher level of high density lipoprotein cholesterol in Japanese. No association of the polymorphism with BP was observed. This study demonstrated for the first time that T323C polymorphism of ETA receptor gene was associated with an adverse insulin response in Chinese and a favorite atherogenic index in Japanese.
Cancer Risk Associated with Insulin Glargine among Adult Type 2 Diabetes Patients – A Nationwide Cohort Study
Chia-Hsuin Chang, Sengwee Toh, Jou-Wei Lin, Shu-Ting Chen, Chuei-Wen Kuo, Lee-Ming Chuang, Mei-Shu Lai
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0021368
Abstract: Background Preclinical and observational studies raise the concern about the safety of insulin glargine in terms of cancer initiation and promotion. This study is designed to examine cancer incidence associated with use of insulin glargine vs. intermediate/long-acting human insulin (HI). Methodology A retrospective cohort study using the Taiwan National Health Insurance claims database was conducted to identify adult patients with type 2 diabetes mellitus and without a history of cancer who initiated insulin glargine (n = 10,190) or intermediate/long-acting HI (n = 49,253) during 2004–2007. Exclusive users were followed from the date of insulin initiation to the earliest of cancer diagnosis, death, disenrollment, or December 31 2007. We estimated adjusted hazard ratios and 95% confidence intervals (CIs) with Cox proportional hazards models adjusting for baseline propensity score. Findings The incidence rate of all cancer per 1,000 person-years was 13.8 for insulin glargine initiators (179 cases) and 16.0 for intermediate/long-acting HI initiators (1,445 cases) during an average follow-up of 2 years. No significant difference in overall cancer risk between insulin glargine initiators and HI initiators was found. For men, however, the adjusted hazard ratio of insulin glargine use as compared with intermediate/long-acting HI was 2.15 (95% CI 1.01–4.59) for pancreatic cancer, and 2.42 (95% CI 1.50–8.40) for prostate cancer. The increased risk was not observed among women. Conclusions Insulin glargine use did not increase the risk of overall cancer incidence as compared with HI. The positive associations with pancreatic and prostate cancer need further evaluation and validation.
Insulin Resistance: Regression and Clustering
Sangho Yoon, Themistocles L. Assimes, Thomas Quertermous, Chin-Fu Hsiao, Lee-Ming Chuang, Chii-Min Hwu, Bala Rajaratnam, Richard A. Olshen
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0094129
Abstract: In this paper we try to define insulin resistance (IR) precisely for a group of Chinese women. Our definition deliberately does not depend upon body mass index (BMI) or age, although in other studies, with particular random effects models quite different from models used here, BMI accounts for a large part of the variability in IR. We accomplish our goal through application of Gauss mixture vector quantization (GMVQ), a technique for clustering that was developed for application to lossy data compression. Defining data come from measurements that play major roles in medical practice. A precise statement of what the data are is in Section 1. Their family structures are described in detail. They concern levels of lipids and the results of an oral glucose tolerance test (OGTT). We apply GMVQ to residuals obtained from regressions of outcomes of an OGTT and lipids on functions of age and BMI that are inferred from the data. A bootstrap procedure developed for our family data supplemented by insights from other approaches leads us to believe that two clusters are appropriate for defining IR precisely. One cluster consists of women who are IR, and the other of women who seem not to be. Genes and other features are used to predict cluster membership. We argue that prediction with “main effects” is not satisfactory, but prediction that includes interactions may be.
Inference of Cross-Level Interaction between Genes and Contextual Factors in a Matched Case-Control Metabolic Syndrome Study: A Bayesian Approach
Shi-Heng Wang, Wei J. Chen, Lee-Ming Chuang, Po-Chang Hsiao, Pi-Hua Liu, Chuhsing K. Hsiao
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056693
Abstract: Genes, environment, and the interaction between them are each known to play an important role in the risk for developing complex diseases such as metabolic syndrome. For environmental factors, most studies focused on the measurements observed at the individual level, and therefore can only consider the gene-environment interaction at the same individual scale. Indeed the group-level (called contextual) environmental variables, such as community factors and the degree of local area development, may modify the genetic effect as well. To examine such cross-level interaction between genes and contextual factors, a flexible statistical model quantifying the variability of the genetic effects across different categories of the contextual variable is in need. With a Bayesian generalized linear mixed-effects model with an unconditional likelihood, we investigate whether the individual genetic effect is modified by the group-level residential environment factor in a matched case-control metabolic syndrome study. Such cross-level interaction is evaluated by examining the heterogeneity in allelic effects under various contextual categories, based on posterior samples from Markov chain Monte Carlo methods. The Bayesian analysis indicates that the effect of rs1801282 on metabolic syndrome development is modified by the contextual environmental factor. That is, even among individuals with the same genetic component of PPARG_Pro12Ala, living in a residential area with low availability of exercise facilities may result in higher risk. The modification of the group-level environment factors on the individual genetic attributes can be essential, and this Bayesian model is able to provide a quantitative assessment for such cross-level interaction. The Bayesian inference based on the full likelihood is flexible with any phenotype, and easy to implement computationally. This model has a wide applicability and may help unravel the complexity in development of complex diseases.
SLC2A10 genetic polymorphism predicts development of peripheral arterial disease in patients with type 2 diabetes. SLC2A10 and PAD in type 2 diabetes
Yi-Der Jiang, Yi-Cheng Chang, Yen-Feng Chiu, Tien-Jyun Chang, Hung-Yuan Li, Wen-Hsing Lin, Hsiang-Yu Yuan, Yuan-Tsong Chen, Lee-Ming Chuang
BMC Medical Genetics , 2010, DOI: 10.1186/1471-2350-11-126
Abstract: We genotyped 10 single nucleotide polymorphisms and one microsatellite spanning 34 kb across the SLC2A10 gene in a prospective cohort of 372 diabetic patients. Their association with the development of peripheral arterial disease (PAD) in type 2 diabetic patients was analyzed.At baseline, several common SNPs of SLC2A10 gene were associated with PAD in type 2 diabetic patients. A common haplotype was associated with higher risk of PAD in type 2 diabetic patients (haplotype frequency: 6.3%, P = 0.03; odds ratio [OR]: 14.5; 95% confidence interval [CI]: 1.3- 160.7) at baseline. Over an average follow-up period of 5.7 years, carriers with the risk-conferring haplotype were more likely to develop PAD (P = 0.007; hazard ratio: 6.78; 95% CI: 1.66- 27.6) than were non-carriers. These associations remained significant after adjustment for other risk factors of PAD.Our data demonstrate that genetic polymorphism of the SLC2A10 gene is an independent risk factor for PAD in type 2 diabetes.Peripheral arterial disease (PAD), defined as lower extremity arterial atherosclerosis, is one of most common diseases of the arteries and is a major complication of type 2 diabetes [1]. Conventional cardiovascular risk factors such as aging, smoking, hyperglycemia, hypertension and dyslipidemia have been shown to be associated with PAD [1]. However, the increased risk for atherosclerotic diseases in diabetic patients can be only partially explained by the conventional risk factors [2]. In fact, a high heritability for ankle-brachial blood pressure index (ABI), an index of PAD, has been obtained in Twin studies in Caucasians [3], indicating that additional genetic factors might be involved in the pathogenesis of PAD. In this respect, the search for genetic causes of PAD remains limited [4].Recently, a genetic form of arterial tortuosity syndrome (ATS; OMIM 208050) was reported to be caused by loss-of-function mutations in the SLC2A10 gene encoding the facilitative glucose transporter GLUT10. A
Plasma Adiponectin Levels Correlate Positively with an Increasing Number of Components of Frailty in Male Elders
Jaw-Shiun Tsai, Chih-Hsun Wu, Su-Chiu Chen, Kuo-Chin Huang, Chin-Ying Chen, Ching-I Chang, Lee-Ming Chuang, Ching-Yu Chen
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056250
Abstract: Objective Frailty is an important geriatric syndrome. Adiponectin is an important adipokine that regulates energy homeostasis. The aim of this study is to investigate the relationship between plasma adiponectin levels and frailty in elders. Methods The demographic data, body weight, metabolic and inflammatory parameters, including plasma glucose, total cholesterol, triglyceride, tumor necrosis factor alpha (TNF-α), c-reactive protein (CRP) and adiponectin levels, were assessed. The frailty score was assessed using the Fried Frailty Index (FFI). Results The mean (SD) age of the 168 participants [83 (49.4%) men and 85 (50.6%) women] was 76.86 (6.10) years. Judged by the FFI score, 42 (25%) elders were robust, 92 (54.7%) were pre-frail, and 34 (20.3%) were frail. The mean body mass index was 25.19 (3.42) kg/m2. The log-transformed mean (SD) plasma adiponectin (μg/mL) level was 1.00 (0.26). The log-transformed mean plasma adiponectin (μg/mL) levels were 0.93 (0.23) in the robust elders, 1.00 (0.27) in the pre-frail elders, and 1.10 (0.22) in the frail elders, and the differences between these values were statistically significant (p = 0.012). Further analysis showed that plasma adiponectin levels rose progressively with an increasing number of components of frailty in all participants as a whole (p for trend = 0.024) and males (p for trend = 0.037), but not in females (p for trend = 0.223). Conclusion Plasma adiponectin levels correlate positively with an increasing number of components of frailty in male elders. The difference between the sexes suggests that certain sex-specific mechanisms may exist to affect the association between adiponectin levels and frailty.
Validation of Type 2 Diabetes Risk Variants Identified by Genome-Wide Association Studies in Han Chinese Population: A Replication Study and Meta-Analysis
Yi-Cheng Chang, Pi-Hua Liu, Yu-Hsiang Yu, Shan-Shan Kuo, Tien-Jyun Chang, Yi-Der Jiang, Jiun-Yi Nong, Juey-Jen Hwang, Lee-Ming Chuang
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0095045
Abstract: Background Several genome-wide association studies (GWAS) involving European populations have successfully identified risk genetic variants associated with type 2 diabetes mellitus (T2DM). However, the effects conferred by these variants in Han Chinese population have not yet been fully elucidated. Methods We analyzed the effects of 24 risk genetic variants with reported associations from European GWAS in 3,040 Han Chinese subjects in Taiwan (including 1,520 T2DM cases and 1,520 controls). The discriminative power of the prediction models with and without genotype scores was compared. We further meta-analyzed the association of these variants with T2DM by pooling all candidate-gene association studies conducted in Han Chinese. Results Five risk variants in IGF2BP2 (rs4402960, rs1470579), CDKAL1 (rs10946398), SLC30A8 (rs13266634), and HHEX (rs1111875) genes were nominally associated with T2DM in our samples. The odds ratio was 2.22 (95% confidence interval, 1.81-2.73, P<0.0001) for subjects with the highest genetic score quartile (score>34) as compared with subjects with the lowest quartile (score<29). The incoporation of genotype score into the predictive model increased the C-statistics from 0.627 to 0.657 (P<0.0001). These estimates are very close to those observed in European populations. Gene-environment interaction analysis showed a significant interaction between rs13266634 in SLC30A8 gene and age on T2DM risk (P<0.0001). Further meta-analysis pooling 20 studies in Han Chinese confirmed the association of 10 genetic variants in IGF2BP2, CDKAL1, JAZF1, SCL30A8, HHEX, TCF7L2, EXT2, and FTO genes with T2DM. The effect sizes conferred by these risk variants in Han Chinese were similar to those observed in Europeans but the allele frequencies differ substantially between two populations. Conclusion We confirmed the association of 10 variants identified by European GWAS with T2DM in Han Chinese population. The incorporation of genotype scores into the prediction model led to a small but significant improvement in T2DM prediction.
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