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Response of low active GLP-1 like substances to test meal in obese Japanese patients with type 2 diabetes mellitus compared with obese controls with normal glucose tolerance  [PDF]
Kyuzi Kamoi, Nobumasa Ohara, Tomoo Ikarashi, You Shinozaki, Kazuo Furukawa, Hideo Sasaki
Journal of Diabetes Mellitus (JDM) , 2012, DOI: 10.4236/jdm.2012.23043
Abstract: Background: A secretion of plasma active GLP-1 (p-active GLP-1) after ingestion of breakfast test meal (TM) is decreased in obese European patients with type 2 diabetes mellitus (T2DM). However, there was no significant difference in pactive GLP-1 secretion following TM between obese Japanese patients with T2DM and controls. The findings indicate the difference may be due to different races or dietary’s customs of subjects. Aims: We examined whether pactive GLP-1 is truly affected by TM in obese Japanese patients (n = 24, group 1) and obese controls (n = 12, group 2). Methods: Glucose (PG), insulin (s-IRI), C-peptide (s-CPR) and active GLP-1 like substances (p-active GLP-1-S) levels in blood were measured 0, 30 and 60 min after TM. Obese Japanese patients with mean 9 years of diabetes had micro- and macro-vascular disturbances and were treated with diet, exercise and/or oral drugs for hyperglycemia. Results: There was no significant difference in sex, age or BMI between groups. Means HbA1c and PG were significantly higher in group 1 than in group 2. There were no significant differences in means of basal s-IRI, HOMA-R and s-CPR between groups. However, means of HOMA-β, insulinogenic index, postprandial s-IRI, s-CPR and p-active GLP-1-S or p-active GLP-1-S/PG values after TM were significantly lower in group 1 than in group 2. Conclusions: These results indicate that a response of p-active GLP-1-S after TM in obese Japanese patients with T2DM was decreased and secretion of GLP-1 relative to PG was impaired. The method of enhancing function of active GLP-1 may be useful for treatment in some of patients with diabetes mellitus.
Differences in mtDNA haplogroup distribution among 3 Jewish populations alter susceptibility to T2DM complications
Jeanette Feder, Ilana Blech, Ofer Ovadia, Shirly Amar, Julio Wainstein, Itamar Raz, Sarah Dadon, Dan E Arking, Benjamin Glaser, Dan Mishmar
BMC Genomics , 2008, DOI: 10.1186/1471-2164-9-198
Abstract: We have analyzed the mitochondrial DNA (mtDNA) genetic variability in Ashkenazi (Ash), Sephardic (Seph) and North African (NAF) Jewish populations (total n = 1179). Our analysis showed significant differences (p < 0.001) in the distribution of mtDNA genetic backgrounds (haplogroups) among the studied populations. To test whether these differences alter the pattern of disease susceptibility, we have screened our three Jewish populations for an association of mtDNA genetic haplogroups with T2DM complications. Our results identified population-specific susceptibility factors of which the best example is the Ashkenazi Jewish specific haplogroup N1b1, having an apparent protective effect against T2DM complications in Ash (p = 0.006), being absent in the NAF population and under-represented in the Seph population. We have generated and analyzed whole mtDNA sequences from the disease associated haplogroups revealing mutations in highly conserved positions that are good candidates to explain the phenotypic effect of these genetic backgrounds.Our findings support the possibility that recent bottleneck events leading to over-representation of minor mtDNA alleles in specific genetic isolates, could result in population-specific susceptibility loci to complex disorders.The quest for susceptibility genes of common complex disorders such as type 2 diabetes mellitus (T2DM) has led to recent successful discoveries of novel disease-related genes through the use of large scale genome-wide association studies including thousands of patients belonging to major ethnic groups [1]. Disease-associated loci often fail to replicate in different populations, because of patterns of population-specific susceptibility [2]. This may occur due to genetic drift and founder effects, turning minor alleles in a certain populations to prevalent ones in another population. One may hypothesize that some of these alleles carry functional effects underlying differences in disease susceptibility between pop
Association of New Loci Identified in European Genome-Wide Association Studies with Susceptibility to Type 2 Diabetes in the Japanese  [PDF]
Toshihiko Ohshige, Minoru Iwata, Shintaro Omori, Yasushi Tanaka, Hiroshi Hirose, Kohei Kaku, Hiroshi Maegawa, Hirotaka Watada, Atsunori Kashiwagi, Ryuzo Kawamori, Kazuyuki Tobe, Takashi Kadowaki, Yusuke Nakamura, Shiro Maeda
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0026911
Abstract: Background Several novel susceptibility loci for type 2 diabetes have been identified through genome-wide association studies (GWAS) for type 2 diabetes or quantitative traits related to glucose metabolism in European populations. To investigate the association of the 13 new European GWAS-derived susceptibility loci with type 2 diabetes in the Japanese population, we conducted a replication study using 3 independent Japanese case-control studies. Methodology/Principal Findings We examined the association of single nucleotide polymorphisms (SNPs) within 13 loci (MTNR1B, GCK, IRS1, PROX1, BCL11A, ZBED3, KLF14, TP53INP1, KCNQ1, CENTD2, HMGA2, ZFAND6 and PRC1) with type 2 diabetes using 4,964 participants (2,839 cases and 2,125 controls) from 3 independent Japanese samples. The association of each SNP with type 2 diabetes was analyzed by logistic regression analysis. Further, we performed combined meta-analyses for the 3 studies and previously performed Japanese GWAS data (4,470 cases vs. 3,071 controls). The meta-analysis revealed that rs2943641 in the IRS1 locus was significantly associated with type 2 diabetes, (P = 0.0034, OR = 1.15 95% confidence interval; 1.05–1.26) and 3 SNPs, rs10930963 in the MTNR1B locus, rs972283 in the KLF14 locus, and rs231362 in the KCNQ1 locus, had nominal association with type 2 diabetes in the present Japanese samples (P<0.05). Conclusions These results indicate that IRS1 locus may be common locus for type 2 diabetes across different ethnicities.
Smoking and adipose tissue inflammation suppress leptin expression in Japanese obese males: potential mechanism of resistance to weight loss among Japanese obese smokers
Shintaro Nagayasu, Shigeki Suzuki, Akiko Yamashita, Ataru Taniguchi, Mitsuo Fukushima, Yoshikatsu Nakai, Kazuko Nin, Naoya Watanabe, Shoichiro Nagasaka, Daisuke Yabe, Fusanori Nishimura
Tobacco Induced Diseases , 2012, DOI: 10.1186/1617-9625-10-3
Abstract: We compared the concentration of inflammatory markers and serum leptin levels among Japanese male subjects. Additionally, leptin and intercellular adhesion molecule (ICAM) -1 gene expression was assessed in adipocytes co-cultured with or without macrophages in the presence or absence of nicotine and/or lipopolysaccharide (LPS).In subjects with BMI below 25 kg/m2, both WBC counts and soluble-ICAM-1 levels are significantly higher in smokers than in non-smokers. However, leptin concentration did not differ according to smoking status. However, in subjects with BMI over 25 kg/m2, smokers exhibited significantly lower serum leptin level as well as higher WBC counts and s-ICAM-1 concentration as compared with non-smokers. Leptin gene expression was markedly suppressed in adipocytes co-cultured with macrophages than in adipocyte culture alone. Furthermore, nicotine further suppressed leptin gene expression. ICAM-1 gene expression was markedly up-regulated in adipocytes co-cultured with macrophages when stimulated with LPS.Adipose tissue inflammation appears to down-regulate leptin expression in adipose tissues. Nicotine further suppresses leptin expression. Thus, both smoking and inflammation may diminish leptin effect in obese subjects. Therefore, obese, but not normal weight, smokers might be more resistant to weight loss than non-smokers.Although there is no doubt that overall serum leptin concentration increases with increased body mass index and body fat content, there also observed large inter-individual differences in circulating leptin concentration even among obese subjects [1]. This may indicate production of leptin protein is regulated by various factors both at genetic and environmental levels. Among environmental factors, smoking appears to be one of such environmental factors, as smoking and its cessation have often been reported to be associated with low body mass index and weight gain [2]. However, previous reports on the effects of smoking on leptin level
ITGAV polymorphism and disease susceptibility in a Japanese rheumatoid arthritis population
Noriko Iikuni, Shu Kobayashi, Katsunori Ikari, Taisuke Tomatsu, Masako Hara, Hisashi Yamanaka, Naoyuki Kamatani, Shigeki Momohara
Arthritis Research & Therapy , 2007, DOI: 10.1186/ar2303
Abstract: One feature of the pathophysiology of RA is the hyper-angiogenesis observed in the synovial tissue and, along with excess macrophages and T lymphocytes, αvβ3 ligands are also abundant in synovial fluid [2]. As a key player in angiogenesis [3], it has been suggested that ITGAV may be a RA susceptibility gene. The linkage study also supports this view because the 2q31 region containing ITGAV exhibited linkage in a dense genome scan [4].Although the European association study by Jacq and colleagues [1] indicated ITGAV to be a new minor RA susceptibility gene, a replication study conducted in a population of different ethnicity is helpful in exploring whether the association is caused by a common variance through various ethnic groups. We therefore undertook a large population-based study to investigate the association between ITGAV and RA in a Japanese population.DNA samples were obtained from 1,504 Japanese RA patients and 449 population control individuals [5]. Genotypes were determined using the TaqMan method, in accordance with the manufacturer's instructions (Applied Biosystems, Tokyo, Japan). Table 1 shows the genotype distributions and allelic frequencies of patients and control individuals. Unlike the European population, the rs3738919-C allele was more frequent in control individuals in our Japanese population, and no significant differences were observed in allele frequencies for Japanese RA patients and control individuals (0.908 and 0.922, respectively).There are several factors that must be accounted for when a study fails to corroborate a previously identified association. One of these is an ethnicity-specific effect. Ethnic differences can result in differences in allele frequencies, and the genetic background of the disease itself may vary between ethnic groups. Another issue that must be considered is that, usually, negative association studies of a target gene outside the HLA region lack sufficient power to detect the genetic effect because the diseas
Relationship between Dermal Structural Changes on Ultrasonographic Images and Skin Viscoelasticity in Overweight and Obese Japanese Males  [PDF]
Masaru Matsumoto, Kazuhiro Ogai, Miku Aoki, Masami Yokogawa, Mariko Tawara, Junko Sugama, Takeo Minematsu, Misako Dai, Hiromi Sanada
Health (Health) , 2016, DOI: 10.4236/health.2016.811106
Abstract: It has been reported that overweight Japanese males have poorly organised dermis and their skin may be fragile to external forces because of decreased dermal echogenicity. However, it is unknown whether the changes in the dermal structure actually affect the dermal function. The objective of this study was to clarify the relationship between dermal structural parameters and dermal functional parameters in overweight and obese Japanese males. A cross-sectional, observational study was conducted on Japanese male volunteers. Two ultrasound scanners, a 20-MHz Dermascan C and an 18-MHz MylabTM five were used to evaluate dermal structure. Echogenicity of the lower dermis and dermal thickness of the participants’ abdomens and thighs were measured. A Cutometer MPA580 was used to evaluate skin viscoelasticity, skin deformation (R0) and elasticity (R2, R7). The correlation between dermal structural parameters and skin viscoelasticity were validated using Pearson’s correlation coefficient or Spearman’s correlation coefficient by rank test. A total of 79 male volunteers were recruited of which 43 were control subjects with BMI <25 (age, 22 - 63 years), 25 were overweight subjects with BMI ≥ 25 to <30 (age, 23 - 64 years) and the 11 obese subjects had a BMI ≥ 30 (age, 26 - 47 years). There was no correlation between dermal structural parameters and skin viscoelasticity in the abdomens or thighs of all 79 participants. On the other hand, in the 36 overweight and obese participants, thigh dermal echogenicity was significantly and negatively correlated with R0 (r = -0.456, p < 0.01) and dermal thickness in the abdomen was significantly and positively correlated with R0 (r = 0.464, p < 0.01). The dermal functional parameter was significantly correlated with dermal structural parameters in overweight and obese males; in other words, a decrease in dermal function may be caused by structural changes in the dermis during obesity.
Vitamin D receptor initiation codon polymorphism influences genetic susceptibility to type 1 diabetes mellitus in the Japanese population
Yoshiyuki Ban, Matsuo Taniyama, Tatsuo Yanagawa, Satoru Yamada, Taro Maruyama, Akira Kasuga, Yoshio Ban
BMC Medical Genetics , 2001, DOI: 10.1186/1471-2350-2-7
Abstract: We found a significantly higher prevalence of the F allele / the FF genotype in the patients compared to the controls (P = 0.0069 and P = 0.014, respectively). Genotype and allele frequencies differed significantly between GAD65-Ab-positive patients and controls (P = 0.017 and P = 0.012, respectively), but neither between GAD65-Ab-negative patients and controls (P = 0.68 and P = 0.66, respectively) nor between GAD65-Ab-positive and -negative patients (P = 0.19 and P = 0.16, respectively).Our findings suggest that the vitamin D receptor initiation codon polymorphism influences genetic susceptibility to T1DM among the Japanese. This polymorphism is also associated with GAD65-Ab-positive T1DM, although the absence of a significant difference between GAD65-Ab-negative patients and controls might be simply due to the small sample size of patients tested for GAD65 antibodies.Type 1 diabetes mellitus (T1DM) is a multifactorial disease with a strong genetic component [1]. The main genetic contribution to T1DM susceptibility lies in the major histocompatibility complex (MHC) on the short arm of chromosome 6; several non-MHC chromosomal regions are also involved [2]. Several approaches have been used to identify T1DM susceptibility regions, including case-control studies of candidate genes [human leukocyte antigen (HLA), insulin gene regulatory region, interleukin-1 receptor type 1 (ILIR1)] [3,4,5,6], combined linkage and association-based studies of candidate genes [cytotoxic T lymphocyte associated-4 (CTLA-4)] [7], and systematic total genome searches in addition to analyses of individual chromosomal regions [8,9,10,11,12,13,14,15,16].There are clear differences in immunogenetic predisposition to T1DM between countries, and disease incidence seems to vary along with these differences in predisposition [1]. The incidence of T1DM in Southern India (10.4/100000 cases per year) is similar to that in Asian children in the UK and Caucasian children of European extraction [17,18].
Postnatal PPARδ Activation and Myostatin Inhibition Exert Distinct yet Complimentary Effects on the Metabolic Profile of Obese Insulin-Resistant Mice  [PDF]
Barbara L. Bernardo,Timothy S. Wachtmann,Patricia G. Cosgrove,Max Kuhn,Alan C. Opsahl,Kyle M. Judkins,Thomas B. Freeman,John R. Hadcock,Nathan K. LeBrasseur
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0011307
Abstract: Interventions for T2DM have in part aimed to mimic exercise. Here, we have compared the independent and combined effects of a PPARδ agonist and endurance training mimetic (GW501516) and a myostatin antibody and resistance training mimetic (PF-879) on metabolic and performance outcomes in obese insulin resistant mice.
Correlation between Occupational Stress, Lifestyle, and Hyperglycemia among Obese and Non-Obese Middle-Aged Japanese Male Workers  [PDF]
Itsuko Bonkohara, Yoko Kubo, Toshio Kobayashi
Health (Health) , 2016, DOI: 10.4236/health.2016.811112
Abstract: The aim of this study was to identify the correlation between stress, lifestyle, and hyperglycemia among middle-aged Japanese male workers. We also analyzed the obese (OB) and non-obese (non- OB) groups pertaining to the risk of hyperglycemia. A total of 353 male employees aged between 50 and 59 years taking health checkup sat a company in Japan were examined. The data were collected using validated scales of occupational stress and medical examination. Of the 353 employees, 335 (effective response rate 95%) were analyzed. “Support from colleagues” and “reward from work” reported by the OB group were lower than the non-OB group. The items “eating until satiety” and “having greasy meal often” were significantly more common in the OB group than in the non-OB group. There was a significant correlation between less sleep time and hyperglycemia in the OB group than in the non-OB group. The non-OB group reported more overtime hours than the OB group. Hyperglycemia in the non-OB group was positively correlated with long working hours, “workload,” and “mental workload.” The results indicated that the OB group would benefit from lifestyle interventions, for example, improvement in sleep time and eating habits may prevent hyperglycemia and eventually in obesity. Furthermore, it was suggested that stress in response to “workload” and “mental workload” owing to long working hours leads to hyperglycemia in the non-OB group. Therefore, the improvement of the workplace environment, reducing the number of hours at work, and stress management are required to prevent hyperglycemia in the non-OB group.
Alanine aminotransferase/aspartate aminotransferase ratio is the best surrogate marker for insulin resistance in non-obese Japanese adults
Ryuichi Kawamoto, Katsuhiko Kohara, Tomo Kusunoki, Yasuharu Tabara, Masanori Abe, Tetsuro Miki
Cardiovascular Diabetology , 2012, DOI: 10.1186/1475-2840-11-117
Abstract: This cross-sectional study included 587 men aged 58?±?14 (mean?±?standard deviation; range, 20–89) years and 755 women aged 60?±?12 (range, 21–88) years. The study sample consisted of 998 (74.4%) non-obese [body mass index (BMI) <25.0 kg/m2] and 344 (25.6%) overweight (BMI ≥25 kg/m2) subjects. Insulin resistance was defined by homeostasis model assessment of insulin resistance (HOMA-IR) of at least 2.5, and HOMA-IR and potential confounders were compared between the groups. Areas under the curve (AUC) of the receiver operating characteristic curves (ROC) were used to compare the power of these serum markers.In non-obese subjects, the best marker of insulin resistance was alanine aminotransferase (ALT)/aspartate aminotransferase (AST) ratio of 0.70 (95% confidence interval (CI), 0.63-0.77). In overweight subjects, AUC values for the ALT/AST ratio and ALT were 0.66 (0.59-0.72) and 0.66 (0.59-0.72), respectively. Multiple linear regression analyses for HOMA-IR showed that ALT/AST ratios were independently and significantly associated with HOMA-IR as well as other confounding factors in both non-obese and overweight subjects. The optimal cut-off point to identifying insulin resistance for these markers yielded the following values: ALT/AST ratio of ≥0.82 in non-obese subjects and ≥1.02 in overweight subjects. In non-obese subjects, the positive likelihood ratio was greatest for ALT/AST ratio.In non-obese Japanese adults, ALT/AST ratio may be the best reliable marker of insulin resistance.Obesity is also a major worldwide public health problem and is associated with a high risk of developing insulin resistance [1]. Insulin resistance plays an important role in the pathogenesis of incident diabetes, hypertension, dyslipidemia, and cardiovascular disease (CVD) [2-4]. Detailed measurement of insulin resistance requires the use of diffuse techniques (e.g., glucose clamp technique.) that require expense and time. Alternatives have been sought to simplify the measurement of in
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