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Articles by K. Kato
Total Records ( 3 ) for K. Kato
  M. Hiramatsu , M. Oguri , K. Kato , T. Yoshida , T. Fujimaki , H. Horibe , K. Yokoi , S. Watanabe , K. Satoh , Y. Aoyagi , M. Tanaka , H. Yoshida , S. Shinkai , Y. Nozawa , T. Murohara and Y. Yamada
  Aims  We previously showed that the C[RIGHTWARDS ARROW]T polymorphism (rs6929846) of BTN2A1 was significantly associated with myocardial infarction in Japanese individuals by a genome-wide association study. Given that diabetes mellitus is an important risk factor for myocardial infarction, the association of rs6929846 of BTN2A1 with myocardial infarction might be attributable, at least in part, to its effect on susceptibility to diabetes. The purpose of this study was to examine the relation of rs6929846 of BTN2A1 to Type 2 diabetes mellitus.

Methods  A total of 8650 Japanese individuals from two independent subject panels were examined: Panel A comprised 1141 individuals with Type 2 diabetes and 3161 control subjects and panel B comprised 1664 individuals with Type 2 diabetes and 2684 control subjects.

Results  The chi-square test revealed that rs6929846 of BTN2A1 was significantly related to the prevalence of Type 2 diabetes in subject panel A (P = 0.0002) and subject panel B (P = 0.006). Multivariable logistic regression analysis with adjustment for age, sex, body mass index and smoking status revealed that rs6929846 was significantly associated with Type 2 diabetes (P = 0.0006; odds ratio 1.25) in all individuals, with the T allele representing a risk factor for this condition. Multiple regression analysis with adjustment for age, sex and body mass index revealed that rs6929846 was significantly (P = 0.04) related to blood glycosylated haemoglobin content in control subjects.

Conclusions BTN2A1 may be a susceptibility gene for Type 2 diabetes in Japanese individuals.

  K. Kato , T. Otsuka , N. Kobayashi , Y. Kon and T. Kawada


Elevated post-load plasma glucose levels may increase the risk of cardiovascular disease, even when they are within the normoglycaemic range. We examined the association of carotid artery intima-media thickness, a marker of early atherosclerosis, with glycaemic variables, including post-load plasma glucose levels, in Japanese subjects with normal glucose tolerance.


The study participants were 663 Japanese subjects with normal glucose tolerance (565 men, mean age 47 ± 9 years) who underwent both a 75-g oral glucose tolerance test and carotid artery intima-media thickness measurement by B-mode ultrasonography during a health examination. Associations between maximal common carotid artery intima-media thickness and fasting plasma glucose, 1-h and 2-h plasma glucose during an oral glucose tolerance test, and HbA1c were examined.


The carotid artery intima-media thickness gradually increased across the tertiles of 1-h plasma glucose, 2-h plasma glucose and HbA1c. In multiple linear regression analysis, 2-h plasma glucose (β = 0.09, P = 0.012), as well as age, male gender, hypertension, dyslipidaemia, and current smoking were independent determinants of carotid artery intima-media thickness. In contrast, other glycaemic variables were not independent determinants of carotid artery intima-media thickness. The carotid artery intima-media thickness in hypertensive subjects with the highest tertile of 2-h plasma glucose [0.70 (95% CI 0.64-0.76) mm] was significantly greater than in normotensive subjects, with the lowest tertile of 2-h plasma glucose [0.60 (95% CI 0.58-0.63) mm, P = 0.037], even after adjusting for the multiple potential confounders.


The 2-h plasma glucose during an oral glucose tolerance test was positively and independently associated with carotid artery intima-media thickness in Japanese subjects with normal glucose tolerance. In particular, the combination of elevated 2-h plasma glucose and hypertension may contribute to an increased carotid artery intima-media thickness.

  N Hosokawa , Y Kamiya and K. Kato

The endoplasmic reticulum (ER) quality control system ensures that newly synthesized proteins in the early secretory pathway are in the correct conformation. Polypeptides that have failed to fold into native conformers are subsequently retrotranslocated and degraded by the cytosolic ubiquitin–proteasome system, a process known as endoplasmic reticulum-associated degradation (ERAD). Most of the polypeptides that enter the ER are modified by the addition of N-linked oligosaccharides, and quality control of these glycoproteins is assisted by lectins that recognize specific sugar moieties and molecular chaperones that recognize unfolded proteins, resulting in proper protein folding and ERAD substrate selection. In Saccharomyces cerevisiae, Yos9p, a lectin that contains a mannose 6-phosphate receptor homology (MRH) domain, was identified as an important component of ERAD. Yos9p was shown to associate with the membrane-embedded ubiquitin ligase complex, Hrd1p–Hrd3p, and provide a proofreading mechanism for ERAD. Meanwhile, the function of the mammalian homologues of Yos9p, OS-9 and XTP3-B remained elusive until recently. Recent studies have determined that both OS-9 and XTP3-B are ER resident proteins that associate with the HRD1–SEL1L ubiquitin ligase complex and are important for the regulation of ERAD. Moreover, recent studies have identified the N-glycan species with which both yeast Yos9p and mammalian OS-9 associate as M7A, a Man7GlcNAc2 isomer that lacks the 1,2-linked terminal mannose from both the B and C branches. M7A has since been demonstrated to be a degradation signal in both yeast and mammals.

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