PubMed Health⌕ Search

Biomedical subjects

Michio Otsuki

Publications and source records attributed to Michio Otsuki.

12 recordsLinked to original sources

Negative association of obesity and its related chronic inflammation with serum glycated albumin but not glycated hemoglobin levels.

BACKGROUND: Measurements of glycated albumin (GA) as well as glycated hemoglobin (HbA1c) have been applied in order to monitor chronic glycemic control in diabetic patients. Both glycated proteins are known influenced by various factors other than glycemia. It has recently been reported that GA level is low in obese, non-diabetic children and is negatively associated with body mass index (BMI) in adult diabetic patients. However, the reasons for the connection between obesity and GA remain unknown. The aim of this study was to examine whether BMI and the obesity-related inflammatory marker plasma high-sensitivity C-reactive protein (hs-CRP) are independently associated with GA and HbA1c. METHODS: Two hundred and twelve non-diabetic subjects (158 with normal glucose tolerance and 54 with impaired glucose tolerance) were enrolled in this study. The effects of fasting plasma glucose (FPG), oral glucose tolerance test (OGTT) 2-h glucose, age, BMI and hs-CRP on HbA1c as well as those on GA were analyzed. RESULTS: FPG significantly correlated with HbA1c, and also significantly but weakly correlated with GA. BMI showed a significantly positive correlation with HbA1c, whereas it negatively correlated with GA. Plasma hs-CRP showed a weak positive correlation with HbA1c, whereas it was negatively associated with GA. By stepwise multivariate regression analyses, BMI and hs-CRP were negatively associated with GA but not with HbA1c. CONCLUSIONS: These results demonstrated that BMI as well as hs-CRP were independent negative risks of GA but not of HbA1c in non-diabetic subjects. Obesity and its related chronic inflammation are involved in lower serum GA levels, but not HbA1c levels, in relation to glycemia.

Body Mass Index↗

Memory effect on the formation of drying cracks.

We propose a model for the formation of drying cracks in a viscoplastic material. In this model, we observe that when an external force is applied to a viscoplastic material before drying, the material memorizes the effect of the force as a plastic deformation. The formation of the drying cracks is influenced by this plastic deformation. This outcome clarifies the result of recent experiments which demonstrated that a drying fracture pattern on a powder-water mixture depends on the manner in which an external force is applied before drying. We analytically express the position of the first crack as a function of the strength of an external force applied before drying. From the expression, we predict that there exists a threshold on the strength of the force. When the force applied is smaller than the threshold, the first crack is formed at the center of the mixture; however, when the force applied exceeds the threshold, the position of the first crack deviates from the center. The extent of the deviation increases as a linear function of the difference between the strength of the force and the threshold.

Journal Article↗

Anomalous time correlation in two-dimensional driven diffusive systems.

We study the time-correlation function of a density field in two-dimensional driven diffusive systems within the framework of fluctuating hydrodynamics. It is found that the time correlation exhibits power-law behavior in an intermediate time regime in the case that the fluctuation-dissipation relation is violated and that the power-law exponent depends on the extent of this violation. We obtain this result by employing a renormalization group method to treat a logarithmic divergence in time.

Journal Article↗

Regeneration of tubular complex is promoted by a free space.

OBJECTIVES: Regeneration of the pancreas is initiated by the tubular complexes that consist of a cluster of epithelia surrounded by the mesenchymal cells. They have the potential to become pancreatic lobes, but their growth stops before the complete regeneration of the organ. To elucidate the possibility that we could promote the regeneration of the pancreas, the potential for growth or differentiation of tubular complex was analyzed. METHODS: The intact lobes were growing around the silk knot after ligation of the pancreas in adult mice. To develop this reaction to a quantitative assay, tubular complexes were induced on the silk strings in the pancreas and were growing into a free space under the silicon cover. The proliferation and differentiation of new lobes with or without the space were analyzed. RESULTS: The number of tubular complexes, which express PDX-1, was increased 5.4 times by the space effect. The proliferating cell nuclear antigen labeling index of acinar cells was 1.7 times stimulated, but that of tubular complex was not changed. The amputated pancreas recovered 49.5% of the resected part under the silicon cover; however, it remained the same weight without the cover. CONCLUSION: The proliferation and differentiation of tubular complex are promoted by a free space.

Animals↗

Identification of a functional variant of estrogen receptor beta in an African population.

In this study, we identified five novel polymorphisms in the estrogen receptor beta (ERbeta) gene in an African population. Interestingly, two of these variants are expected to change the amino acid sequence of the ERbeta protein. These changes correspond to an isoleucine to valine substitution at amino acid position 3 (I3V) and a valine to glycine substitution at position 320 (V320G), respectively. The functional consequences of these amino acid substitutions were determined in different in vitro assays. The I3V mutation displayed no differences with regard to transcriptional activity in a reporter assay, as compared with the wild-type receptor. The V320G mutation, however, showed significantly decreased maximal transcriptional activity in a reporter assay, although its binding affinity for 17beta-estradiol was not affected. A pull-down assay indicated that the interaction of full-length TIF2 with hERbetaV320G was weaker than with hERbetawt. Moreover, surface plasmon resonance analysis revealed reduced interaction of the V320G ERbeta variant with the NR box I and II modules of TIF2. To our knowledge, this represents the first identification of a functional polymorphism in the ERbeta gene. This novel polymorphism provides a tool for human genetic studies of diseases in the African population.

Amino Acid Sequence↗

Specific regulation of lipocalin-type prostaglandin D synthase in mouse heart by estrogen receptor beta.

Estrogens have important physiological roles in the cardiovascular system. We use DNA microarray technology to study the molecular mechanism of estrogen action in the heart and to identify novel estrogen-regulated genes. In this investigation we identify genes that are regulated by chronic estrogen treatment of mouse heart. We present our detailed characterization of one of these genes, lipocalin-type prostaglandin D synthase (L-PGDS). Northern and Western blot analysis revealed that L-PGDS was induced both by acute and chronic estrogen treatment. Northern blot analysis, using estrogen receptor (ER)-disrupted mice, suggests that L-PGDS is specifically induced by ERbeta in vivo. In further support of ERbeta-selective regulation, we identify a functional estrogen-responsive element in the L-PGDS promoter, the activity of which is up-regulated by ERbeta, but not by ERalpha. We demonstrate that a one-nucleotide change (A to C) in the L-PGDS estrogen-responsive element affects receptor selectivity.

Animals↗

Cardiovascular roles of estrogen receptors: insights gained from knockout models.

The effects of estrogen are mediated through two functionally distinct receptors, estrogen receptor alpha (ER- alpha ), and estrogen receptor beta (ER- beta ), both of which are expressed in the cardiovascular system. The etiology of cardiovascular disease is believed to result in part from the loss of endogenous estrogen, indicating that estrogen and its receptors may play important roles in the prevention of cardiovascular disease in women.

Journal Article↗

RU486 antagonizes the inhibitory effect of peroxisome proliferator-activated receptor alpha on interleukin-6 production in vascular endothelial cells.

Peroxisome proliferator-acitivated receptor alpha (PPARalpha) is a member of nuclear receptor superfamily. Recent studies have shown that the activators for PPARalpha inhibit the expression of some inflammatory molecules in vascular endothelial cells (ECs) and vascular smooth muscle cells, indicating the anti-inflammatory roles of PPARalpha on vascular walls. In this investigation, we showed that RU486, already proved to be an active anti-glucocorticoid and anti-progesterone agent, blocked the inhibition of tumor necrosis factor (TNF)-alpha-stimulated interleukin-6 (IL-6) production by the PPARalpha activator fenofibrate in human umbilical vein ECs. Transient transfection of bovine aortic ECs with an IL-6 promoter construct demonstrated that RU486 blocked the inhibitory effect of fenofibrate on TNF-alpha-induced IL-6 promoter activity. By fluorescence microscopy, RU486 was found to prevent fenofibrate-induced nuclear translocation of PPARalpha. Thus, RU486 has an antagonizing effect on PPARalpha-mediated down-regulation of IL-6 in vascular ECs. This effect may be exerted by its interference with the nuclear translocation of PPARalpha.

Animals↗

The thiazolidinedione drug troglitazone up-regulates nitric oxide synthase expression in vascular endothelial cells.

Endothelial dysfunction is a phenomenon often observed in diabetic patients, which is a cause for vascular complications of diabetes mellitus. Endothelium-derived nitric oxide (NO) is responsible for vasodilatation, and NO-dependent vasodilatation is diminished in diabetic patients. In the present study, we evaluated the effects of thiazolidinediones (TZDs), antidiabetic drugs known to improve insulin resistance and to have vasodilating properties, on endothelial NO synthase (eNOS) expression in cultured vascular endothelial cells. Human umbilical vein endothelial cells were treated with the TZDs troglitazone and pioglitazone, or the peroxisome proliferator-activated receptor (PPAR) gamma activator 15-deoxy-Delta(12,14)-prostaglandin J(2) (15-dPGJ2). The expression of eNOS protein and its mRNA was determined by Western and Northern blot analyses, respectively. The effect of alpha-tocopherol that possesses structural similarity to troglitazone was also examined. Troglitazone up-regulated eNOS protein and its mRNA levels, whereas pioglitazone and 15-dPGJ2 failed to increase their levels. By contrast, alpha-tocopherol also increased in eNOS protein and mRNA. These results suggest that troglitazone up-regulates eNOS expression probably through its 6-hydroxychromanes structure but not activating PPARgamma.

Analysis of Variance↗

Menopause, but not age, is an independent risk factor for fasting plasma glucose levels in nondiabetic women.

OBJECTIVE: Glucose metabolism is influenced by various genetic and environmental factors. In women the prevalence of abnormal glucose metabolism is known to increase around and after age 50. The aim of this study was to determine whether menopause augments fasting plasma glucose (FPG) levels in women. DESIGN: Of 672 Japanese women who underwent health examinations, we studied 505 nondiabetic participants who had no history of hysterectomy and had never used estrogens or progestins. All participants were administered an oral glucose tolerance test, and their blood measurements and information about their menopause status were obtained. RESULTS: Of these 505 women, 208 were premenopausal and 297 were postmenopausal. Age, body mass index, triglycerides level, total cholesterol level, low-density lipoprotein cholesterol level, blood pressure, and homeostasis model assessment insulin sensitivity index rose across quintiles of FPG levels, whereas high-density lipoprotein cholesterol level and homeostasis model assessment pancreatic beta-cell function index did not. The number of premenopausal women declined and the number of postmenopausal women increased across quintiles of FPG levels. Univariate regression analysis demonstrated that age, body mass index, triglycerides level, low-density lipoprotein cholesterol level, and menopause status were associated with FPG level, whereas high-density lipoprotein cholesterol level was not. Stepwise multivariate regression analysis showed that the independent risk factors for elevated FPG levels were body mass index, menopause, and triglycerides level, whereas age and low-density lipoprotein cholesterol level did not contribute to FPG levels. CONCLUSIONS: Menopause, but not age, is directly involved in augmented FPG levels in nondiabetic women.

Adult↗