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Insulin-like growth factor (IGF)-binding protein-2 (IGFBP-2), one of the most abundant circulating IGFBPs, is known to attenuate the biological action of IGF-1. Although the effect of IGFBP-2 in preventing metabolic disorders is well known, its regulatory mechanism remains unclear. In the present study, we demonstrated the transcriptional regulation of the Igfbp-2 gene by peroxisome-proliferator-activated receptor (PPAR) α in the liver. During fasting, both Igfbp-2 and PPARα expression levels were increased. Wy14643, a selective PPARα agonist, significantly induced Igfbp-2 gene expression in primary cultured hepatocytes. However, Igfbp-2 gene expression in Pparα null micewas not affected by fasting or Wy14643. In addition, through transient transfection and chromatin immunoprecipitation assay in fasted livers, we determined that PPARα bound to the putative PPAR-responsive element between -511 bp and -499 bp on the Igfbp-2 gene promoter, indicating that the Igfbp-2 gene transcription is activated directly by PPARα. To explore the role of PPARα in IGF-1 signalling, we treated primary cultured hepatocytes with Wy14643 and observed a decrease in the number of IGF-1 receptors (IGF-1Rs) and in Akt phosphorylation. No inhibition was observed in the hepatocytes isolated from Pparα null mice. These results suggest that PPARα controls IGF-1 signalling through the up-regulation of hepatic Igfbp-2 transcription during fasting and Wy14643 treatment. [ABSTRACT FROM AUTHOR]

B-cell translocation gene 2 (BTG2) is a member of an emerging gene family that is involved in cellular functions. In this study, we demonstrate that BTG2 regulates glucose homeostasis via upregulation of Nur77 in diabetic mice. Hepatic BTG2 gene expression was elevated by fasting and forskolin. Overexpression of Btg2 increased the expression of hepatic gluconeogenic genes and blood glucose output and subsequently impaired glucose and insulin tolerance. Upregulation of the transcriptional activity of Nur77, gluconeogenic genes, and glucose production by forskolin was observed by Btg2 transduction, but not in Btg2 knockdown. BTG2-stimulated glucose production and glucose-6- phosphatase promoter activity were attenuated by dominant-negative Nur77. Coimmunoprecipitation and chromatin immunoprecipitation assays showed that BTG2 induced Nur77 occupancy on the glucose-6-phosphatase promoter via a physical interaction. Btg2 gene expression was increased in streptozotocin-treated and db/db mice. Finally, impairment of glucose homeostasis, such as the increase of blood glucose, glucose intolerance, and insulin intolerance, was elevated in diabetic mice, whereas this phenomenon was abolished in knockdown of Btg2. Together, these data suggest that BTG2 participates in the regulation of hepatic glucose homeostasis, which means that BTG2 might serve as a potential therapeutic target for combating metabolic dysfunction. [ABSTRACT FROM AUTHOR]

Glucose-6-phosphatase (G6Pase) is a key enzyme that is responsible for the production of glucose in the liver during fasting or in type 2 diabetes mellitus (T2DM). During fasting or in T2DM, peroxisome proliferator-activated receptor α (PPARα) is activated, which may contribute to increased hepatic glucose output. However, the mechanism by which PPARα up-regulates hepatic G6Pase gene expression in these states is not well understood. We evaluated the mechanism by which PPARα up-regulates hepatic G6Pase gene expression in fasting and T2DM states. In PPARα-null mice, both hepatic G6Pase and phosphoenolpyruvate carboxykinase levels were not increased in the fasting state. Moreover, treatment of primary cultured hepatocytes with Wy14,643 or fenofibrate increased the G6Pase mRNA level. In addition, we have localized and characterized a PPAR-responsive element in the promoter region of the G6Pase gene. Chromatin immunoprecipitation (ChIP) assay revealed that PPARα binding to the putative PPAR-responsive element of the G6Pase promoter was increased in fasted wild-type mice and db/db mice. These results indicate that PPARα is responsible for glucose production through the up-regulation of hepatic G6Pase gene expression during fasting or T2DM animal models. [ABSTRACT FROM AUTHOR]

Lipid homeostasis in vertebrates is regulated by 3 sterol regulatory element binding protein (SREBP) isoforms. Here, we identify targets of SREBP-1 in mammalian liver using chromatin immunoprecipitation-high-throughput DNA sequencing. Antisera to SREBP-1 were used with liver chromatin from mice fed a high-carbohydrate diet after a fast, which leads to superinduction of hepatic SREBP-lc expression. SREBP-1-DNA complexes were subjected to massive parallel DNA sequencing using the Illumina Genome Analyzer II, resulting in 5.7 million sequence reads. Mapping these reads to the mouse reference genome identified 426 peaks of SREBP-1 binding vs. a control antibody. These binding peaks show a striking enrichment in proximal promoter regions, with 52% located within 1 kb upstream of a transcription start site. A previously undescribed sequence motif (5′-ACTACANNTCCC-3′) was present in 76% of the total peaks, and we show that it is a functional SREBP-1 response element. Our analysis also reveals that an Spi consensus site is present as a "coregulatory" motif in 50% of the SREBP-1 binding peaks, consistent with previous functional studies. SREBP-1 bound not only to many well-characterized SREBP-1 target genes but to several other previously unknown targets in lipid and carbohydrate metabolism as well as many putative target genes in other diverse biological pathways. [ABSTRACT FROM AUTHOR]

Thermomechanical properties and crystallization behavior of poly(ethylene terephthalate) (PET) nanocomposites containing layered double hydroxide (LDH) were investigated. To enhance the compatibility between PET matrix and LDH, dimethyl 5‐sulfoisophthalate (DMSI) anion intercalated LDH (LDH‐DMSI) was synthesized by coprecipitation method, and its structure was confirmed by Fourier transform infrared (FTIR) spectrometer and X‐ray diffraction (XRD) measurements. Then, PET nanocomposites with LDH‐DMSI content of 0, 0.5, 1.0, and 2.0 wt% were prepared by in‐situ polymerization. The dispersion morphologies were observed by transmission electron microscopy (TEM) and XRD, showing that LDH‐DMSI was exfoliated in PET matrix. Thermal and mechanical properties, such as thermal stability, tensile modulus, and tensile yield strength of nanocomposites, were enhanced by exfoliated LDH‐DMSI nanolayers. However, elongation at break was drastically decreased with LDH loading owing to the increased stiffness and microvoids. The effect of exfoliated nanolayers, which acted as a nucleating agent confirmed by differential scanning calorimeter (DSC), on the microstructural parameters during isothermal crystallization, was analyzed by synchrotron small‐angle X‐ray scattering (SAXS). It is believed that nanocomposites could be crystallized more easily owing to the increased nucleation sites, which lead to the decrease of average amorphous region size and the long period with the increase of LDH‐DMSI content. © 2006 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 45: 28–40, 2007 [ABSTRACT FROM AUTHOR]

GLUT2 is mainly expressed in the liver, β-cells of the pancreas, and the basolateral membrane of kidney proximal tubules and plays an important role in glucose homeostasis in living organisms. The transcription of the GLUT2 gene is known to be upregulated in the liver during postprandial hyperglycemic states or in type 2 diabetes. However, a molecular mechanism by which glucose activates GLUT2 gene expression is not known. In this study, we report evidence that sterol response element-binding protein (SREBP)-1c plays a key role in glucose-stimulated GLUT2 gene expression. The GLUT2 promoter reporter is activated by SREBP-1c, and the activation is inhibited by a dominant-negative form of SREBP-1c (SREBP-1c DN). Adenoviral expression of SREBP-1c DN suppressed glucose-stimulated GLUT2 mRNA level in primary hepatocytes. An electrophoretic mobility shift assay and mutational analysis of the GLUT2 promoter revealed that SREBP-1c binds to the -84/-76 region of the GLUT2 promoter. Chromatin immunoprecipitation revealed that the binding of SREBP-1c to the -84/-76 region was increased by glucose concentration in a dose-dependent manner. These results indicate that SREBP-1c mediates glucose-stimulated GLUT2 gene expression in hepatocytes. Diabetes 54: 1684-1691, 2005 [ABSTRACT FROM AUTHOR]

Thiazolidinediones (TZDs), synthetic ligands of peroxisome proliferator-activated receptor (PPAR)-γ, are known to decrease hepatic glucose production and increase glycogen synthesis in diabetic animals. Recently it was reported that glucokinase (GK) expression was increased by TZDs in the liver of diabetic ZDF rats. However, the mechanism whereby TZDs increase GK expression is not yet studied. We have assumed that liver type glucokinase (LGK) induction by TZDs could be achieved by direct transcriptional activation. Thus, we have dissected the LGK promoter to explore the presence of a PPAR response element (PPRE) in the promoter. From this study, we were able to localize a PPRE in the −116/−104 region of the rat LGK gene. The PPAR-γ/retinoid X receptor-α heterodimer was bound to the element and activated the LGK promoter. The LGK promoter lacking the PPRE or having mutations in the PPRE could not be activated by PPAR-γ. Furthermore, troglitazone increased endogenous GK mRNA in primary hepatocytes. These results indicate that PPAR-γ can directly activate GK expression in liver and may contribute to improving glucose homeostasis in type 2 diabetes. [ABSTRACT FROM AUTHOR]

Presents information on a study which investigated the effects of the glycerol addition on characteristics of gelatinized starch and its blends. Mechanical properties and thermal properties of Poly (L-lactic acid) and starch blends; Experimental procedure; Results and discussion; Conclusions.

Presents a study of the formation of silica nanofibers using the sol-gel method and electrospinning technique. Tetraethyl orthosilicate (TEOS) solution does not contain any gelator or binder to help spinnability; Growing interest in one-dimensional, inorganic nanosized materials such as carbon nanotubes, carbide nanorods, silica and titania nanofibers/nanotubes.

The author comments on the celebration of the 70th anniversary of the Society of Fiber Science and Technology, Japan (SFSTJ). He describes the relationship between SFSTJ and the South Korean fiber society. He also discusses the growth of membership in SFSTJ and his personal relationship with the society.

We generated a line of mice in which sterol regulatory element binding protein 1a (SREBP-1a) was specifically inactivated by insertional mutagenesis. Homozygous mutant mice were completely viable despite expressing SREBP-1a mRNA below 5% of normal, and there were minimal effects on expression of either SREBP-1c or -2. Microarray expression studies in liver, where SREBP-1a mRNA is 1/10 the level of the highly similar SREBP-1c, demonstrated that only a few genes were affected. The only downregulated genes directly linked to lipid metabolism were Srebf1 (which encodes SREBP-1) and Acacb (which encodes acetyl coenzyme A [acetyl-CoA] carboxylase 2 [ACC2], a critical regulator of fatty acyl-CoA partitioning between cytosol and mitochondria). ACC2 regulation is particularly important during food restriction. Similar to Acacb knockout mice, SREBP-1a-deficient mice have lower hepatic triglycerides and higher serum ketones during fasting than wild-type mice. SREBP-1a and -1c have identical DNA binding and dimerization domains; thus, the failure of the more abundant SREBP-1c to substitute for activating hepatic ACC2 must relate to more efficient recruitment of transcriptional coactivators to the more potent SREBP-1a activation domain. Our chromatin immunoprecipitation results support this hypothesis. [ABSTRACT FROM AUTHOR]

The inter-layer anion of layered double hydroxides (LDH) with a hydrotalcite (HT)-like structure was ion-exchanged with various organic surfactants, particularly with long chain aliphatic surfactants. After the ion-exchange process, the basal spacing of the LDH was increased and the increase of the basal spacing depended on various factors, such as the intercalation capacity functionality and orientation capability of the surfactant. Of the employed surfactants, stearic acid intercalated LDH showed the highest increase of the basal spacing, which was confirmed by XRD analysis. FTIR results supported the interaction of the surfactants with the LDH. In addition, an increase in the thermal stability of the dodecanedioic acid intercalated HT was evidenced by the TGA method. [ABSTRACT FROM AUTHOR]