126 research outputs found

    Berberine Improves Glucose Metabolism in Diabetic Rats by Inhibition of Hepatic Gluconeogenesis

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    Berberine (BBR) is a compound originally identified in a Chinese herbal medicine Huanglian (Coptis chinensis French). It improves glucose metabolism in type 2 diabetic patients. The mechanisms involve in activation of adenosine monophosphate activated protein kinase (AMPK) and improvement of insulin sensitivity. However, it is not clear if BBR reduces blood glucose through other mechanism. In this study, we addressed this issue by examining liver response to BBR in diabetic rats, in which hyperglycemia was induced in Sprague-Dawley rats by high fat diet. We observed that BBR decreased fasting glucose significantly. Gluconeogenic genes, Phosphoenolpyruvate carboxykinase (PEPCK) and Glucose-6-phosphatase (G6Pase), were decreased in liver by BBR. Hepatic steatosis was also reduced by BBR and expression of fatty acid synthase (FAS) was inhibited in liver. Activities of transcription factors including Forkhead transcription factor O1 (FoxO1), sterol regulatory element-binding protein 1c (SREBP1) and carbohydrate responsive element-binding protein (ChREBP) were decreased. Insulin signaling pathway was not altered in the liver. In cultured hepatocytes, BBR inhibited oxygen consumption and reduced intracellular adenosine triphosphate (ATP) level. The data suggest that BBR improves fasting blood glucose by direct inhibition of gluconeogenesis in liver. This activity is not dependent on insulin action. The gluconeogenic inhibition is likely a result of mitochondria inhibition by BBR. The observation supports that BBR improves glucose metabolism through an insulin-independent pathway

    Finishing the euchromatic sequence of the human genome

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    The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

    Deletion of Tet1 in Mice with Impaired Prefrontal Cortex Functions by Activating the NGF/TrkA Signaling Pathway

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    Abstract Tet1 (ten-eleven translocation methylcytosine dioxygenase 1) is the enzyme methylcytosine dioxygenase of DNA demethylation in the nervous system. Tet1 controls and mediates gene transcription, memory formation, and extinction. However, little is known about Tet1 in prefrontal cortex (PFC) functions especially in the medial prefrontal cortex (mPFC), which controls cortex flexibility and emotional reactivity in the CNS. This study conducted behavioral tests including an open field test, sociability and social novelty preference tests, social dominance, and prepulse inhibition test to examine brain functions, especially PFC functions after the deletion of Tet1. The mPFC from Tet1 KO mice and WT adult mice was analyzed using qRT-PCR to assess neuron growth-related genes, including Gsk3β, Pi3k, Crx4, Fgfr1, Fgfr2, Egfr, Dbn1, Akt2, Vegf, Vegfr, and Akt3. Subsequently, primary PFC neuronal cells were administered shTet1 to knockdown the Tet1 gene and function. We found that the deletion of Tet1 in the mouse brains impaired social interaction, novelty, and prepulse inhibition (PPI) in the mice. Knockdown of the Tet1 gene influenced the growth and complexity of neurons. The increase in Ngf and Bdnf by Western blotting were found in Tet1 deficient mice. The results support and complement the view that Tet1 deficiency may be related to schizophrenia.</jats:p

    The Study of Face Processing in Social Anxiety Disorder Based on Face-Specific N170 Component

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    Although previous studies showed that social anxiety disorder (SAD) exhibits the attentional bias for angry faces, few studies investigated effective face recognition combined with event-related potential (ERP) technique in SAD patients, especially the treatment effect. This study examines the differences in face processing in SAD patients before and after treatment and healthy control people (H-group). High-density EEG scans were registered in response to emotional schematic faces, particularly interested in the face processing N170 component. Analysis of N170 amplitude revealed a larger N170 for P-group-pre in response to inverted and upright stimuli than H-group in the right hemisphere. The result of the intragroup t-test showed that N170 was delayed for inverted relative to upright faces only in P-group-post and H-group but not in P-group-pre. Remarkably, the results of ANOVAs manifested that emotional expression cannot modulate N170 for SAD patients. Besides, the N170-based asymmetry index (AI) was introduced to analyze the left- and right-hemisphere dominance of N170 for three groups. It was found that, with the improvement of patients’ treatment, the value of A I N 170 − b a s e     d presented a decreasing trend. These results together suggested that there was no inversion effect observed for patients with SAD. The change in the value of A I N 170 − b a s e     d can be used as potential electrophysiological markers for the diagnosis and treatment effects on patients with SAD.</jats:p

    Investigation on microstructure and its transformation mechanisms of B2O3-SiO2-Al2O3-CaO brazing flux system

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    AbstractThe B2O3-SiO2-Al2O3-CaO brazing fluxes and slags were investigated by using X-ray photoelectron spectroscopy (XPS) and Fourier transform infrared spectroscopy (FTIR). The microstructure of the fluxes and slags and its transformation mechanism during the brazing process were investigated, especially the effect of ratio of B2O3to SiO2(B2O3/SiO2) on the microstructural transformation was analyzed. The results show that the structure units of the fluxes and slags are [BO4], [BO3], [SiO4], [AlO4] and [AlO6], and the network structure is a silicon-boron network structure. The O in the slags consist of bridged oxygen, non-bridged oxygen and free oxygen. During the brazing process, part of the [BO4] in slag combined with silica-oxygen network to form Si-O-B structure, which contribute to the network structure of slag, and another part of the [BO4] was transformed to [BO3]. The increase of (B2O3/SiO2) contribute to the transformation of [BO4] to [BO3], and more B2O3 take part in the interface reaction with the increase of (B2O3/SiO2). Therefore, the increase of (B2O3/SiO2) leads to the decrease in the viscosity of the slag, which is beneficial to the spreading behavior during the brazing process.</jats:p
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