Biomedical subjects

W Yan

Publications and source records attributed to W Yan.

At least 19 recordsLinked to original sources

PubMed2006

p53 is required for nerve growth factor-mediated differentiation of PC12 cells via regulation of TrkA levels.

p53 is necessary for the elimination of neural cells inappropriately differentiated or in response to stimuli. However, the role of p53 in neuronal differentiation is not certain. Here, we showed that nerve growth factor (NGF)-mediated differentiation in PC12 cells is enhanced by overexpression of wild-type p53 but inhibited by mutant p53 or knockdown of endogenous wild-type p53, the latter of which can be rescued by expression of exogenous wild-type p53. Interestingly, p53 knockdown or overexpression of mutant p53 attenuates NGF-mediated activation of TrkA, the high-affinity receptor for NGF and a tyrosine kinase, and activation of the mitogen-activated protein kinase pathway. In addition, p53 knockdown reduces the constitutive levels of TrkA, which renders PC12 cells inert to NGF. And finally, we showed that both constitutive and stimuli-induced expressions of TrkA are regulated by p53 and that induction of TrkA by activated endogenous p53 enhances NGF-mediated differentiation. Taken together, our data demonstrate that p53 plays a critical role in NGF-mediated neuronal differentiation in PC12 cells at least in part via regulation of TrkA levels.

Animals↗

PubMed2005

[13C] phenylalanine breath test and hepatic phenylalanine metabolism enzymes in cirrhotic rats.

BACKGROUND: Stable isotope 13C-labelled phenylalanine breath test has been applied to enable the quantitative evaluation of hepatic functional reserve, but the mechanism underlying the changes in function has not been resolved. This study evaluated the correlation between expression of the mRNA of key enzymes mediating phenylalanine metabolism and the metabolism of L-[1-13C] phenylalanine (13C-phe) assessed by the excretion of 13C-CO2 in the breath of rats with, and without, chronic hepatic injury induced by administration of carbon tetrachloride (CCl4). MATERIALS AND METHODS: Male Sprague-Dawley (SD) rats (n = 29) were given subcutaneous injections of CCl4 to induce chronic hepatic injury. L-[1-13C] phenylalanine breath tests (PheBT) were then applied to the rats to assess hepatic function. Expression of phenylalanine hydroxylase (PHH) and tyrosine transaminase (TYT) mRNA in liver was detected by real-time fluorescence quantification RT-PCR, using TaqMan as the probe. It was then determined whether the PheBT results correlated with PHH and/or TYT mRNA expression. In addition, immunohistochemical labelling was used to visualize PHH protein expression in the control and injured liver tissue. RESULTS: There were significant decreases in PheBT and PHH mRNA expression in the cirrhotic rats relative to the uninjured controls and these two measures of liver function were correlated. However, TYT mRNA expression was not changed by CCl4-induced liver injury. The immunohistochemical analysis revealed that PHH protein was expressed predominantly in the cytoplasm of liver cells. CONCLUSIONS: The results of the PheBT were consistent with the changes in PHH gene expression following liver injury. The present findings indicate that decreased expression of the rate-limiting enzyme PHH, but not of TYT, might underlie the functional deficits detected as decreased PheBT. The 13C excretion rate constant per mass liver (PheBT-k/LW) was the most sensitive index that could be used to evaluate the PHH mRNA expression in the liver.

Animals↗

PubMed2005

Polymorphism of human leukocyte antigen-DRB1, -DQB1, and -DPB1 genes of Shandong Han population in China.

In the present study, polymerase chain reaction-sequence-based typing (PCR-SBT) was used to analyze human leukocyte antigen (HLA)-DRB1, -DQB1, and -DPB1 alleles of 98 unrelated healthy Shandong Han individuals. A total of 60 alleles, in which 28 in DRB1, 15 in DQB1 and 17 in DPB1 were found. Among the 28 detected DRB1 alleles, DRB1*150101, DRB1*070101, DRB1*090102, DRB1*120201, and DRB1*080302 were commonly observed, with frequencies of 16.3%, 11.2%, 10.2%, 8.2%, and 5.6%, respectively. The most predominant DQB1 allele was DQB1*030101/0309 with the frequency of 20.4%, followed by DQB1*0201/0202 (14.8%), DQB1*0602 (14.3%), DQB1*030302 (12.2%), and DQB1*060101/060103 (10.7%). Of the 17 detected DPB1 alleles, DPB1*0501 was the most frequent allele with the frequency of 37.2%. DPB1*020102 (18.4%), DPB1*040101 (11.2%), DPB1*0402 (7.1%), and DPB1*1701 (6.6%) were also very frequent alleles. A total of 53 estimated DRB1-DQB1 two-locus haplotypes were observed in Shandong Han population, of which DRB1*150101-DQB1*0602 was the most predominant, followed by DRB1*090102-DQB1*030302, DRB1*070101-DQB1*0201/0202 DRB1*120201-DQB1*030101/0309, and DRB1*080302- DQB1*060101/060103. The distribution of the HLA class II alleles and haplotypes frequencies as well as the dendrogram showed that the Shandong Han population belongs to the northern group of Chinese. The data have implications for anthropological studies and disease associations.

Alleles↗

PubMed2005

Association analysis of the variant in the regulatory subunit of phosphoinositide 3-kinase (p85alpha) with Type 2 diabetes mellitus and hypertension in the Chinese Han population.

AIMS: To determine whether variants in the gene for the regulatory subunit of phosphoinositide 3-kinase (p85alpha) are associated with Type 2 diabetes mellitus (Type 2 DM) and hypertension in a Chinese population. METHODS: We performed a case-control study genotyping the Met326Ile and IVS4+82A>G polymorphisms in 494 patients with Type 2 DM and hypertension and 557 normal controls from the north of China. Individual genotypes were identified by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The IVS4+82A>G polymorphism was further confirmed by direct sequencing in 20 randomly selected cases. RESULTS: The IVS4+82A>G polymorphism that is common in Caucasians was not detected in our population. Frequencies of genotypes and alleles of Met326Ile polymorphism were not significantly different between cases and controls in whole samples by univariate analysis. Logistic regression analysis demonstrated that Ile326Ile genotype was associated with a 2.085-fold (95% CI, 1.043-4.168, P = 0.0377) relative risk of diabetes and hypertension. After stratification by obesity, the frequency of Ile326Ile genotype in cases was higher than that in controls (18/304 vs. 13/510, P = 0.015) among non-obese individuals (BMI < 28 kg/m2). We did not find that this missense mutation was associated with blood pressure, glucose and blood lipids in the control group. CONCLUSION: Our data indicate that the Met326Ile variation in the gene encoding the p85alpha protein might contribute to the increased risk of Type 2 DM and hypertension in Chinese.

Aged↗

PubMed2004

Early anti-apoptosis treatment reduces myocardial infarct size after a prolonged reperfusion.

OBJECTIVE: Significant myocardial apoptosis occurs in ischemia/reperfused hearts. However, the contribution of apoptosis to the development of myocardial injury remains controversial. The present study attempted to obtain evidence that inhibition of apoptosis at early reperfusion can reduce myocardial infarction after prolonged reperfusion. METHODS: Adult male rats were subjected to 30 min ischemia and 4 (apoptosis assay) or 24 h (myocardial infarction determination) of reperfusion and treated with vehicle, SB 239063, insulin or insulin plus wortmannin. RESULTS: Treatment with SB 239063 or insulin markedly decreased myocardial apoptosis (10.6 +/- 1.5% and 7.9 +/- 0.9% respectively, P < 0.01 vs. vehicle) and significantly reduced infarct size (43 +/- 3.6% and 35 +/- 2.9%, respectively, P < 0.01 vs. vehicle). Most interestingly, inhibition of insulin signaling with wortmannin to block insulin signaling not only blocked insulin's anti-apoptotic effect, but also abolished its infarct reduction property. CONCLUSION: These data indicate that apoptosis contributes to the development of myocardial infarction, and inhibition of apoptosis at early reperfusion reduces the myocardial infarction.

Androstadienes↗

PubMed2004

An oligonucleotide microarray for the detection of vaccinia virus.

Vaccinia virus is a member of the orthopoxvirus group, to which also belongs variola virus, one of the most hazardous pathogens known to man. To establish a model system to detect orthopoxviruses, a vaccinia oligonucleotide microarray is designed, produced and tested. Vaccinia virus is used to test the prepared microarrays. The virus DNA samples in different propagation phases are extracted and hybridised with the oligonucleotide microarray. The results showed that the oligonucleotide microarray can detect vaccinia virus with high specificity and sensitivity.

Base Sequence↗

PubMed2004

Quantitative analysis of the effects of hyaluronan and aggrecan concentration and hyaluronan size on the elasticity of hyaluronan-aggrecan solutions.

We determined elasticity (G') and viscosity (G'') of various aggrecan-hyaluronan solutions using a controlled-stress rheometer with high (10 Hz) to low (0.1 Hz) frequencies. Aggrecan solution (50 mg/ml) alone showed little elasticity at any frequency, but the addition of 3300 kDa hyaluronan at 0.001-0.1 mg/ml markedly increased the elasticity, but not the viscosity, at all frequencies. Increasing hyaluronan concentration at >0.1 mg/ml did not further increase the elasticity of the aggrecan solution, and the elasticity of the aggrecan-hyaluronan complex solution reached a plateau at a 500:1 (w/w) ratio. In studies with increasing concentrations of aggrecan and a constant concentration (0.5 mg/ml) of 3300 kDa hyaluronan, aggrecan induced elasticity only at >20 mg/ml, indicating the presence of a critical concentration for elasticity. In the presence of 50 mg/ml aggrecan, 1000 kDa hyaluronan had far less effect on the elasticity of the aggrecan solution than did 3300 kDa hyaluronan. These findings suggest that only approximately 50% reduction in aggrecan concentration (<20 mg/ml), or reduced hyaluronan size (<1000 kDa)--compared with their physiological levels in young cartilage--can abolish the elastic network of the aggrecan-hyaluronan complex.

Aggrecans↗

PubMed2003

Inheritance of plant regeneration from maize (Zea mays L.) shoot meristem cultures derived from germinated seeds and the identification of associated RAPD and SSR markers.

The inheritance of shoot regeneration through shoot-tip meristem culture derived from maize seedling was evaluated, and the markers (RAPD and SSR) associated with this regeneration character were identified both in a group of North American maize inbreds and a crossing population. A discrete distribution of percent regeneration and no. of shoots per explant was observed in the inbred group and the F(2) population. The results suggested that this regenerable trait was controlled by several major genes. Five RAPD markers were identified to be relevant to percent regeneration in maize shoot-tip culture system. One RAPD marker and three SSR markers were associated with no. of shoot per explant and its relevant traits. Of them marker BC603-1600 explained 18% of the variation for no. of shoot per explant and 16% of the variation for callus size. The BC603-1600 was sequenced and assigned in linkage group 7 based on a NCBI blast search. The information provided here should benefit to determine the genetic mechanisms involved in the maize regeneration response related to shoot meristem culture pathway and benefit to select high regenerable germplasm by using marker assisted selection.

Analysis of Variance↗

PubMed2001

Novel inactivating mutations of transforming growth factor-beta type I receptor gene in head-and-neck cancer metastases.

Carcinoma cell lines are frequently refractory to transforming growth factor-beta (TGF beta)-mediated cell cycle arrest. Whether and how TGF beta signaling is disrupted in the majority of human tumors, however, remains unclear. To investigate whether TGF beta signaling might be disrupted by inactivation of the key signaling molecule, the TGF beta type I (T beta R-I) receptor, and whether or not T beta R-I inactivation is associated with late stage disease, we conducted a comprehensive structural analysis of the T beta R-I gene in fine-needle aspirates of 23 head-&-neck cancer metastases. We encountered 4 different mutations of T beta R-I, 3 of which have not been previously identified. In 1 case, we found a somatic intragenic 4-bp deletion predicting for a truncation of the receptor protein. This is the first example of a true loss-of-function mutation of T beta R-I in a human epithelial neoplasm. In 2 other cases, we identified missense mutations located between the juxtamembrane- and serine-threonine kinase domains. One of these resulted in an alanine-to-threonine substitution (A230T), which disrupts receptor signaling activity by causing rapid protein degradation within the endoplasmatic reticulum. This represents a novel mechanism of inactivation of a TGF beta signaling intermediate. Finally, we identified a serine-to-tyrosine substitution at codon 387 (S387Y) in a metastasis but not in the corresponding primary tumor. We had previously shown this S387Y mutant to be predominantly associated with breast cancer metastases and to have a diminished ability to mediate TGF beta-dependent signaling. In aggregate, these findings provide further support for the hypothesis that inactivation of the TGF beta signaling pathway occurs in a significant subset of human cancers.

Activin Receptors, Type I↗

PubMed2001

The Nck-interacting kinase (NIK) phosphorylates the Na+-H+ exchanger NHE1 and regulates NHE1 activation by platelet-derived growth factor.

NIK, a recently identified Nck-interacting kinase, acts upstream of the MEK kinase MEKK1 to activate the c-Jun N-terminal kinase JNK. We now show that NIK binds to and divergently activates the plasma membrane Na(+)-H(+) exchanger NHE1. In a genetic screen, NHE1 interacted with NIK at a site N-terminal (amino acids 407-502) to the Nck-binding domain, and this site is critical for its association with NHE1 in vivo. NIK also phosphorylates NHE1; however, the phosphorylation sites, which are distal to amino acid 638, are distinct from the NIK-binding site on NHE1 (amino acids 538-638). Expression of wild-type, but not a kinase-inactive, NIK in fibroblasts increased NHE1 phosphorylation and activity. The kinase domain of NIK, however, was not sufficient for this response in vivo. Full phosphorylation and activation of NHE1 required both the kinase and the NHE1-binding domains of NIK, suggesting that the NHE1-binding site functions as a targeting signal. The functional significance of an interaction between NIK and NHE1 was confirmed by the ability of a kinase-inactive NIK to selectively inhibit activation of NHE1 by platelet-derived growth factor but not by thrombin. Moreover, although NIK activates JNK through a mechanism dependent on MEKK1, it phosphorylated and activated NHE1 independently of MEKK1. These findings indicate that NIK acts downstream of platelet-derived growth factor receptors to phosphorylate and activate NHE1 divergently of its activation of JNK.

Animals↗

PubMed2001

Effect of ethanol on proliferation and estrogen receptor-alpha expression in human breast cancer cells.

There is substantial epidemiological evidence suggesting that alcohol consumption is associated with increased risk for breast cancer. However, possible biological mechanisms have not been clearly established. In the present studies, a direct effect of ethanol on the proliferation and intracellular content of cyclic AMP (cAMP) in two estrogen receptor-positive (ER+) and two estrogen receptor-negative (ER-) human breast cancer cell lines was examined. Treatment of ER+ human breast cancer cells (MCF-7 and ZR75.1) with ethanol at concentrations between 10 and 100 mM was associated with increased cell numbers compared to controls. The ERalpha content and the amount of intracellular cAMP also increased in ER+ cells exposed to ethanol, compared to controls. On the other hand, ethanol treatment did not increase cell proliferation or cAMP levels in the ER- (BT-20 and MDA-MB-231) human breast cancer cells. Therefore, ethanol added at physiologically relevant concentrations to ER+ human breast cancer cell cultures can enhance cell proliferation and increase the content of ERalpha.

Breast Neoplasms↗

PubMed2001

Differential expression and regulation of the retinoblastoma family of proteins during testicular development and spermatogenesis: roles in the control of germ cell proliferation, differentiation and apoptosis.

Normal spermatogenesis is highly dependent on well-balanced germ cell proliferation, differentiation, and apoptosis. However, the molecular mechanisms that govern these processes are largely unknown. Retinoblastoma family proteins (pRb, p107 and p130) are potentially important regulators of cell growth, differentiation and apoptosis. pRb has been shown to be expressed in the rat testis and involved in the regulation of spermatogenesis. In the present study, the expression and localization of the other two pRb family members, p107 and p130, were analysed at both mRNA and protein levels during testicular development and spermatogenesis using Northern, Western blotting, immunohistochemistry, and in situ hybridization. Furthermore, changes of levels and phosphorylation status of pRb family proteins in response to growth suppression and/or apoptosis induction were investigated using a seminiferous tubule culture system and three animal models. Our data suggest that: (1) pRb family proteins are differentially expressed in the rat testis and they function in a cell-type-specific manner during testicular development and spermatogenesis; (2) they participate in the control of germ cell cycle and act in a cell cycle-phase-specific fashion during germ cell proliferation, and (3) they are also involved in the regulation of apoptosis of germ cells and Leydig cells.

Acetates↗

PubMed2001

Cloning and characterization of a human beta,beta-carotene-15,15'-dioxygenase that is highly expressed in the retinal pigment epithelium.

Retinoids play a critical role in vision, as well as in development and cellular differentiation. beta,beta-Carotene-15,15'-dioxygenase (Bcdo), the enzyme that catalyzes the oxidative cleavage of beta,beta-carotene into two retinal molecules, plays an important role in retinoid synthesis. We report here the first cloning of a mammalian Bcdo. Human BCDO encodes a protein of 547 amino acid residues that demonstrates 68% identity with chicken Bcdo. It is expressed highly in the retinal pigment epithelium (RPE) and also in kidney, intestine, liver, brain, stomach, and testis. The gene spans approximately 20 kb, is composed of 11 exons and 10 introns, and maps to chromosome 16q21-q23. A mouse orthologue was also identified, and its predicted amino acid sequence is 83% identical with human BCDO. Biochemical analysis of baculovirus expressed human BCDO demonstrates the predicted beta,beta-carotene-15,15'-dioxygenase activity. The expression pattern of BCDO suggests that it may provide a local supplement to the retinoids available to photoreceptors, as well as a supplement to the retinoid pools utilized elsewhere in the body. In addition, the finding that many of the enzymes involved in retinoid metabolism are mutated in retinal degenerations suggests that BCDO may also be a candidate gene for retinal degenerative disease.

Amino Acid Sequence↗

PubMed2001

Local structures of mechanically alloyed Fe100-xCux solid solutions studied by X-ray absorption fine structure.

The local structures of the immiscible Fe(100-x)Cu(x) alloys (x= 0, 10, 20, 40, 60, 80 and 100) produced by mechanical alloying have been investigated by XAFS. For the Fe(100-x)Cu(x) (x > or = 40) solid solutions, the local structures around Fe atoms change from bcc structure to fcc one and the Cu atoms maintain the original coordination geometry after milling for 160 hours. On the contrary, the local structures around Cu atoms in both of Fe80Cu20 and Fe90Cu10 alloys appear a transition from fcc to bcc structure. We found that the Debye-waller factor sigma of fcc Fe-Cu phase is larger than that of bcc Fe-Cu phase, and the sigma (0.099 A) around Fe atoms is larger than that (0.089 A) of Cu in the Fe(100-x)Cu(x) (x > or = 40) solid solutions. This suggests that the mechanically alloyed Fe(100-x)Cu(x) supersaturated solid solution is not a homogeneous alloy, and consists of Fe-rich and Cu-rich regions for various compositions. A possible mechanism for bcc-to-fcc and fcc-to-bcc changes in Fe(100-x)Cu(x) solid solutions is discussed in relation to the interdiffusion and transition induced by the ball milling.

Journal Article↗

PubMed2001

A new fluoroaluminophosphate chain with an Al/P ratio of unity.

A new compound, Al2P2O8F2.[(CH3)2CHNH2CH2CH2NH2CH(CH3)2] (denoted AlPO-CJ8), with a 1-dimensional fluoroaluminophosphate chain and an Al/P ratio of unity has been synthesized solvothermally by using isopropylamine as an organic additive. It is characterized by X-ray powder diffraction (XRD), inductively coupled plasma (ICP), ion selective electrodes (ISE), and TGA-DTA analyses and structurally determined by single-crystal X-ray diffraction analysis. AlPO-CJ8 crystallizes in the triclinic space group P1 with a = 5.0306(8) A, b = 9.3626(15) A, c = 10.6131(17) A, alpha = 65.949(4) degrees, beta = 88.218(4) degrees, gamma = 77.19 degrees, and Z = 2. Its structure is built up by alternation of tetrahedral PO3(=O) and AlO3F units to form infinite 1-D Al2P2O8F2(2-) macroanionic chains. The inorganic chains are held together by diprotonated N,N'-diisopropylethylenediamine through H-bonds. The organic species N,N'-diisopropylethylenediamine is believed to be formed through solvothermal reaction of the organic additive isopropylamine and the solvent ethylene glycol. The existence of terminal P=O and Al-F bond groups in the 1-D chain indicates that it has potential to further set up higher dimensional networks through condensations.

Journal Article↗

PubMed2001

Glutamine metabolism to glucosamine is necessary for glutamine inhibition of endothelial nitric oxide synthesis.

L-Glutamine is a physiological inhibitor of endothelial NO synthesis. The present study was conducted to test the hypothesis that metabolism of glutamine to glucosamine is necessary for glutamine inhibition of endothelial NO generation. Bovine venular endothelial cells were cultured for 24 h in the presence of 0, 0.1, 0.5 or 2 mM D-glucosamine, or of 0.2 or 2 mM L-glutamine with or without 20 microM 6-diazo-5-oxo-L-norleucine (DON) or with 100 microM azaserine. Both DON and azaserine are inhibitors of L-glutamine:D-fructose-6-phosphate transaminase (isomerizing) (EC 2.6.1.16), the first and rate controlling enzyme in glucosamine synthesis. Glucosamine at 0.1, 0.5 and 2 mM decreased NO production by 34, 45 and 56% respectively compared with controls where glucosamine was lacking. DON (20 microM) and azaserine (100 microM) blocked glucosamine synthesis and prevented the inhibition of NO generation by glutamine. Neither glutamine nor glucosamine had an effect on NO synthase (NOS) activity, arginine transport or cellular tetrahydrobiopterin and Ca(2+) levels. However, both glutamine and glucosamine inhibited pentose cycle activity and decreased cellular NADPH concentrations; these effects of glutamine were abolished by DON or azaserine. Restoration of cellular NADPH levels by the addition of 1 mM citrate also prevented the inhibiting effect of glutamine or glucosamine on NO synthesis. A further increase in cellular NADPH levels by the addition of 5 mM citrate resulted in greater production of NO. Collectively, our results demonstrate that the metabolism of glutamine to glucosamine is necessary for the inhibition of endothelial NO generation by glutamine. Glucosamine reduces the cellular availability of NADPH (an essential cofactor for NOS) by inhibiting pentose cycle activity, and this may be a metabolic basis for the inhibition of endothelial NO synthesis by glucosamine.

Animals↗

PubMed2001

Gradation processing algorithm of digital radiological chest image.

Gradation processing technology can enhance display contrast of interested region by using linear or nonlinear transform. Current algorithms generally calculate transform parameters depended on experimental statistical values or some simple image processing method such as histogram analysis. They cannot accord with the human subjective vision mechanism nor can they intelligently acquire required parameters. Therefore, processing results are not very accurate or reliable. We propose a gradation processing algorithm of digital radiological chest images based on region growing segmentation technology. It combines self-adapted segmentation with prior knowledge of directed segmentation, and its computation cost is low. It can perform contrast enhancement of the interested regions more accurately, and accords with the human subjective vision mechanism better.

Algorithms↗

PubMed2001

Presence of glutamine:fructose-6-phosphate amidotransferase for glucosamine-6-phosphate synthesis in endothelial cells: effects of hyperglycaemia and glutamine.

AIMS/HYPOTHESIS: Recent studies show that glucosamine infusion impairs endothelium-dependent blood flow in normoglycaemic rats. The pathophysiological relevance of this finding, however, depends on whether de novo glucosamine synthesis occurs in endothelial cells. The aim of this study was to test the hypothesis of whether glutamine:fructose-6-phosphate amidotransferase (the first and key regulatory enzyme in hexosamine synthesis) is present for endothelial glucosamine synthesis. METHODS: Bovine venular, bovine aortic, human microvascular, human umbilical vein, and rat coronary microvascular endothelial cells were used to measure glutamine:fructose-6-phosphate amidotransferase activity. To determine glucosamine-6-phosphate synthesis in intact cells, they were incubated for 1 h in Krebs bicarbonate buffer containing 5, 15 or 30 mmol/l [U-14C]glucose and 0.5, 2 or 4 mmol/l glutamine. The [14C]Glucosamine-6-phosphate and its end products ([14C]UDP-N-acetylglucosamine and [14C]UDP-Nacetylgalactosamine) were separated by HPLC. RESULTS: There were high glutamine:fructose-6-phosphate amidotransferase activities in all endothelial cells studied. Exposure of cells to 15 to 30 mmol/l glucose or 2 to 4 mmol/l glutamine increased enzyme activity. Glucosamine-6-phosphate, UDP-N-acetylglucosamine and UDP-N-acetylgalactosamine syntheses increased with increasing extracellular concentrations of glucose from 5 to 30 mmol/l or of glutamine from 0.5 to 4 mmol/l. CONCLUSION/INTERPRETATION: Our results show the presence of glutamine:fructose-6-phosphate amidotransferase for de novo glucosamine synthesis in endothelial cells and the modulation of this pathway by hyperglycaemia and glutamine. As glucosamine inhibits endothelial nitric oxide synthesis, these findings could have important implications for impaired endothelium-dependent relaxation and vascular dysfunction in diabetes mellitus.

Animals↗