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1.
Little is known about the cellular and molecular regulation of the uptake process of the water-soluble vitamin biotin into liver cells, the major site of biotin utilization and metabolism. Such studies are best done using a highly viable and homogeneous cellular system that allows examination of prolonged exposure to an agent(s) or a particular condition(s) on the uptake process. Isolated hepatocytes when maintained in primary culture lose their ability to transport biotin by the specialized carrier system. The aim of the present study was, therefore, to examine the mechanism(s) of biotin uptake by the cultured human-derived liver cells, Hep G2. Uptake to biotin by Hep G2 cells was appreciable and linear for up to 10 min of incubation. The uptake process was Na+ gradient-dependent as indicated by studies of Na+ replacement and pretreatment of cells with gramicidin and ouabain. Biotin uptake was also dependent on both incubation temperature and intracellular energy. Unlabeled biotin and the structural analogs with free carboxyl groups (thioctic acid, desthiobiotin) but not those with blocked carboxyl group (biocytin, biotin methyl ester, and thioctic amide) caused significant inhibition of 3H-biotin uptake at 37°C but not 4°C. Initial rate of biotin uptake was saturable as a function of concentration at 37°C but was lower and linear at 4°C. Pretreatment of Hep G2 cells with sulfhydryl group inhibitors (e.g., p-chloromer-curibenzene sulfonate) led to a significant inhibition in biotin uptake; this inhibition was effectively reversed by reducing agents (e.g., dithiothreitol). Biotin uptake was also inhibited by the membrane transport inhibitors probenecid (noncompetitively), DIDS and furosemide but not by amiloride. Pretreatment of Hep G2 cells with valinomycin did not alter biotin uptake. The stoichiometric ratio of biotin to Na+ uptake in Hep G2 cells was also determined and found to be 1:1. These findings demonstrate that biotin uptake by these cultured liver cells is mediated through a specialized carrier system that is dependent on Na+-gradient, temperature, and energy and transports the vitamin by an electroneutral process. These findings are similar to those seen with native liver tissue preparations and demonstrate the suitability of Hep G2 cells for in-depth investigations of the cellular and molecular regulation of biotin uptake by the liver. © 1994 Wiley-Liss, Inc. 1 This article is a US Government work, and as such, is in the public domain in the United State of America . 相似文献
2.
The effect of neurotensin on submaximally-stimulated hepatobiliary and pancreatic secretion was studied in 6 healthy subjects. An intravenous infusion of neurotensin 1.4 ± 0.3 pmol/kg/min, designed to reproduce plasma neurotensin immunoreactivity levels within the physiological range, produced a significant increase in pancreatic bicarbonate output. Plasma concentrations of pancreatic polypeptide rose by 83 ± 16 pmol/l and were associated with a small reduction in trypsin, but no significant change in bilirubin outputs. 相似文献
3.
Ding Y Vaziri ND Coulson R Kamanna VS Roh DD 《American journal of physiology. Endocrinology and metabolism》2000,279(1):E11-E17
Diabetes is associated with endothelial dysfunction and increased risk of hypertension, cardiovascular disease, and renal complications. Earlier studies have revealed that hyperglycemia impairs nitric oxide (NO) production and diabetes causes endothelial dysfunction in humans and experimental animals. This study was designed to test the effects of altered concentrations of glucose, insulin, and glucagon, the principal variables in types I and II diabetes, on NO production and endothelial NO synthase (eNOS) expression in cultured human coronary endothelial cells. Cultured endothelial cells were incubated in the presence of glucose at either normal (5.6 mM) or high (25 mM) concentrations for 7 days. The rates of basal and bradykinin-stimulated NO production (nitrate + nitrite) and eNOS protein expression (Western blot) were then determined at the basal condition and in the presence of insulin (10(-8) and 10(-7) M), glucagon (10(-8) and 10(-7) M), or both. Incubation with a high-glucose concentration for 7 days significantly downregulated, whereas insulin significantly upregulated, basal and bradykinin-stimulated NO production and eNOS expression in cultured endothelial cells. The stimulatory action of insulin was mitigated by high-glucose concentration and abolished by cotreatment of cells with glucagon. Thus hyperglycemia, insulinopenia, and hyperglucagonemia, which frequently coexist in diabetes, can work in concert to suppress NO production by human coronary artery endothelial cells. 相似文献
4.
A Puri R Sethi B Singh SK Dwivedi VS Narain RK Saran VK Puri 《Indian pacing and electrophysiology journal》2009,9(3):186-189
A 25-year-old previously asymptomatic pregnant woman at 36 weeks'' gestation was noticed to have repetitive monomorphic ventricular tachycardia. A dilated left ventricle with moderately reduced systolic function was found on echocardiographic examination. This is a very rare presentation of peripartum cardiomyopathy (PPCMP) presenting with repetitive monomorphic ventricular tachycardia. 相似文献
5.
A recently silenced, duplicate PgiC locus in Clarkia 总被引:1,自引:0,他引:1
Previous electrophoretic analysis showed that 17 diploid species of the
wildflower Clarkia (Onagraceae) have two cytosolic isozymes of
phosphoglucose isomerase (PGIC; EC 5.3.1.9), whereas 15 other diploid
species have a single PGIC. Molecular studies revealed that the two
isozymes in the former species are encoded by duplicate genes, PgiC1 and
PgiC2, whereas the single isozyme in the latter is always encoded by PgiC1.
Phylogenetic analysis of the nucleotide sequences implied that PgiC2 was
silenced four times independently in the genus. Here we describe a psi
PgiC2 from C. mildrediae, a species in which only PgiC1 is expressed. The
discovery of the psi PgiC2 is significant because it confirms a formal
prediction of the phylogenetic analysis. The psi PgiC2 includes 5,039
nucleotides corresponding to 18 of the 23 exons of PgiC, as well as the
intervening introns and 3' nontranslated region. The absence of an increase
of nucleotide substitutions in its "exons" suggests that the gene was
silenced recently. The present study appears to be the first to establish
that a specific duplicate gene locus regularly expressed in a group of
related plant species has been silenced in one of them. The multiple
independent silencings of PgiC2 suggest that it remained functional but
inessential in ancestral lineages. We discuss the possibility that PgiC2
may have been preserved in these lineages by selection against mutants
causing defective PGIC1- PGIC2 heterodimers.
相似文献
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7.
Kyu-hyang Cho Hyun-ju Kim Vaijinath S. Kamanna Nosratola D. Vaziri 《Biochimica et Biophysica Acta (BBA)/General Subjects》2010
Background
Mounting evidence points to lipid accumulation in the diseased kidney and its contribution to progression of nephropathy. We recently found heavy lipid accumulation and marked dysregulation of lipid metabolism in the remnant kidneys of rats with chronic renal failure (CRF). Present study sought to determine efficacy of niacin supplementation on renal tissue lipid metabolism in CRF.Methods
Kidney function, lipid content, and expression of molecules involved in cholesterol and fatty acid metabolism were determined in untreated CRF (5/6 nephrectomized), niacin-treated CRF (50 mg/kg/day in drinking water for 12 weeks) and control rats.Results
CRF resulted in hypertension, proteinuria, renal tissue lipid accumulation, up-regulation of scavenger receptor A1 (SR-A1), acyl-CoA cholesterol acyltransferase-1 (ACAT1), carbohydrate-responsive element binding protein (ChREBP), fatty acid synthase (FAS), acyl-CoA carboxylase (ACC), liver X receptor (LXR), ATP binding cassette (ABC) A-1, ABCG-1, and SR-B1 and down-regulation of sterol responsive element binding protein-1 (SREBP-1), SREBP-2, HMG-CoA reductase, PPAR-α, fatty acid binding protein (L-FABP), and CPT1A. Niacin therapy attenuated hypertension, proteinuria, and tubulo-interstitial injury, reduced renal tissue lipids, CD36, ChREBP, LXR, ABCA-1, ABCG-1, and SR-B1 abundance and raised PPAR-α and L-FABP.Conclusions and general significance
Niacin administration improves renal tissue lipid metabolism and renal function and structure in experimental CRF. 相似文献8.
Aulus EAD Barbosa Érika VS Albuquerque Maria CM Silva Djair SL Souza Osmundo B Oliveira-Neto Arnubio Valencia Thales L Rocha Maria F Grossi-de-Sa 《BMC biotechnology》2010,10(1):44
Background
Coffee is an important crop and is crucial to the economy of many developing countries, generating around US70 billion per year. There are 115 species in the < i > Coffea < /i > genus, but only two, < i > C. arabica < /i > and < i > C. canephora < /i > , are commercially cultivated. Coffee plants are attacked by many pathogens and insect-pests, which affect not only the production of coffee but also its grain quality, reducing the commercial value of the product. The main insect-pest, the coffee berry borer ( < i > Hypotheneumus hampei < /i > ), is responsible for worldwide annual losses of around US70 billion per year. There are 115 species in the Coffea genus, but only two, C. arabica and C. canephora, are commercially cultivated. Coffee plants are attacked by many pathogens and insect-pests, which affect not only the production of coffee but also its grain quality, reducing the commercial value of the product. The main insect-pest, the coffee berry borer (Hypotheneumus hampei), is responsible for worldwide annual losses of around US500 million. The coffee berry borer exclusively damages the coffee berries, and it is mainly controlled by organochlorine insecticides that are both toxic and carcinogenic. Unfortunately, natural resistance in the genus Coffea to H. hampei has not been documented. To overcome these problems, biotechnological strategies can be used to introduce an α-amylase inhibitor gene (α-AI1), which confers resistance against the coffee berry borer insect-pest, into C. arabica plants. 相似文献9.
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