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61.
首次报道了昆明小鼠体内发育的早期胚胎1-细胞至桑椹期阶段葡萄糖代谢的3种关键酶-6-磷酸葡萄糖脱氢酶(G6PDH)、6-磷酸果糖激酶(PFK)和磷酸葡萄糖变位酶(PGM)的基因转录情况,其分别体现了磷酸戊糖、糖酵解、糖原的合成和分解等途径,根据G6PDH、PFK、PGM的cDNA序列分别设计和合成3套共6对内、外引物,采用巢式RT-PCR方法对其进行检测。结果表明:早期胚胎1-8细胞阶段均有G6PDH基因的转录,叠椹期胚胎不存在该基因的转录,说明早期胚胎1-8细胞阶段可能存在磷酸戊糖,而桑椹期则不存在;1-细胞至桑椹期均存在PFK基因的转录,说明该阶段的胚胎可能存在糖酵解代谢途径;1-细胞至桑椹期均不存在PGM基因的转录,说明该阶段的胚胎可能不存在糖原的合成与分解代谢途径。 相似文献
62.
E.V. Sviderskaya E. Jazrawi S.A. Baldwin C.C. Widnell C.A. Pasternak 《The Journal of membrane biology》1996,149(2):133-140
The stimulation of glucose transport in response to various types of stress has been studied. There is no relationship between
effects of stress-inducing agents on glucose transport and their effects on cellular protein synthesis. Although the effect
of stress on glucose transport appears analogous to its stimulation by insulin, cells that are slightly insulin-sensitive
in terms of glucose transport (BHK cells) show a similar degree of stimulation as highly insulin-sensitive cells (differentiated
3T3-L1 cells). External labeling of the transporter protein with a photoactivatable derivative of mannose, 2-N-4-(1-azi-2,2,2-trifluoroethyl)
benzoyl-1, 3-bis-(D-mannos-4-yloxy)-propylamine, shows that most of the increased glucose transport activity correlates with
an increase in the amount of the transporter on the cell surface. Cells subjected to K+-depletion, which inhibits endocytosis and results in an accumulation of receptors at the cell surface, show the same increase
in glucose transport as cells exposed to stress; stressed cells show no further increase in glucose transport when subjected
to K+ depletion. These results support the view (Widnell, C.C., Baldwin, S.A., Davies, A., Martin, S., Pasternak, C.A. 1990. FASEB J
4:1634–1637) that cellular stress increases glucose transport by promoting the accumulation of glucose transporter molecules
at the cell surface.
Received: 20 June 1995/Revised: 29 September 1995 相似文献
63.
Taxonomic identification of Streptomyces exfoliatus K10 and characterization of its poly(3-hydroxybutyrate) depolymerase gene 总被引:1,自引:0,他引:1
Britta Klingbeil Reiner M. Kroppenstedt Dieter Jendrossek 《FEMS microbiology letters》1996,142(2-3):215-221
Abstract Using fungi grown on synthetic agar medium, we evaluated and compared the concentration of various H2 O2 -producing enzymes. Our results showed that oxidase production in solid medium was better than that found in liquid medium and as high as that detected in wood samples. High yields of oxidases made it possible to compare different oxidases in the same culture extracts and under different conditions. Our results also indicated that H2 O2 production is ubiquitous in the white rot fungi tested and that enzyme levels are influenced by the substrate composition. 相似文献
64.
目的:通过PET/CT检查观察脂肪肝患者肝脏及其他组织对18F脱氧葡萄糖(18F-FDG)摄入变化,探讨脂肪肝与糖脂代谢的相关性。方法:36例做PET/CT的健康和2型糖尿病男性患者,分为对照组(n=18例);脂肪肝组(n=9例);糖尿病脂肪肝组(n=9例)。常规测血糖、血脂及肝肾功能。PET/CT测肝脏CT值和肝脏、肾皮质,骨骼肌组织18F-FDG的最大标准摄入值(SUVmax)及平均标准摄入值(SUVmean)。结果:1.糖尿病脂肪肝组的TG显著高于单纯脂肪肝组和正常对照组,P=0.0003,0.0000。单纯脂肪肝组的TG亦显著高于正常对照组,P=0.028。2.糖尿病脂肪肝组的肝脏18F-FDG的SUVmean和SUVmax显著高于正常对照组的SUVmean和SUVmax,P=0.0054,0.0133。单纯脂肪肝组的肝脏SUVmean和SUVmax亦高于正常对照组,但比较无统计学差异。脑皮质、肾皮质和骨骼肌组织的18F-FDG的SUVmean和SUVmax三组间比较无显著性差异。3.Spearman相关性分析发现FBG与TG显著正相关(r=0.59919,P=0.0004);FBG和TG与肝脏的CT值显著负相关(r=-0.55625,P=0.0004;r=-0.45739,P=0.0097)。结论:脂肪肝与空腹血糖和甘油三酯升高显著相关。脂肪肝及2型糖尿病脂肪肝患者肝脏对葡萄糖摄取增高。 相似文献
65.
Colleen L O Reilly Selina Uranga James D Fluckey 《World journal of biological chemistry》2021,12(5):70-86
The prevalence of type 2 diabetes (T2D) continues to rise despite the amount of research dedicated to finding the culprits of this debilitating disease. Skeletal muscle is arguably the most important contributor to glucose disposal making it a clear target in insulin resistance and T2D research. Within skeletal muscle there is a clear link to metabolic dysregulation during the progression of T2D but the determination of culprits vs consequences of the disease has been elusive. Emerging evidence in skeletal muscle implicates influential cross talk between a key anabolic regulatory protein, the mammalian target of rapamycin (mTOR) and its associated complexes (mTORC1 and mTORC2), and the well-described cano nical signaling for insulin-stimulated glucose uptake. This new understanding of cellular signaling crosstalk has blurred the lines of what is a culprit and what is a consequence with regard to insulin resistance. Here, we briefly review the most recent understanding of insulin signaling in skeletal muscle, and how anabolic responses favoring anabolism directly impact cellular glucose disposal. This review highlights key cross-over interactions between protein and glucose re gulatory pathways and the implications this may have for the design of new therapeutic targets for the control of glucoregulatory function in skeletal muscle. 相似文献
66.
67.
Grace Fergusson Mélanie Ethier Bader Zarrouki Ghislaine Fontés Vincent Poitout 《Journal of visualized experiments : JoVE》2013,(78)
Chronic exposure to excessive levels of nutrients is postulated to affect the function of several organs and tissues and to contribute to the development of the many complications associated with obesity and the metabolic syndrome, including type 2 diabetes. To study the mechanisms by which excessive levels of glucose and fatty acids affect the pancreatic beta-cell and the secretion of insulin, we have established a chronic nutrient infusion model in the rat. The procedure consists of catheterizing the right jugular vein and left carotid artery under general anesthesia; allowing a 7-day recuperation period; connecting the catheters to the pumps using a swivel and counterweight system that enables the animal to move freely in the cage; and infusing glucose and/or Intralipid (a soybean oil emulsion which generates a mixture of approximately 80% unsaturated/20% saturated fatty acids when infused with heparin) for 72 hr. This model offers several advantages, including the possibility to finely modulate the target levels of circulating glucose and fatty acids; the option to co-infuse pharmacological compounds; and the relatively short time frame as opposed to dietary models. It can be used to examine the mechanisms of nutrient-induced dysfunction in a variety of organs and to test the effectiveness of drugs in this context. 相似文献
68.
Haspel HC Stephenson KN Davies-Hill T El-Barbary A Lobo JF Croxen RL Mougrabi W Koehler-Stec EM Fenstermacher JD Simpson IA 《The Journal of membrane biology》1999,169(1):45-53
Barbiturates inhibit GLUT-1-mediated glucose transport across the blood-brain barrier, in cultured mammalian cells, and in
human erythrocytes. Barbiturates also interact directly with GLUT-1. The hypotheses that this inhibition of glucose transport
is (i) selective, preferring barbiturates over halogenated hydrocarbon inhalation anesthetics, and (ii) specific, favoring
some GLUT-# isoforms over others were tested. Several oxy- and thio-barbiturates inhibited [3H]-2-deoxyglucose uptake by GLUT-1 expressing murine fibroblasts with IC50s of 0.2–2.9 mm. Inhibition of GLUT-1 by barbiturates correlates with their overall lipid solubility and pharmacology, and requires hydrophobic
side chains on the core barbiturate structure. In contrast, several halogenated hydrocarbons and ethanol (all ≤10 mm) do not significantly inhibit glucose transport. The interaction of these three classes of anesthetics with purified GLUT-1
was evaluated by quenching of intrinsic protein fluorescence and displayed similar specificities and characteristics. The
ability of barbiturates to inhibit other facilitative glucose transporters was determined in cell types expressing predominantly
one isoform. Pentobarbital inhibits [3H]-2-deoxyglucose and [14C]-3-O-methyl-glucose uptake in cells expressing GLUT-1, GLUT-2, and GLUT-3 with IC50s of ∼1 mm. In contrast, GLUT-4 expressed in insulin-stimulated rat adipocytes was much less sensitive than the other isoforms to inhibition
by pentobarbital (IC50 of >10 mm). Thus, barbiturates selectively inhibit glucose transport by some, but not all, facilitative glucose transporter isoforms.
Received: 10 November 1998/Revised: 3 February 1999 相似文献
69.
葡萄糖异构酶(glucoseisomerase,GI)是使用量最大的工业酶之一,可用于高果糖浆的生产,也可以用含木聚糖物质及废料为底物发酵生产乙醇,具有重要的经济价值.本文选择了表达载体pBV220[1],利用PCR方法删除了原表达质粒pTKDGI1中GI结构基因5′端多余的核苷酸,并添加了合适的酶切位点,重新构建了能在大肠杆菌DH5α中高效表达GIG138P的表达质粒pBZGI1.传代实验表明,新表达体系的稳定性明显优于原表达体系.粗酶液经热处理、DEAESepharoseFF和分子筛Se… 相似文献
70.
Chun-Hao Tsai Yi-Chun Chiang Hsien-Te Chen Po-Hao Huang Horng-Chaung Hsu Chih-Hsin Tang 《Biochimica et Biophysica Acta (BBA)/General Subjects》2013