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《生物化学与生物物理学报:生物膜》1986,862(2):329-334
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(1) Alkyl sugar inhibition of d-allose uptake into adipocytes has been used to explore the spatial requirements of the external sugar transport site in insulin-treated cells. α-methyl and β-methyl glucosides show low affinity indicating very little space around C-1. The high affinity of d-glucosamine (Ki = 9.05 ± 0.66 mM) is lost by N-acetylation. shows no detectable affinity, indicating that a bulky group at C-2 is not accepted. Similarly (Ki = 42.1 ± 7.5 mM) has lower affinity than (Ki = 5.14 ± 0.32 mM) indicating very little space around C-2 but much more around C-3. A reduction in affinity does occur if a propyl group is introduced into the C-3 position. The Ki for is 11.26 ± 2.12 mM. (Ki = 87.2 ± 17.9 mM) and (Ki = 78.07 ± 12.6 mM) show low affinity compared with d-galactose and d-glucose, indicating steric constraints around C-6. High affinity is restored in (Ki = 4.66 ± 0.23 mM) possibly indicating a hydrophobic binding site around C-6). (2) In insulin treated cells (Ki = 6.11 ± 0.5 mM) and maltose (Ki = 23.5 ± 2.1 mM) are well accommodated by the site but trehalose shows no detectable inhibition. These results indicate that the site requires a specific orientation of the sugar as it approaches the transporter from the external solution. C-1 faces the inside while C-4 faces the external solution. (3) To determine the spatial and hydrogen bonding requirements for basal cells 40 μM was used as the substrate. Poor hydrogen bonding analogues and analogues with sterically hindering alkyl groups showed similar Ki values to those determined for insulin-treated cells. These results indicate that insulin does not change the specificity of the adipocyte transport system. 相似文献
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F. Malaisse-Lagae A. Sener W.J. Malaisse 《Biochimica et Biophysica Acta (BBA)/Molecular Cell Research》1983,762(1):36-43
Both d-glucose and its nonmetabolized analog are known to protect the pancreatic B-cell against the toxic action of alloxan, as if the protective action of hexoses were to involve a membrane-associated glucoreceptor site. In the present study, the protective actions of the two hexoses were found to differ from one another in several respects. Using the process of glucose-stimulated insulin release by rat pancreatic islets as an index of alloxan cytotoxicity, we observed that the protective action of d-glucose was suppressed by d-mannoheptulose and menadione, impaired by NH4Cl, and little affected by aminooxyacetate. These findings and the fact that d-glucose failed to decrease [2-14C]alloxan uptake by the islets suggest that the protective action of d-glucose depends on an increase in the generation rate of reducing equivalents (NADH and NADPH). The latter view is supported by the observation that the protective action of a noncarbohydrate nutrient, 2-ketoisocaproate, was also abolished by menadione. Incidentally, the protective action of 2-ketoisocaproate was apparently a mitochondrial phenomenon, it not being suppressed by aminooxyacetate. In contrast to that of glucose, the protective action of was unaffected by d-mannoheptulose, failed to be totally suppressed by menadione, and coincided with a decreased uptake of [2-14C]-alloxan by the islets. It is concluded that the protective action of d-glucose in linked to the metabolism of the sugar in islet cells, whereas that of results from inhibition of alloxan uptake. This conclusion reinforces our opinion that the presence in the B-cell of an alleged stereospecific membrane glucoreceptor represents a mythical concept. 相似文献
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