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2 y different from that proposed for 2-deoxy-d-glucitol 6-phosphate in the previously published structu
3 ylitol 5-phosphate and ALSE complexed with d-glucitol 6-phosphate) are superimposable (as expected fr
7 ined isofagomine and 2,5-anhydro-2,5-imino-D-glucitol active site binding substructures with hydropho
9 monoglycated insulin (insulin B-chain Phe(1)-glucitol adduct) was evaluated in seven overnight-fasted
10 igatory role for GutQ in the metabolism of d-glucitol and there is no readily apparent link between D
11 oxy-L-proline, 1,5-anhydro-4-deoxy-4-amino-D-glucitol, and 1,5-anhydro-4-deoxy-4-amino-L-iditol] has
12 lycated cholecystokinin octapeptide (CCK-8) (glucitol-Asp1 adduct) modified at the NH2-terminus was p
14 ribes the synthesis and quantification of N-(glucitol)ethanolamine (GE) and N-(carboxymethyl)serine (
15 ,4;5,6-di-O-isopropylidene-1-amino-1-deoxy-D-glucitol-gamma-glutamate 20, suitable for Fmoc-strategy
16 e-spacer that incorporates 1-amino-1-deoxy-D-glucitol-gamma-glutamate subunits into a peptidic backbo
17 ificantly lower after administration of Tyr1-glucitol GIP compared with GIP (AUC 255 +/- 33 vs. 368 +
20 more protracted insulin response after Tyr1-glucitol GIP than GIP (AUC 773 +/- 41 vs. 639 +/- 39 ng
23 -spacer: Pte-gammaGlu-(Glu(1-amino-1-deoxy-D-glucitol)-Glu)(2)-Glu(1-amino-1-deoxy-D-gluci tol)-Cys-O
24 te catabolic systems, including those of the glucitol (GutR), fucose (FucR), and deoxyribonucleoside
26 ntification of the degradation products of d-glucitol indicates simultaneous oxidation processes at a
27 there is no readily apparent link between D-glucitol metabolism and LPS biosynthesis, it is suggeste
29 bly affect the activities of the mannitol or glucitol PTS permeases or of non-PTS sugar permeases.
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