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1 (+) and a high-affinity inhibitor, 2-deoxy-d-glucitol 6-(E)-vinylhomophosphonate.
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
4 d structure of MIP synthase-NAD(+)-2-deoxy-d-glucitol 6-phosphate.
5 nd the enzyme bound to an inhibitor, 2-deoxy-glucitol-6-phosphate.
6                2-Amino-1,5-anhydro-2-deoxy-D-glucitol, a highly functionalized tetrahydropyran, is a
7 ined isofagomine and 2,5-anhydro-2,5-imino-D-glucitol active site binding substructures with hydropho
8 wo peptides (162.7 Da) representing a single glucitol adduct (theoretical 164 Da).
9 monoglycated insulin (insulin B-chain Phe(1)-glucitol adduct) was evaluated in seven overnight-fasted
10                                            d-glucitol and d-galactitol decreased the microhardness an
11 igatory role for GutQ in the metabolism of d-glucitol and there is no readily apparent link between D
12 oxy-L-proline, 1,5-anhydro-4-deoxy-4-amino-D-glucitol, and 1,5-anhydro-4-deoxy-4-amino-L-iditol] has
13 lycated cholecystokinin octapeptide (CCK-8) (glucitol-Asp1 adduct) modified at the NH2-terminus was p
14 ting that GutQ is not directly involved in d-glucitol catabolism.
15 t kefiran films, 2 and 5% w/w of glycerol, d-glucitol, d-galactitol, d-mannitol, and d-limonene were
16 ribes the synthesis and quantification of N-(glucitol)ethanolamine (GE) and N-(carboxymethyl)serine (
17 ,4;5,6-di-O-isopropylidene-1-amino-1-deoxy-D-glucitol-gamma-glutamate 20, suitable for Fmoc-strategy
18 e-spacer that incorporates 1-amino-1-deoxy-D-glucitol-gamma-glutamate subunits into a peptidic backbo
19 ificantly lower after administration of Tyr1-glucitol GIP compared with GIP (AUC 255 +/- 33 vs. 368 +
20             These data demonstrate that Tyr1-glucitol GIP displays resistance to plasma DPP IV degrad
21 whereas >99% of NH2-terminally modified Tyr1-glucitol GIP remained intact.
22  more protracted insulin response after Tyr1-glucitol GIP than GIP (AUC 773 +/- 41 vs. 639 +/- 39 ng
23                                         Tyr1-glucitol GIP was similarly resistant to serum degradatio
24                      Effects of GIP and Tyr1-glucitol GIP were examined in Wistar rats after intraper
25 -spacer: Pte-gammaGlu-(Glu(1-amino-1-deoxy-D-glucitol)-Glu)(2)-Glu(1-amino-1-deoxy-D-gluci tol)-Cys-O
26 te catabolic systems, including those of the glucitol (GutR), fucose (FucR), and deoxyribonucleoside
27      Based on utilization of I-erythritol, D-glucitol, i-myo-inositol, D-mannitol, and ribitol and su
28 ntification of the degradation products of d-glucitol indicates simultaneous oxidation processes at a
29  there is no readily apparent link between D-glucitol metabolism and LPS biosynthesis, it is suggeste
30                                          The glucitol operon (gutAEBDMRQ) of Escherichia coli encodes
31 bly affect the activities of the mannitol or glucitol PTS permeases or of non-PTS sugar permeases.
32          The binding site for the open chain glucitol residue extends to a subsite that is distinct f
33 ferase system that metabolizes the hexitol D-glucitol (sorbitol).
34      They were negative for L-rhamnose and D-glucitol (sorbitol).
35 hritis-associated pilus (pap) operon and the glucitol utilization (gut) operon were formed.