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1 nder hyperglycemic conditions through the AR polyol pathway.
2 n preventing diabetes-induced changes in the polyol pathway.
3 ulates aldose reductase, a key enzyme in the polyol pathway.
4 n the calculated flux of glucose through the polyol pathway.
5 ction by stimulating aldose reductase in the polyol pathway.
6 ized to sorbitol by aldose reductase via the polyol pathway.
7 ption is accompanied by aldose reductase and polyol pathway activation in steatotic areas.
8 ients, mice undergoing iAKI show significant polyol pathway activation in the kidney cortex character
9  in the development of DR, namely, increased polyol pathway, activation of protein kinase C (PKC), in
10                           This suggests that polyol pathway activity in the lens may translate to oxi
11 s and to assess the potential involvement of polyol pathway activity in the pathogenesis of spinally
12  documents discrete cellular consequences of polyol pathway activity in the retina, and it suggests t
13 a short duration of diabetes are mediated by polyol pathway activity.
14 e genes, blocks NF-kappaB, and represses the polyol pathway, AGEs production, and hyperlipidemia.
15 ucose concentrations are known to induce the polyol pathway and increase fructose generation in the l
16 is the first and rate-limiting enzyme of the polyol pathway and is involved in the pathogenesis of di
17 ole of endogenous fructose production by the polyol pathway and its metabolism through fructokinase i
18  may be a useful strategy for inhibiting the polyol pathway and preventing the development of diabete
19 novel mechanism, involving activation of the polyol pathway and repression of microRNA-24 (miR-24), t
20 glucose uptake, nerve energy metabolism, the polyol pathway, and protein kinase C (PKC) activity in E
21  alterations in galactose metabolism and the polyol pathway are related to DM with KF.
22 e idea of activation of aldose reductase and polyol pathway as an important mechanism of hyperglycemi
23 cation of proteins and signaling through the polyol pathway, but interference with these mechanisms h
24 f glucose via several pathways including the polyol pathway causes cellular toxicity.
25                    The aldose reductase (AR) polyol pathway contributes to these microvascular compli
26      Herein we report that inhibition of the polyol pathway enzyme aldose reductase (AR) by two struc
27       Increased reduction of glucose via the polyol pathway enzyme aldose reductase (AR) has been lin
28 esent study was to elucidate the role of the polyol pathway enzyme aldose reductase (AR) in the media
29      Herein we report that inhibition of the polyol pathway enzyme aldose reductase (AR) prevents the
30 e of this study was to determine whether the polyol pathway enzyme aldose reductase mediates diabetes
31            Sorbitol dehydrogenase (SDH) is a polyol pathway enzyme that catalyzes conversion of sorbi
32 irms that 3-FG is metabolized to 3-FF by the polyol pathway enzymes.
33        These findings suggest that increased polyol pathway flux in diabetic animals leads to the act
34                                              Polyol pathway flux in spinal oligodendrocytes provides
35                    The impact of exaggerated polyol pathway flux on ciliary neurotrophic factor (CNTF
36 trolled cases of diabetes, lead to increased polyol pathway flux, activation of protein kinase C and
37 dose reductase inhibitors can prevent excess polyol pathway flux, and hence these agents may prevent
38 volved in the pathogenesis of complications: polyol pathway flux, increased formation of AGEs (advanc
39                            Activation of the polyol pathway has been linked to the development of sec
40  the increased metabolism of glucose via the polyol pathway has received considerable attention.
41          These observations suggest that the polyol pathway hyperactivity induced by HG contributes t
42 ases, polyol formation, and flux through the polyol pathway in cultured dog retinal capillary cells w
43 ications for how to evaluate the role of the polyol pathway in diabetic retinopathy.
44 t that fructose also can be produced via the polyol pathway in the liver, where it may induce hepatic
45                              The role of the polyol pathway in the pathogenesis of diabetic retinopat
46 ed for 3 months at a dose that inhibited the polyol pathway in the retina of diabetic rats to a simil
47 as associated with significant inhibition of polyol pathway intermediates in both lens and sciatic ne
48 es showed a dramatic increase in glucose and polyol pathway intermediates in diabetes, a striking upr
49  depletion, and enhanced the accumulation of polyol pathway intermediates without worsening myo-inosi
50 in accumulation of intramuscular glucose and polyol pathway intermediates.
51                                          The polyol pathway is a metabolic route able to convert gluc
52 of aldose reductase, the first enzyme of the polyol pathway, is a key response to ischemia and that i
53 dose reductase (AR), the first enzyme of the polyol pathway, is a promising approach in treatment of
54 ry stress is the distinct signature that the polyol pathway leaves on retinal vessels.
55                      These data suggest that polyol pathway metabolites and AGE can stimulate rat vas
56 ficant effect on either energy metabolism or polyol pathway of normal nerves.
57  study investigated the relation between the polyol pathway, PKC-beta, ROS, JAK2, and Ang II in the d
58 activation of Janus kinase 2 (JAK2), and the polyol pathway play important parts in the hyperprolifer
59 e reductase, the rate-limiting enzyme of the polyol pathway, plays a key role in the pathogenesis of
60 diabetic rat if documented inhibition of the polyol pathway prevents a sequence of retinal vascular a
61 verts sorbitol into fructose in the two-step polyol pathway previously implicated in diabetic neuropa
62       The data confirm that flux through the polyol pathway primarily results in sorbitol accumulatio
63 f 3-deoxyglucosone, at least in part via the polyol pathway, provides an amplification loop to sustai
64 exerted by phosphofructokinase on the PP and polyol pathways revealed that the extent of glycolytic f
65 blocking the excess glucose flux through the polyol pathway that prevails under diabetic conditions h
66 easing evidence to link abnormalities in the polyol pathway to the pathogenesis of diabetic neuropath
67 ehydrogenase (SDH) in the second step of the polyol pathway, under conditions of high glucose flux.
68  by gas chromatography, and flux through the polyol pathway was investigated by 19F nuclear magnetic
69                         Intermediates of the polyol pathway were increased in DMG, particularly fruct
70 e glycerolipid/fatty acid metabolism and the polyol pathway, were found not only to operate at unchan
71  the pentose phosphate pathway (PPP) and the polyol pathway, while also regulating ion channel functi