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1 nder hyperglycemic conditions through the AR polyol pathway.
2 n preventing diabetes-induced changes in the polyol pathway.
3 n the calculated flux of glucose through the polyol pathway.
5 ients, mice undergoing iAKI show significant polyol pathway activation in the kidney cortex character
6 in the development of DR, namely, increased polyol pathway, activation of protein kinase C (PKC), in
8 s and to assess the potential involvement of polyol pathway activity in the pathogenesis of spinally
9 documents discrete cellular consequences of polyol pathway activity in the retina, and it suggests t
11 e genes, blocks NF-kappaB, and represses the polyol pathway, AGEs production, and hyperlipidemia.
12 ucose concentrations are known to induce the polyol pathway and increase fructose generation in the l
13 is the first and rate-limiting enzyme of the polyol pathway and is involved in the pathogenesis of di
14 ole of endogenous fructose production by the polyol pathway and its metabolism through fructokinase i
15 may be a useful strategy for inhibiting the polyol pathway and preventing the development of diabete
16 novel mechanism, involving activation of the polyol pathway and repression of microRNA-24 (miR-24), t
17 glucose uptake, nerve energy metabolism, the polyol pathway, and protein kinase C (PKC) activity in E
18 e idea of activation of aldose reductase and polyol pathway as an important mechanism of hyperglycemi
23 esent study was to elucidate the role of the polyol pathway enzyme aldose reductase (AR) in the media
25 e of this study was to determine whether the polyol pathway enzyme aldose reductase mediates diabetes
31 trolled cases of diabetes, lead to increased polyol pathway flux, activation of protein kinase C and
32 dose reductase inhibitors can prevent excess polyol pathway flux, and hence these agents may prevent
33 volved in the pathogenesis of complications: polyol pathway flux, increased formation of AGEs (advanc
37 ases, polyol formation, and flux through the polyol pathway in cultured dog retinal capillary cells w
40 ed for 3 months at a dose that inhibited the polyol pathway in the retina of diabetic rats to a simil
41 as associated with significant inhibition of polyol pathway intermediates in both lens and sciatic ne
42 es showed a dramatic increase in glucose and polyol pathway intermediates in diabetes, a striking upr
43 depletion, and enhanced the accumulation of polyol pathway intermediates without worsening myo-inosi
45 of aldose reductase, the first enzyme of the polyol pathway, is a key response to ischemia and that i
49 study investigated the relation between the polyol pathway, PKC-beta, ROS, JAK2, and Ang II in the d
50 activation of Janus kinase 2 (JAK2), and the polyol pathway play important parts in the hyperprolifer
51 e reductase, the rate-limiting enzyme of the polyol pathway, plays a key role in the pathogenesis of
52 diabetic rat if documented inhibition of the polyol pathway prevents a sequence of retinal vascular a
54 f 3-deoxyglucosone, at least in part via the polyol pathway, provides an amplification loop to sustai
55 exerted by phosphofructokinase on the PP and polyol pathways revealed that the extent of glycolytic f
56 blocking the excess glucose flux through the polyol pathway that prevails under diabetic conditions h
57 easing evidence to link abnormalities in the polyol pathway to the pathogenesis of diabetic neuropath
58 ehydrogenase (SDH) in the second step of the polyol pathway, under conditions of high glucose flux.
59 by gas chromatography, and flux through the polyol pathway was investigated by 19F nuclear magnetic
60 the pentose phosphate pathway (PPP) and the polyol pathway, while also regulating ion channel functi
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