PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16718375-8 2006 Blood glucose, glycosylated haemoglobin levels and polyol pathway enzymes AR and SDH increased significantly causing accumulation of sorbitol and fructose in the diabetic lens and treatment with SOV and TSP significantly (p < 0.05) decreased these to control levels. Sorbitol 133-141 aldo-keto reductase family 1 member B1 Rattus norvegicus 74-76 21376710-1 2011 Aldose reductase (AKR1B1), which catalyzes the reduction of glucose to sorbitol and lipid aldehydes to lipid alcohols, has been shown to be involved in secondary diabetic complications including cataractogenesis. Sorbitol 71-79 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-16 21376710-1 2011 Aldose reductase (AKR1B1), which catalyzes the reduction of glucose to sorbitol and lipid aldehydes to lipid alcohols, has been shown to be involved in secondary diabetic complications including cataractogenesis. Sorbitol 71-79 aldo-keto reductase family 1 member B1 Rattus norvegicus 18-24 21376710-12 2011 Biochemical analysis of lens homogenates showed that the AKR1B1 activity and sorbitol levels were significantly lower in sugar-treated AKR1B1 knockdown rat lenses as compared to WT rat lenses treated with 50mM glucose. Sorbitol 77-85 aldo-keto reductase family 1 member B1 Rattus norvegicus 135-141 20197634-6 2010 The attenuation of retinal vascular responses to ACh were not modified by treatment with GP-1447, whereas the aldose reductase inhibitor completely prevented diabetes-induced thinning of the retina and sorbitol accumulation in the retina and the lens. Sorbitol 202-210 aldo-keto reductase family 1 member B1 Rattus norvegicus 110-126 19902381-8 2010 In addition, sorbitol synthesized from glucose catalyzed by AR is directly related to cell volume regulation. Sorbitol 13-21 aldo-keto reductase family 1 member B1 Rattus norvegicus 60-62 18569331-2 2008 AR enzyme appears to be the key factor in the reduction of glucose to sorbitol. Sorbitol 70-78 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-2 18569331-3 2008 Synthesis and accumulation of sorbitol in cells due to AR activity is the main cause of diabetic complications, such as diabetic cataract, retinopathy, neuropathy and nephropathy. Sorbitol 30-38 aldo-keto reductase family 1 member B1 Rattus norvegicus 55-57 18569331-4 2008 Aldose reductase inhibitors have been found to prevent sorbitol accumulation in tissues. Sorbitol 55-63 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-16 12773033-1 2003 We report here on the discovery path that led to a structurally unprecedented non-hydantoin, non-carboxylic acid aldose reductase inhibitor, 24, which shows remarkably potent oral activity in normalizing elevated sorbitol levels and, more significantly, fructose levels in the sciatic nerve of chronically diabetic rats, with ED(90) values of 0.8 and 3 mpk, respectively. Sorbitol 213-221 aldo-keto reductase family 1 member B1 Rattus norvegicus 113-129 15755558-2 2005 Diabetes-induced alterations in the sorbitol pathway occur in sympathetic ganglia and therapeutic agents which inhibit aldose reductase or sorbitol dehydrogenase improve or exacerbate, respectively, diabetes-induced NAD. Sorbitol 36-44 aldo-keto reductase family 1 member B1 Rattus norvegicus 119-135 15171691-0 2004 Alteration of urinary sorbitol excretion in WBN-kob diabetic rats - treatment with an aldose reductase inhibitor. Sorbitol 22-30 aldo-keto reductase family 1 member B1 Rattus norvegicus 86-102 15321028-1 2004 The initiation of sugar cataract formation by the aldose reductase catalyzed accumulation of sorbitol in diabetic rats, and its prevention by the administration of aldose reductase inhibitors at the onset or early stages of diabetes, has been well established. Sorbitol 93-101 aldo-keto reductase family 1 member B1 Rattus norvegicus 50-66 14551351-2 2003 For characterization we studied regulation of sorbitol synthesis by aldose reductase (AR) and degradation by sorbitol dehydrogenase (SDH) in papillary interstitial cells. Sorbitol 46-54 aldo-keto reductase family 1 member B1 Rattus norvegicus 68-84 12881532-0 2003 Aldose reductase induced by hyperosmotic stress mediates cardiomyocyte apoptosis: differential effects of sorbitol and mannitol. Sorbitol 106-114 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-16 12881532-7 2003 Furthermore, sorbitol treatment resulting in induction and activation of aldose reductase, decreased expression of the antiapoptotic protein Bcl-xL, increased DNA fragmentation, and glutathione depletion. Sorbitol 13-21 aldo-keto reductase family 1 member B1 Rattus norvegicus 73-89 12684816-5 2003 Collectively, these data indicate that fructose is produced by coordinately expressed AR and SDH in the egg and epithelia of the oviduct and suggest that the resulting sorbitol and fructose can be used as energy sources for spermatozoa motility during the fertilization process. Sorbitol 168-176 aldo-keto reductase family 1 member B1 Rattus norvegicus 86-88 12663474-1 2003 Diabetes is known to affect cataract formation by means of osmotic stress induced by activated aldose reductase in the sorbitol pathway. Sorbitol 119-127 aldo-keto reductase family 1 member B1 Rattus norvegicus 95-111 12604220-5 2003 We show that exposure of rat erythrocytes to NO donors inhibits AR activity and AR mediated accumulation of sorbitol, possibly by S-glutathiolation of Cys-298. Sorbitol 108-116 aldo-keto reductase family 1 member B1 Rattus norvegicus 80-82 12604220-2 2003 The first step of this pathway, which generates sorbitol from glucose, is catalyzed by aldose reductase (AR) (AKR1B). Sorbitol 48-56 aldo-keto reductase family 1 member B1 Rattus norvegicus 87-103 12604220-2 2003 The first step of this pathway, which generates sorbitol from glucose, is catalyzed by aldose reductase (AR) (AKR1B). Sorbitol 48-56 aldo-keto reductase family 1 member B1 Rattus norvegicus 105-107 12167599-3 2002 Sorbitol is produced from glucose in a reaction catalyzed by aldose reductase (AR). Sorbitol 0-8 aldo-keto reductase family 1 member B1 Rattus norvegicus 61-77 12167599-3 2002 Sorbitol is produced from glucose in a reaction catalyzed by aldose reductase (AR). Sorbitol 0-8 aldo-keto reductase family 1 member B1 Rattus norvegicus 79-81 12035507-2 2001 The increase of sorbitol and fructose levels caused by aldose reductase activation and sorbitol dehydrogenase inhibition were observed in sciatic nerve of streptozotocin-diabetic rats. Sorbitol 16-24 aldo-keto reductase family 1 member B1 Rattus norvegicus 55-71 11520112-10 2001 AR activity was also increased causing the elevation of sorbitol in lenses of OLETF rats during the early stages of cataract formation. Sorbitol 56-64 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-2 10440899-4 1999 SNK-860 (fidarestat), an inhibitor of AR, decreased the sorbitol levels at 10(-6)M, while addition of SDI-158, an inhibitor of sorbitol dehydrogenase, did not affect the level in the cells grown in high glucose. Sorbitol 56-64 aldo-keto reductase family 1 member B1 Rattus norvegicus 38-40 10440899-5 1999 These observations suggested that sorbitol produced by AR in the isolated Schwann cells may be predominantly excreted. Sorbitol 34-42 aldo-keto reductase family 1 member B1 Rattus norvegicus 55-57 10440899-7 1999 A significant correlation was observed between sorbitol level and AR activity (r = 0.998). Sorbitol 47-55 aldo-keto reductase family 1 member B1 Rattus norvegicus 66-68 10068486-6 1999 These observations linking iris vessel changes with galactose-feeding, coupled with the fact that aldose reductase inhibitors also prevent these changes, strongly suggest a link between the sorbitol pathway and the appearance and progression of iris vessel changes. Sorbitol 190-198 aldo-keto reductase family 1 member B1 Rattus norvegicus 98-114 9716718-4 1998 The enzymes aldose reductase (which mediates the conversion of glucose to sorbitol) and sorbitol dehydrogenase (which converts sorbitol into fructose) were expressed not only in macula densa cells but also in the surrounding tubular cells, and the expression was insensitive to furosemide. Sorbitol 74-82 aldo-keto reductase family 1 member B1 Rattus norvegicus 12-28 10599142-7 1998 The picamilon and aldose reductase inhibitors administration to diabetic rats is accompanied by the partial reduction of brain sorbitol level. Sorbitol 127-135 aldo-keto reductase family 1 member B1 Rattus norvegicus 18-34 9686698-7 1998 Both aldose reductase inhibitors reduced sorbitol pathway intermediates in a dose-related manner. Sorbitol 41-49 aldo-keto reductase family 1 member B1 Rattus norvegicus 5-21 9505366-5 1997 Administration of aldose reductase inhibitors to diabetic rats is accompanied by partial reduction of sorbitol level in sciatic nerve. Sorbitol 102-110 aldo-keto reductase family 1 member B1 Rattus norvegicus 18-34 9695123-3 1998 In both normal and diabetic rats, the aldose reductase inhibitors suppressed glucose-stimulated sorbitol output, but failed to affect the metabolism of D-[5(-3H]glucose or D-[U-14C]glucose and the secretory response to the hexose. Sorbitol 96-104 aldo-keto reductase family 1 member B1 Rattus norvegicus 38-54 9949255-2 1998 Very little information is available concerning the expression of the enzymes of sorbitol metabolism (aldose reductase (AR) and sorbitol dehydrogenase (SDH)) on the RNA level under different osmotic conditions. Sorbitol 81-89 aldo-keto reductase family 1 member B1 Rattus norvegicus 102-118 9949255-2 1998 Very little information is available concerning the expression of the enzymes of sorbitol metabolism (aldose reductase (AR) and sorbitol dehydrogenase (SDH)) on the RNA level under different osmotic conditions. Sorbitol 81-89 aldo-keto reductase family 1 member B1 Rattus norvegicus 120-122 10959252-1 1998 Increased activation of the first half of the polyol pathway, the conversion of glucose to sorbitol by aldose reductase, has been implicated in aldose reductase inhibitor-preventable neurochemical changes that may contribute to the aetiology of diabetic neuropathy. Sorbitol 91-99 aldo-keto reductase family 1 member B1 Rattus norvegicus 103-119 10959252-1 1998 Increased activation of the first half of the polyol pathway, the conversion of glucose to sorbitol by aldose reductase, has been implicated in aldose reductase inhibitor-preventable neurochemical changes that may contribute to the aetiology of diabetic neuropathy. Sorbitol 91-99 aldo-keto reductase family 1 member B1 Rattus norvegicus 144-160 8889497-1 1996 Sorbitol formation in rat lenses incubated with high levels of glucose was related to activation of aldose reductase (AR). Sorbitol 0-8 aldo-keto reductase family 1 member B1 Rattus norvegicus 100-116 8954157-6 1996 In neonates, sorbitol contents were tenfold lower than in the adult, probably as a result of a lower affinity and a lower number of enzymatic aldose-reductase sites. Sorbitol 13-21 aldo-keto reductase family 1 member B1 Rattus norvegicus 142-158 8889497-1 1996 Sorbitol formation in rat lenses incubated with high levels of glucose was related to activation of aldose reductase (AR). Sorbitol 0-8 aldo-keto reductase family 1 member B1 Rattus norvegicus 118-120 8809342-3 1996 We have shown earlier that under hyperglycemia, lipid peroxides increase; and aldose reductase, an enzyme that reduces glucose to sorbitol, efficiently reduces HNE. Sorbitol 130-138 aldo-keto reductase family 1 member B1 Rattus norvegicus 78-94 8872957-4 1996 We focused on the synthesis of sorbitol catalyzed by the enzyme, aldose reductase. Sorbitol 31-39 aldo-keto reductase family 1 member B1 Rattus norvegicus 65-81 7752919-4 1995 Aldose reductase inhibitors are thought to have an effect by decreasing peripheral nerve sorbitol content and increasing nerve myo-inositol. Sorbitol 89-97 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-16 8786718-4 1995 Sor-3P and Fru-3P are also present in the galactosemic lens, apparently synthesized directly from their precursors, sorbitol and fructose, which are elevated in the lens due to increased flux of glucose through the aldose reductase (AR) pathway. Sorbitol 116-124 aldo-keto reductase family 1 member B1 Rattus norvegicus 215-231 7564101-2 1995 Galactosemia and hyperglycemia can cause excessive levels of galactitol or sorbitol in several organs via aldose reductase (AR) catalysis. Sorbitol 75-83 aldo-keto reductase family 1 member B1 Rattus norvegicus 106-122 7564101-2 1995 Galactosemia and hyperglycemia can cause excessive levels of galactitol or sorbitol in several organs via aldose reductase (AR) catalysis. Sorbitol 75-83 aldo-keto reductase family 1 member B1 Rattus norvegicus 124-126 8733731-3 1996 These findings indicate that the enzymatic kinetics of aldose reductase sorbitol (ARS) in diabetic brain undergo alteration favoring intracellular sorbitol and fructose accumulation, the frequently implicated biochemical basis of diabetic complications. Sorbitol 72-80 aldo-keto reductase family 1 member B1 Rattus norvegicus 55-71 8733731-3 1996 These findings indicate that the enzymatic kinetics of aldose reductase sorbitol (ARS) in diabetic brain undergo alteration favoring intracellular sorbitol and fructose accumulation, the frequently implicated biochemical basis of diabetic complications. Sorbitol 147-155 aldo-keto reductase family 1 member B1 Rattus norvegicus 55-71 8785398-8 1996 In water-deprived, sodium-loaded, and potassium-loaded rats, the inner medullary sorbitol content increased significantly in accordance with the rise in the enzymatic activity and the level of aldose reductase mRNA. Sorbitol 81-89 aldo-keto reductase family 1 member B1 Rattus norvegicus 193-209 7503236-4 1995 Similar results were obtained for the activity of aldose reductase (sorbitol synthesis) [25 +/- 4 U/g (control), 19 +/- 3 U/g (diuresis), and 48 +/- 7 U/g (antidiuresis)]. Sorbitol 68-76 aldo-keto reductase family 1 member B1 Rattus norvegicus 50-66 8027986-4 1994 The first enzyme in this pathway, aldose reductase, reduces glucose to sorbitol. Sorbitol 71-79 aldo-keto reductase family 1 member B1 Rattus norvegicus 34-50 8040341-4 1994 In accordance with this construct, N-nitro-L-arginine methyl ester, a competitive inhibitor of nitric oxide synthase reversed the increased nerve conduction velocity afforded by aldose reductase inhibitor treatment in the acutely diabetic rat without affecting the attendant correction of nerve sorbitol and myo-inositol. Sorbitol 295-303 aldo-keto reductase family 1 member B1 Rattus norvegicus 178-194 7859946-8 1995 These observations, together with other evidence, suggest that sorbitol pathway-linked vascular dysfunction (in ocular tissues, peripheral nerve, and aorta) and electrophysiological dysfunction (in peripheral nerve) induced by diabetes are more closely linked to increased oxidation of sorbitol to fructose than to putative osmotic effects of elevated sorbitol levels or redox and metabolic imbalances associated with reduction of glucose to sorbitol by aldose reductase. Sorbitol 63-71 aldo-keto reductase family 1 member B1 Rattus norvegicus 454-470 8241288-0 1993 Control of sorbitol metabolism in renal inner medulla of diabetic rats: regulation by substrate, cosubstrate and products of the aldose reductase reaction. Sorbitol 11-19 aldo-keto reductase family 1 member B1 Rattus norvegicus 129-145 8129726-11 1994 3,3"-Tetramethylene-glutaric acid (5 mM), an inhibitor of aldose reductase, inhibited glucokinase translocation induced by glucose, but not that by sorbitol or fructose, suggesting that glucose may induce glucokinase translocation by conversion into sorbitol. Sorbitol 250-258 aldo-keto reductase family 1 member B1 Rattus norvegicus 58-74 8241288-12 1993 Combining the results obtained on the properties of the aldose reductase in vitro and the observation made in the intact cells, the investigators suggest that the decrease in NADPH/NADP ratio, as well as changes in the redox state in the cells of diabetic animals, can play a significant role in the control of sorbitol synthesis. Sorbitol 311-319 aldo-keto reductase family 1 member B1 Rattus norvegicus 56-72 8389817-3 1993 Sorbitol, the product of glucose metabolism by aldose reductase, was detected in all nerves from control animals, whereas it was below detection limits in 7 of 11 nerves from Ponalrestat-treated rats. Sorbitol 0-8 aldo-keto reductase family 1 member B1 Rattus norvegicus 47-63 8325441-4 1993 Aldose reductase inhibitors are thought to lower tissue sorbitol while increasing myo-inositol. Sorbitol 56-64 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-16 8359577-10 1993 Prevention of sorbitol accumulation with the aldose reductase inhibitor sorbinil increased nerve taurine levels by 22% (p < 0.05) when compared with untreated diabetic animals. Sorbitol 14-22 aldo-keto reductase family 1 member B1 Rattus norvegicus 45-61 8464370-2 1993 Quantitative determination of testis aldose reductase activities, expressed as the sorbitol index, showed a value similar to that of brain. Sorbitol 83-91 aldo-keto reductase family 1 member B1 Rattus norvegicus 37-53 8464370-3 1993 Sorbitol imaging demonstrated aldose reductase activities in testis to be confined primarily to the central region of this organ. Sorbitol 0-8 aldo-keto reductase family 1 member B1 Rattus norvegicus 30-46 1363299-4 1992 Sorbitol synthesis was inhibited by feeding male Wistar rats the aldose reductase inhibitor sorbinil at 40 mg/kg/day for 71 d, and renal inner medullas were extracted for analysis. Sorbitol 0-8 aldo-keto reductase family 1 member B1 Rattus norvegicus 65-81 1936600-2 1991 We previously demonstrated sorbitol accumulation, due in part to enhanced expression of aldose reductase (AR) in the diabetic kidney. Sorbitol 27-35 aldo-keto reductase family 1 member B1 Rattus norvegicus 88-104 1410879-2 1992 The evidence of sorbitol excess in the crystalline lens of alloxan-diabetic rats has led to anticipate the role of the enzyme aldose-reductase in the pathogenesis of the diabetic cataract. Sorbitol 16-24 aldo-keto reductase family 1 member B1 Rattus norvegicus 126-142 1401064-2 1992 With development of the concentrating system and a hypertonic medullary interstitium, there is a need to generate intracellular osmolytes such as sorbitol, which is produced in a reaction catalyzed by the enzyme aldose reductase. Sorbitol 146-154 aldo-keto reductase family 1 member B1 Rattus norvegicus 212-228 1370506-5 1992 On the other hand, aldose reductase inhibitors significantly reduced the sorbitol content and increased the cAMP and myoinositol contents in the sciatic nerves of diabetic rats. Sorbitol 73-81 aldo-keto reductase family 1 member B1 Rattus norvegicus 19-35 1370506-7 1992 There was a negative correlation between cAMP and sorbitol in the sciatic nerves of diabetic rats treated with aldose reductase inhibitors and a positive correlation between cAMP and motor nerve conduction velocity. Sorbitol 50-58 aldo-keto reductase family 1 member B1 Rattus norvegicus 111-127 1370506-9 1992 Aldose reductase inhibitors inhibited sorbitol accumulation and increased cAMP in sciatic nerves. Sorbitol 38-46 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-16 1936600-2 1991 We previously demonstrated sorbitol accumulation, due in part to enhanced expression of aldose reductase (AR) in the diabetic kidney. Sorbitol 27-35 aldo-keto reductase family 1 member B1 Rattus norvegicus 106-108 1954333-1 1991 Sorbitol production in the renal medulla increases in dehydrated rats, indicating that aldose reductase activity varies with the state of hydration. Sorbitol 0-8 aldo-keto reductase family 1 member B1 Rattus norvegicus 87-103 1954333-9 1991 The stability of aldose reductase activity despite changes in ionic composition or osmolality supports the hypothesis that acute regulation of intracellular sorbitol content occurs by variation in cell sorbitol permeability and not by variation in cell sorbitol production. Sorbitol 157-165 aldo-keto reductase family 1 member B1 Rattus norvegicus 17-33 2120282-2 1990 Aldose reductase (AR) is an enzyme responsible for converting glucose into sorbitol and galactose into galactitol. Sorbitol 75-83 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-16 1903044-4 1991 The sorbitol index, a measure of aldose reductase activities in vivo, determined by the 3-FDG 19F NMR method, revealed that aldose reductase activities were significantly higher (p less than 0.05) in aged brain. Sorbitol 4-12 aldo-keto reductase family 1 member B1 Rattus norvegicus 33-49 1903044-4 1991 The sorbitol index, a measure of aldose reductase activities in vivo, determined by the 3-FDG 19F NMR method, revealed that aldose reductase activities were significantly higher (p less than 0.05) in aged brain. Sorbitol 4-12 aldo-keto reductase family 1 member B1 Rattus norvegicus 124-140 2124193-5 1990 Although the addition of an aldose reductase inhibitor (0.7 mmol/l) to the hyperglycaemic culture media containing an additional 66.7 mmol/l glucose significantly reduced the sorbitol content of embryos to approximately one-eighth, the myo-inositol content of embryos remained decreased and the frequency of neural lesions was unchanged (23.1% vs 23.9%, NS). Sorbitol 175-183 aldo-keto reductase family 1 member B1 Rattus norvegicus 28-44 2120282-2 1990 Aldose reductase (AR) is an enzyme responsible for converting glucose into sorbitol and galactose into galactitol. Sorbitol 75-83 aldo-keto reductase family 1 member B1 Rattus norvegicus 18-20 2114645-1 1990 Aldose reductase (alditol:NADP+ oxidoreductase, EC 1.1.1.21), an enzyme that converts glucose to sorbitol, the first step of the polyol pathway, has been implicated in secondary complications of diabetes, such as cataracts, retinopathy, neuropathy, and nephropathy. Sorbitol 97-105 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-16 2129508-2 1990 To examine the mechanism for changes in net sorbitol production, we measured activities of enzymes regulating sorbitol production (aldose reductase) and degradation (sorbitol dehydrogenase) in untreated, water diuretic, and antidiuretic (water restriction and/or vasopressin administration) rats. Sorbitol 110-118 aldo-keto reductase family 1 member B1 Rattus norvegicus 131-147 2138728-9 1990 The aldose reductase inhibitor Sorbinil prevented the increase in lens sorbitol in both the 21- and 44-d streptozotocin diabetic rats; cataract formation was prevented in the 44-d diabetic animals. Sorbitol 71-79 aldo-keto reductase family 1 member B1 Rattus norvegicus 4-20 2109701-7 1990 Of special interest is the induction of large amounts of AR in rat kidney cortex mesangial cells, a target tissue of diabetes and a site where excessive accumulation of sorbitol is suspected to be a critical factor in diabetic nephropathy. Sorbitol 169-177 aldo-keto reductase family 1 member B1 Rattus norvegicus 57-59 2144507-3 1990 The specific activities of the sorbitol pathway enzymes, sorbitol dehydrogenase and aldose reductase, are increased 2.5-fold and unchanged, respectively, if the cells are grown in the presence of sorbitol instead of glucose. Sorbitol 31-39 aldo-keto reductase family 1 member B1 Rattus norvegicus 84-100 2105661-1 1990 Sorbitol accumulates in renal medullary cells by synthesis from glucose in a reaction catalyzed by aldose reductase. Sorbitol 0-8 aldo-keto reductase family 1 member B1 Rattus norvegicus 99-115 2759193-4 1989 The results showed that (1) the activity of aldose reductase increased initially and decreased after 11 days of diabetes; (2) the fructose pool increased initially but started to decline after 3 days; (3) the HMPS activity increased nearly 40% immediately after diabetes induction; and (4) the turnover rates of glucose, alpha-glycerophosphate (GP), lactate, sorbitol, and fructose were 80.8 +/- 2.6, 10.1 +/- 1.4, 47.7 +/- 3.7, 7.9 +/- 0.9 and 5.2 +/- 2.2 nmol hr-1 lens-1 (34 mg wet weight lens-1), respectively. Sorbitol 359-367 aldo-keto reductase family 1 member B1 Rattus norvegicus 44-60 34738094-3 2021 In several tissues, including heart and brain, ischemia activates polyol pathway enzymes-aldose reductase (AR) and sorbitol dehydrogenase (SDH)-that convert glucose to sorbitol and fructose in reactions, causing oxidative stress and tissue loss. Sorbitol 168-176 aldo-keto reductase family 1 member B1 Rattus norvegicus 89-105 2507378-6 1989 All three aldose reductase inhibitors completely prevented or markedly reduced these hemodynamic and vascular filtration changes and increases in tissue sorbitol levels in the anterior uvea, posterior uvea, retina, sciatic nerve, and granulation tissue. Sorbitol 153-161 aldo-keto reductase family 1 member B1 Rattus norvegicus 10-26 2514349-1 1989 Aldose reductase (AR), an enzyme that catalyzes the conversion of glucose to sorbitol, has been implicated in the pathogenesis of many of the complications of diabetes mellitus, but its normal physiological function in various tissues remains uncertain. Sorbitol 77-85 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-16 2514349-1 1989 Aldose reductase (AR), an enzyme that catalyzes the conversion of glucose to sorbitol, has been implicated in the pathogenesis of many of the complications of diabetes mellitus, but its normal physiological function in various tissues remains uncertain. Sorbitol 77-85 aldo-keto reductase family 1 member B1 Rattus norvegicus 18-20 2514350-1 1989 Aldose reductase (AR), an enzyme which converts glucose to sorbitol, has been implicated in the pathogenesis of diabetic cataracts and retinopathy. Sorbitol 59-67 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-16 2514350-1 1989 Aldose reductase (AR), an enzyme which converts glucose to sorbitol, has been implicated in the pathogenesis of diabetic cataracts and retinopathy. Sorbitol 59-67 aldo-keto reductase family 1 member B1 Rattus norvegicus 18-20 2514350-8 1989 Since it has been suggested that AR-catalyzed sorbitol production could be an osmoprotective device of lens epithelium during systemic hyperosmolar stress, AR mRNA levels from dehydrated hyperosmolar rats were compared with euvolemic control values, and no difference was found. Sorbitol 46-54 aldo-keto reductase family 1 member B1 Rattus norvegicus 33-35 2514350-8 1989 Since it has been suggested that AR-catalyzed sorbitol production could be an osmoprotective device of lens epithelium during systemic hyperosmolar stress, AR mRNA levels from dehydrated hyperosmolar rats were compared with euvolemic control values, and no difference was found. Sorbitol 46-54 aldo-keto reductase family 1 member B1 Rattus norvegicus 156-158 2495737-1 1989 Osmoregulation in inner medullary cells depends in part on cellular accumulation of sorbitol, the production of which from glucose is catalyzed by aldose reductase. Sorbitol 84-92 aldo-keto reductase family 1 member B1 Rattus norvegicus 147-163 2528720-1 1989 Intracellular accumulation of sorbitol, generated from D-glucose via the aldose reductase pathway, is thought to play an important role in diabetic complications such as lens cataracts and neuropathy. Sorbitol 30-38 aldo-keto reductase family 1 member B1 Rattus norvegicus 73-89 2515932-2 1989 Supplementing the high-glucose cultures with an aldose reductase inhibitor markedly decreased the sorbitol levels without affecting the malformations or the retarded growth of the embryos. Sorbitol 98-106 aldo-keto reductase family 1 member B1 Rattus norvegicus 48-64 3143049-0 1988 Sorbitol metabolism in the retina, optic nerve, and sural nerve of diabetic rats treated with an aldose reductase inhibitor. Sorbitol 0-8 aldo-keto reductase family 1 member B1 Rattus norvegicus 97-113 2527143-1 1989 Intracellular accumulation of sorbitol, resulting from the increased glucose flux through polyol pathway with the action of aldose reductase, has been found pathogenic to chronic diabetic complications. Sorbitol 30-38 aldo-keto reductase family 1 member B1 Rattus norvegicus 124-140 3143049-1 1988 Sorbitol concentration has been measured in retina, optic, and sural nerve of normal, diabetic, and aldose reductase inhibitor-treated diabetic rats. Sorbitol 0-8 aldo-keto reductase family 1 member B1 Rattus norvegicus 100-116 3143049-5 1988 It is suggested that aldose reductase inhibition may be of greater use for alleviating peripheral nervous system accumulation of sorbitol than for hindering CNS accumulation of the polyol. Sorbitol 129-137 aldo-keto reductase family 1 member B1 Rattus norvegicus 21-37 3096334-4 1986 The aldose reductase inhibitors Sorbinil and Statil obtunded the rises in sorbitol but did not modify the increased incidence of malformations and the fall in DNA, protein and myo-inositol. Sorbitol 74-82 aldo-keto reductase family 1 member B1 Rattus norvegicus 4-20 3362066-1 1988 Metabolic imaging reflecting glucose metabolism in the glycolytic and aldose reductase sorbitol (ARS) pathways was performed noninvasively in rat using fluorinated glucose analogs, 2-fluoro-2-deoxy-D-glucose (2-FDG) or 3-fluoro-3-deoxy-D-glucose (3-FDG), and fluorine-19 (19F) nuclear magnetic resonance (NMR) imaging. Sorbitol 87-95 aldo-keto reductase family 1 member B1 Rattus norvegicus 70-86 2435570-4 1987 Treatment of a group of diabetic rats with the aldose reductase inhibitor, sorbinil, profoundly reduced the concentrations of polyol pathway metabolites (sorbitol and fructose) in sciatic nerve. Sorbitol 154-162 aldo-keto reductase family 1 member B1 Rattus norvegicus 47-63 3030278-3 1986 In the presence of NADPH aldose reductase reduced glucose, galactose and xylose to the respective polyols sorbitol, galactitol and xylitol. Sorbitol 106-114 aldo-keto reductase family 1 member B1 Rattus norvegicus 25-41 3189800-1 1988 Accumulation of sorbitol or galactitol and depletion of myo-inositol in hyperglycemic conditions such as diabetes and galactosemia involve the activity of aldose reductase and are implicated in hyperglycemia-induced complications such as cataract and neuropathy. Sorbitol 16-24 aldo-keto reductase family 1 member B1 Rattus norvegicus 155-171 3770312-6 1986 Administration of the aldose reductase inhibitor to the pregnant diabetic rats normalized the sorbitol levels in the embryos and their membranes, whereas the sorbitol contents of the fetal livers and placentas were significantly lowered but not completely corrected. Sorbitol 94-102 aldo-keto reductase family 1 member B1 Rattus norvegicus 22-38 3770312-6 1986 Administration of the aldose reductase inhibitor to the pregnant diabetic rats normalized the sorbitol levels in the embryos and their membranes, whereas the sorbitol contents of the fetal livers and placentas were significantly lowered but not completely corrected. Sorbitol 158-166 aldo-keto reductase family 1 member B1 Rattus norvegicus 22-38 25986969-1 2015 Increased aldose reductase activity has been implicated in the development of retinopathy due to accumulation of intracellular sugar alcohol, i.e., sorbitol. Sorbitol 148-156 aldo-keto reductase family 1 member B1 Rattus norvegicus 10-26 3922829-7 1985 Treatment with ONO-2235, a new aldose reductase inhibitor, prevented both slowing of motor nerve conduction velocity and elevation of nerve sorbitol concentration. Sorbitol 140-148 aldo-keto reductase family 1 member B1 Rattus norvegicus 31-47 6423398-1 1983 Aldose reductase (alditol:NADP oxidoreductase EC .1.1.1.21), an enzyme in the sorbitol pathway which has been implicated in the pathogenesis of diabetic complications, has been purified from rat lens (RLAR) by affinity chromatography with Amicon Matrex Gel Orange A and its properties have been compared to those of purified human placental aldose reductase (HPAR). Sorbitol 78-86 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-16 210165-6 1978 Both types of culture (as well as extracts of intact rat liver) exhibited enzymatic activities catalyzing the conversion of glucose to sorbitol (aldose reductase) and sorbitol to fructose (sorbitol dehydrogenase). Sorbitol 135-143 aldo-keto reductase family 1 member B1 Rattus norvegicus 145-161 33713301-1 2021 Aldose reductase (AR) catalyzes the conversion of glucose to sorbitol in a NADPH-dependent reaction, thereby increasing the production of reactive oxygen species (ROS). Sorbitol 61-69 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-16 30109747-0 2018 Artichoke leaf extract, as AKR1B1 inhibitor, decreases sorbitol level in the rat eye lenses under high glucose conditions ex vivo. Sorbitol 55-63 aldo-keto reductase family 1 member B1 Rattus norvegicus 27-33 30109747-1 2018 In the previous study, the artichoke leaf extract showed effective inhibition of AKR1B1, the first enzyme of polyol pathway, which reduces high level of glucose to osmotically active sorbitol, important for development of chronic diabetic complications. Sorbitol 183-191 aldo-keto reductase family 1 member B1 Rattus norvegicus 81-87 3100860-3 1986 The enzyme aldose reductase catalyzes the formation of sorbitol. Sorbitol 55-63 aldo-keto reductase family 1 member B1 Rattus norvegicus 11-27 2431858-2 1986 Treatment with an aldose reductase inhibitor both prevented and reversed this defect which was related to marked accumulations of sorbitol and fructose. Sorbitol 130-138 aldo-keto reductase family 1 member B1 Rattus norvegicus 18-34 2995180-4 1985 Administration of the aldose reductase inhibitor, sorbinil, which normalizes glomerular contents of both sorbitol and myo-inositol in diabetes, completely prevented the diminution of Na/K-ATPase activity. Sorbitol 105-113 aldo-keto reductase family 1 member B1 Rattus norvegicus 22-38 6407887-8 1983 These results suggest that sorbitol accumulation might contribute to the development of peripheral nerve dysfunction in acutely diabetic animals and the new aldose reductase inhibitor could be a potential drug for therapy of diabetic neuropathy. Sorbitol 27-35 aldo-keto reductase family 1 member B1 Rattus norvegicus 157-173 4402538-1 1972 ALDOSE REDUCTASE (ALDITOL: NADP oxidoreductase, EC 1.1.1.21) is the enzyme responsible for the conversion of glucose to its sugar alcohol, sorbitol. Sorbitol 139-147 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-16 26272532-2 2015 Aldose reductase inhibitor (ARI) blocks sorbitol production, and results in prevention of damage of nerve fibers. Sorbitol 40-48 aldo-keto reductase family 1 member B1 Rattus norvegicus 0-16 25986969-5 2015 The supplementation of Compound 2 suppresses sorbitol accumulation in retina by decreased AR activity in STZ induced diabetic rat in dose dependent manner. Sorbitol 45-53 aldo-keto reductase family 1 member B1 Rattus norvegicus 90-92 26291727-1 2015 The aim of the present work was to study the effect of 3-mercapto-5H-1,2,4-triazino[5,6-b]indole-5-acetic acid (CMTI), an efficient aldose reductase inhibitor, on sorbitol accumulation in selected organs of streptozotocin-induced diabetic rats in vivo. Sorbitol 163-171 aldo-keto reductase family 1 member B1 Rattus norvegicus 132-148 22710095-1 2012 In sugar cataract formation in rats, aldose reductase (AR) activity is not only linked to lenticular sorbitol (diabetic) or galactitol (galactosemic) formation but also to signal transduction changes, cytotoxic signals and activation of apoptosis. Sorbitol 101-109 aldo-keto reductase family 1 member B1 Rattus norvegicus 37-53 22710095-1 2012 In sugar cataract formation in rats, aldose reductase (AR) activity is not only linked to lenticular sorbitol (diabetic) or galactitol (galactosemic) formation but also to signal transduction changes, cytotoxic signals and activation of apoptosis. Sorbitol 101-109 aldo-keto reductase family 1 member B1 Rattus norvegicus 55-57 25985564-2 2014 In the present work we studied the effect of a novel zwitterionic inhibitor of aldose reductase [(2-benzyl-2,3,4,5-tetrahydro-1 H-pyrido[4,3-b]indole-8-yl)-acetic acid, compound 1] on sorbitol accumulation in ex vivo and in vivo models of diabetic complications. Sorbitol 184-192 aldo-keto reductase family 1 member B1 Rattus norvegicus 79-95