PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31589122-2 2020 Hepatic AR is induced under hyperglycemia condition and converts excess glucose to lipogenic fructose, which contributes in part to the accumulation of fat in the liver cells of diabetes rodents. Fructose 93-101 aldo-keto reductase family 1 member B Homo sapiens 8-10 32086945-0 2020 Elevated fructose and uric acid via aldose reductase contribute to experimental and human alcoholic liver disease. Fructose 9-17 aldo-keto reductase family 1 member B Homo sapiens 36-52 32086945-2 2020 Fructose (dietary or endogenous), its metabolite uric acid, and aldose reductase (AR, the only endogenous enzyme that produces fructose) are strongly associated with the development of non-alcoholic fatty liver disease (NAFLD). Fructose 127-135 aldo-keto reductase family 1 member B Homo sapiens 64-80 32086945-2 2020 Fructose (dietary or endogenous), its metabolite uric acid, and aldose reductase (AR, the only endogenous enzyme that produces fructose) are strongly associated with the development of non-alcoholic fatty liver disease (NAFLD). Fructose 127-135 aldo-keto reductase family 1 member B Homo sapiens 82-84 32086945-6 2020 Lastly, we demonstrated the therapeutic potential of pharmacological AR inhibition against alcohol-induced hepatic injury in experimental ALD CONCLUSIONS: Our data demonstrate that hepatic AR upregulation, and consequent elevation in fructose, sorbitol and/or uric acid, are important factors contributing to alcohol-induced steatosis, ER stress, apoptosis and liver injury in both experimental and human ALD. Fructose 234-242 aldo-keto reductase family 1 member B Homo sapiens 69-71 32086945-6 2020 Lastly, we demonstrated the therapeutic potential of pharmacological AR inhibition against alcohol-induced hepatic injury in experimental ALD CONCLUSIONS: Our data demonstrate that hepatic AR upregulation, and consequent elevation in fructose, sorbitol and/or uric acid, are important factors contributing to alcohol-induced steatosis, ER stress, apoptosis and liver injury in both experimental and human ALD. Fructose 234-242 aldo-keto reductase family 1 member B Homo sapiens 189-191 6782033-14 1981 The added activities of AR and PD in producing sorbitol and fructose in combination with decreased hexokinase with age may account for diabetic cataract formation in human lenses exposed to a high glucose stress. Fructose 60-68 aldo-keto reductase family 1 member B Homo sapiens 24-26 30551808-1 2019 Aldose reductase is an important enzyme in the polyol pathway, where glucose is converted to fructose, and sorbitol is released. Fructose 93-101 aldo-keto reductase family 1 member B Homo sapiens 0-16 23850972-2 2013 Hyperglycemia increases glucose flux through the polyol pathway, in which aldose reductase converts glucose into intracellular sorbitol, which is subsequently converted to fructose by sorbitol dehydrogenase (SDH). Fructose 172-180 aldo-keto reductase family 1 member B Homo sapiens 74-90 30023751-1 2017 Aldose reductase is the first enzyme of the polyol pathway in which glucose is converted to fructose via sorbitol. Fructose 92-100 aldo-keto reductase family 1 member B Homo sapiens 0-16 22911800-2 2012 High glucose (25 mM) incubation up-regulated mRNA levels of aldose reductase (an enzyme converting glucose to fructose) and aldolase B (a key enzyme that catalyzes MG formation from fructose) and enhanced MG formation in human umbilical vein endothelial cells (HUVECs) and HUVEC-derived EA. Fructose 110-118 aldo-keto reductase family 1 member B Homo sapiens 60-76 22911800-2 2012 High glucose (25 mM) incubation up-regulated mRNA levels of aldose reductase (an enzyme converting glucose to fructose) and aldolase B (a key enzyme that catalyzes MG formation from fructose) and enhanced MG formation in human umbilical vein endothelial cells (HUVECs) and HUVEC-derived EA. Fructose 182-190 aldo-keto reductase family 1 member B Homo sapiens 60-76 20466987-4 2010 Under diabetic conditions AR converts glucose into sorbitol, which is then converted to fructose. Fructose 88-96 aldo-keto reductase family 1 member B Homo sapiens 26-28 16278369-1 2006 Two enzymes are involved in the polyol pathway: an aldose reductase that reduces glucose in sorbitol followed by its oxidation in fructose by sorbitol dehydrogenase. Fructose 130-138 aldo-keto reductase family 1 member B Homo sapiens 51-67 19224447-2 2009 Sorbitol synthesis is regulated by the enzyme aldose reductase (AR) and its degradation to fructose is catalyzed by the enzyme sorbitol dehydrogenase (SDH). Fructose 91-99 aldo-keto reductase family 1 member B Homo sapiens 46-62 19224447-2 2009 Sorbitol synthesis is regulated by the enzyme aldose reductase (AR) and its degradation to fructose is catalyzed by the enzyme sorbitol dehydrogenase (SDH). Fructose 91-99 aldo-keto reductase family 1 member B Homo sapiens 64-66 20520742-1 2010 Reductions in fasting serum fructose or erythrocyte sorbitol have been proposed as markers for early proof of mechanism in clinical development of aldose reductase (AR) inhibitors. Fructose 28-36 aldo-keto reductase family 1 member B Homo sapiens 147-163 12615520-1 2003 The polyol pathway consists of two enzymes aldose reductase (AR) and sorbitol dehydrogenase (SDH); the former is the first enzyme in the polyol pathway, that catalyzes the reduction of glucose to sorbitol, the latter is the second one, that converts sorbitol to fructose using by NAD(+) as a cofactor. Fructose 262-270 aldo-keto reductase family 1 member B Homo sapiens 43-59 16026266-4 2005 In animal studies, there is strong evidence that aldose reductase, the first and rate-limiting enzyme of the polyol pathway that converts glucose to fructose, plays a key role in the pathogenesis of microvascular complications. Fructose 149-157 aldo-keto reductase family 1 member B Homo sapiens 49-65 12962626-1 2003 Sorbitol dehydrogenase (hSDH) and aldose reductase form the polyol pathway that interconverts glucose and fructose. Fructose 106-114 aldo-keto reductase family 1 member B Homo sapiens 34-50 12615520-1 2003 The polyol pathway consists of two enzymes aldose reductase (AR) and sorbitol dehydrogenase (SDH); the former is the first enzyme in the polyol pathway, that catalyzes the reduction of glucose to sorbitol, the latter is the second one, that converts sorbitol to fructose using by NAD(+) as a cofactor. Fructose 262-270 aldo-keto reductase family 1 member B Homo sapiens 61-63 9614624-6 1998 The aldose reductase content in erythrocytes was well correlated with its activity, and there was a significant correlation between the enzyme content and the erythrocyte sorbitol (r = 0.58, P < 0.001) or fructose (r = 0.57, P < 0.001) levels as well as between the enzyme level and the lactate-to-pyruvate ratio (r = 0.38, P < 0.05). Fructose 208-216 aldo-keto reductase family 1 member B Homo sapiens 4-20 12792982-4 2003 AGE are reported also to be produced by increased levels of fructose through increased activity of AR in diabetes. Fructose 60-68 aldo-keto reductase family 1 member B Homo sapiens 99-101 10923253-19 2000 Aldose reductase inhibitors might reduce sorbitol and fructose production and normalize myo-inositol levels. Fructose 54-62 aldo-keto reductase family 1 member B Homo sapiens 0-16 9183016-1 1997 The polyol pathway comprises the enzymes aldose reductase and sorbitol dehydrogenase which convert glucose to fructose via sorbitol. Fructose 110-118 aldo-keto reductase family 1 member B Homo sapiens 41-57 7940997-1 1994 Aldose reductase converts glucose to sorbitol, which is further processed to fructose. Fructose 77-85 aldo-keto reductase family 1 member B Homo sapiens 0-16 8792096-4 1996 Indomethacin (20 microM) significantly (P < 0.01) suppressed the release of fructose (25.4 +/- 15.7% of control) and hexose phosphates (29.4 +/- 4.0) with the inhibition of release of lactate dehydrogenase (35.5 +/- 4.9) as well as probucol, whereas an aldose reductase inhibitor, epalrestat, significantly (P < 0.001) inhibited only the fructose release (0.9 +/- 0.8). Fructose 79-87 aldo-keto reductase family 1 member B Homo sapiens 256-272 8535074-1 1995 The polyol pathway comprises the enzymes aldose reductase and sorbitol dehydrogenase, which convert glucose to sorbitol and sorbitol to fructose, respectively, particularly in hyperglycemic states. Fructose 136-144 aldo-keto reductase family 1 member B Homo sapiens 41-57 34120350-5 2021 In turn, the ethanol ingested could activate aldose reductase that stimulates the conversion of glucose to fructose, while uric acid produced during ethanol metabolism could further enhance fructose production and metabolism. Fructose 107-115 aldo-keto reductase family 1 member B Homo sapiens 45-61 8330752-1 1993 Conversion of glucose to fructose via sorbitol depends upon the enzymes aldose reductase and sorbitol dehydrogenase and is called the polyol pathway. Fructose 25-33 aldo-keto reductase family 1 member B Homo sapiens 72-88 2118946-1 1990 Aldose reductase activity is increased in neuroblastoma cells grown in media containing 30 mM fructose and/or 30 mM glucose. Fructose 94-102 aldo-keto reductase family 1 member B Homo sapiens 0-16 2118946-12 1990 These data suggest that fructose may be activating or increasing sorbinil-resistant aldose reductase activity as well as partially blocking sorbitol dehydrogenase activity. Fructose 24-32 aldo-keto reductase family 1 member B Homo sapiens 84-100 35454074-2 2022 AKR1B1 is the first enzyme of the so-called polyol pathway that allows the conversion of glucose into sorbitol, which in turn is oxidized to fructose by sorbitol dehydrogenase. Fructose 141-149 aldo-keto reductase family 1 member B Homo sapiens 0-6 3142503-3 1988 Inclusion of aldose reductase inhibitors in the incubation medium not only prevented the accumulation of sorbitol and fructose but also prevented the decrease in glutathione and ATP. Fructose 118-126 aldo-keto reductase family 1 member B Homo sapiens 13-29 3136330-8 1988 On repeat biopsy, six diabetics, treated for a year with the aldose reductase inhibitor sorbinil, had decreased endoneurial levels of sorbitol (P less than 0.01) and fructose (0.05 less than P less than 0.1), but unchanged levels of myo-inositol. Fructose 166-174 aldo-keto reductase family 1 member B Homo sapiens 61-77 6425821-4 1984 An increase of aldose reductase and a decrease in the sorbitol-dehydrogenase activity occur within the first two weeks after diabetes induction, which correlates with the maximal rate of sorbitol and fructose accumulation. Fructose 200-208 aldo-keto reductase family 1 member B Homo sapiens 15-31