Protective role of fructokinase blockade in the pathogenesis of acute kidney injury in mice

Acute kidney injury is associated with high mortality, especially in intensive care unit patients. The polyol pathway is a metabolic route able to convert glucose into fructose. Here we show the detrimental role of endogenous fructose production by the polyol pathway and its metabolism through fruct...

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Vydáno v:Nature communications Ročník 8; číslo 1; s. 14181 - 12
Hlavní autoři: Andres-Hernando, Ana, Li, Nanxing, Cicerchi, Christina, Inaba, Shinichiro, Chen, Wei, Roncal-Jimenez, Carlos, Le, Myphuong T., Wempe, Michael F., Milagres, Tamara, Ishimoto, Takuji, Fini, Mehdi, Nakagawa, Takahiko, Johnson, Richard J., Lanaspa, Miguel A.
Médium: Journal Article
Jazyk:angličtina
Vydáno: London Nature Publishing Group UK 13.02.2017
Nature Publishing Group
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Acute Kidney Injury - etiology
Acute Kidney Injury - metabolism
Acute Kidney Injury - prevention & control
Aldehyde Reductase - metabolism
Animals
Cell Line
Creatinine
Fructokinases - antagonists & inhibitors
Fructokinases - genetics
Fructokinases - metabolism
Fructose - metabolism
Fructose - urine
Human subjects
Humanities and Social Sciences
Humans
Intensive care
Ischemia
Ischemia - complications
Kidney - drug effects
Kidney - metabolism
Kidney - pathology
Kidneys
Luteolin - pharmacology
Metabolism
Mice, Inbred C57BL
Mice, Knockout
multidisciplinary
Oxidative stress
Oxidative Stress - drug effects
Pathogenesis
Protective Agents - pharmacology
Science
Science (multidisciplinary)
Surgery
Uric acid
Uric Acid - metabolism
ISSN:2041-1723, 2041-1723
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Tagy: Přidat tag
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Abstract Acute kidney injury is associated with high mortality, especially in intensive care unit patients. The polyol pathway is a metabolic route able to convert glucose into fructose. Here we show the detrimental role of endogenous fructose production by the polyol pathway and its metabolism through fructokinase in the pathogenesis of ischaemic acute kidney injury (iAKI). Consistent with elevated urinary fructose in AKI patients, mice undergoing iAKI show significant polyol pathway activation in the kidney cortex characterized by high levels of aldose reductase, sorbitol and endogenous fructose. Wild type but not fructokinase knockout animals demonstrate severe kidney injury associated with ATP depletion, elevated uric acid, oxidative stress and inflammation. Interestingly, both the renal injury and dysfunction in wild-type mice undergoing iAKI is significantly ameliorated when exposed to luteolin, a recently discovered fructokinase inhibitor. This study demonstrates a role for fructokinase and endogenous fructose as mediators of acute renal disease. The polyol pathway, which converts glucose into sorbitol and fructose, is active in chronic conditions like hepatic steatosis and chronic kidney disease. Here, Andres-Hernando et al . show that fructose production promotes renal injury and fructokinase inhibition protects against kidney damage during ischaemic acute kidney disease.
AbstractList The polyol pathway, which converts glucose into sorbitol and fructose, is active in chronic conditions like hepatic steatosis and chronic kidney disease. Here, Andres-Hernandoet al. show that fructose production promotes renal injury and fructokinase inhibition protects against kidney damage during ischaemic acute kidney disease.
Acute kidney injury is associated with high mortality, especially in intensive care unit patients. The polyol pathway is a metabolic route able to convert glucose into fructose. Here we show the detrimental role of endogenous fructose production by the polyol pathway and its metabolism through fructokinase in the pathogenesis of ischaemic acute kidney injury (iAKI). Consistent with elevated urinary fructose in AKI patients, mice undergoing iAKI show significant polyol pathway activation in the kidney cortex characterized by high levels of aldose reductase, sorbitol and endogenous fructose. Wild type but not fructokinase knockout animals demonstrate severe kidney injury associated with ATP depletion, elevated uric acid, oxidative stress and inflammation. Interestingly, both the renal injury and dysfunction in wild-type mice undergoing iAKI is significantly ameliorated when exposed to luteolin, a recently discovered fructokinase inhibitor. This study demonstrates a role for fructokinase and endogenous fructose as mediators of acute renal disease.Acute kidney injury is associated with high mortality, especially in intensive care unit patients. The polyol pathway is a metabolic route able to convert glucose into fructose. Here we show the detrimental role of endogenous fructose production by the polyol pathway and its metabolism through fructokinase in the pathogenesis of ischaemic acute kidney injury (iAKI). Consistent with elevated urinary fructose in AKI patients, mice undergoing iAKI show significant polyol pathway activation in the kidney cortex characterized by high levels of aldose reductase, sorbitol and endogenous fructose. Wild type but not fructokinase knockout animals demonstrate severe kidney injury associated with ATP depletion, elevated uric acid, oxidative stress and inflammation. Interestingly, both the renal injury and dysfunction in wild-type mice undergoing iAKI is significantly ameliorated when exposed to luteolin, a recently discovered fructokinase inhibitor. This study demonstrates a role for fructokinase and endogenous fructose as mediators of acute renal disease.
Acute kidney injury is associated with high mortality, especially in intensive care unit patients. The polyol pathway is a metabolic route able to convert glucose into fructose. Here we show the detrimental role of endogenous fructose production by the polyol pathway and its metabolism through fructokinase in the pathogenesis of ischaemic acute kidney injury (iAKI). Consistent with elevated urinary fructose in AKI patients, mice undergoing iAKI show significant polyol pathway activation in the kidney cortex characterized by high levels of aldose reductase, sorbitol and endogenous fructose. Wild type but not fructokinase knockout animals demonstrate severe kidney injury associated with ATP depletion, elevated uric acid, oxidative stress and inflammation. Interestingly, both the renal injury and dysfunction in wild-type mice undergoing iAKI is significantly ameliorated when exposed to luteolin, a recently discovered fructokinase inhibitor. This study demonstrates a role for fructokinase and endogenous fructose as mediators of acute renal disease. The polyol pathway, which converts glucose into sorbitol and fructose, is active in chronic conditions like hepatic steatosis and chronic kidney disease. Here, Andres-Hernando et al . show that fructose production promotes renal injury and fructokinase inhibition protects against kidney damage during ischaemic acute kidney disease.
Acute kidney injury is associated with high mortality, especially in intensive care unit patients. The polyol pathway is a metabolic route able to convert glucose into fructose. Here we show the detrimental role of endogenous fructose production by the polyol pathway and its metabolism through fructokinase in the pathogenesis of ischaemic acute kidney injury (iAKI). Consistent with elevated urinary fructose in AKI patients, mice undergoing iAKI show significant polyol pathway activation in the kidney cortex characterized by high levels of aldose reductase, sorbitol and endogenous fructose. Wild type but not fructokinase knockout animals demonstrate severe kidney injury associated with ATP depletion, elevated uric acid, oxidative stress and inflammation. Interestingly, both the renal injury and dysfunction in wild-type mice undergoing iAKI is significantly ameliorated when exposed to luteolin, a recently discovered fructokinase inhibitor. This study demonstrates a role for fructokinase and endogenous fructose as mediators of acute renal disease. The polyol pathway, which converts glucose into sorbitol and fructose, is active in chronic conditions like hepatic steatosis and chronic kidney disease. Here, Andres-Hernando et al. show that fructose production promotes renal injury and fructokinase inhibition protects against kidney damage during ischaemic acute kidney disease.
Acute kidney injury is associated with high mortality, especially in intensive care unit patients. The polyol pathway is a metabolic route able to convert glucose into fructose. Here we show the detrimental role of endogenous fructose production by the polyol pathway and its metabolism through fructokinase in the pathogenesis of ischaemic acute kidney injury (iAKI). Consistent with elevated urinary fructose in AKI patients, mice undergoing iAKI show significant polyol pathway activation in the kidney cortex characterized by high levels of aldose reductase, sorbitol and endogenous fructose. Wild type but not fructokinase knockout animals demonstrate severe kidney injury associated with ATP depletion, elevated uric acid, oxidative stress and inflammation. Interestingly, both the renal injury and dysfunction in wild-type mice undergoing iAKI is significantly ameliorated when exposed to luteolin, a recently discovered fructokinase inhibitor. This study demonstrates a role for fructokinase and endogenous fructose as mediators of acute renal disease.
ArticleNumber 14181
Author Inaba, Shinichiro
Fini, Mehdi
Andres-Hernando, Ana
Roncal-Jimenez, Carlos
Li, Nanxing
Cicerchi, Christina
Ishimoto, Takuji
Johnson, Richard J.
Chen, Wei
Lanaspa, Miguel A.
Milagres, Tamara
Nakagawa, Takahiko
Wempe, Michael F.
Le, Myphuong T.
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  surname: Andres-Hernando
  fullname: Andres-Hernando, Ana
  organization: University of Colorado Denver
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  givenname: Nanxing
  surname: Li
  fullname: Li, Nanxing
  organization: University of Colorado Denver
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  givenname: Christina
  surname: Cicerchi
  fullname: Cicerchi, Christina
  organization: University of Colorado Denver
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  givenname: Shinichiro
  surname: Inaba
  fullname: Inaba, Shinichiro
  organization: University of Colorado Denver
– sequence: 5
  givenname: Wei
  surname: Chen
  fullname: Chen, Wei
  organization: University of Colorado Denver, Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University
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  givenname: Carlos
  surname: Roncal-Jimenez
  fullname: Roncal-Jimenez, Carlos
  organization: University of Colorado Denver
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  givenname: Myphuong T.
  surname: Le
  fullname: Le, Myphuong T.
  organization: University of Colorado Denver
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  surname: Wempe
  fullname: Wempe, Michael F.
  organization: University of Colorado Denver
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  surname: Milagres
  fullname: Milagres, Tamara
  organization: University of Colorado Denver
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  givenname: Takuji
  surname: Ishimoto
  fullname: Ishimoto, Takuji
  organization: University of Colorado Denver
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  givenname: Mehdi
  surname: Fini
  fullname: Fini, Mehdi
  organization: University of Colorado Denver
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  givenname: Takahiko
  surname: Nakagawa
  fullname: Nakagawa, Takahiko
  organization: University of Colorado Denver
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  givenname: Miguel A.
  surname: Lanaspa
  fullname: Lanaspa, Miguel A.
  email: miguel.lanaspagarcia@ucdenver.edu
  organization: University of Colorado Denver
BackLink https://www.ncbi.nlm.nih.gov/pubmed/28194018$$D View this record in MEDLINE/PubMed
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Snippet Acute kidney injury is associated with high mortality, especially in intensive care unit patients. The polyol pathway is a metabolic route able to convert...
The polyol pathway, which converts glucose into sorbitol and fructose, is active in chronic conditions like hepatic steatosis and chronic kidney disease. Here,...
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StartPage 14181
SubjectTerms 42
42/35
631/443/272
64/60
692/4022/1585/4
82
82/51
82/80
96/106
96/21
Acute Kidney Injury - etiology
Acute Kidney Injury - metabolism
Acute Kidney Injury - prevention & control
Aldehyde Reductase - metabolism
Animals
Cell Line
Creatinine
Fructokinases - antagonists & inhibitors
Fructokinases - genetics
Fructokinases - metabolism
Fructose - metabolism
Fructose - urine
Human subjects
Humanities and Social Sciences
Humans
Intensive care
Ischemia
Ischemia - complications
Kidney - drug effects
Kidney - metabolism
Kidney - pathology
Kidneys
Luteolin - pharmacology
Metabolism
Mice, Inbred C57BL
Mice, Knockout
multidisciplinary
Oxidative stress
Oxidative Stress - drug effects
Pathogenesis
Protective Agents - pharmacology
Science
Science (multidisciplinary)
Surgery
Uric acid
Uric Acid - metabolism
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Title Protective role of fructokinase blockade in the pathogenesis of acute kidney injury in mice
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