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Study · Animal study (in vivo) · mouse · 2019

3 results

AMP-activated protein kinase activation ameliorates eicosanoid dysregulation in high-fat-induced kidney disease in mice.

Declèves AE, Mathew AV, Armando AM, Han X, Dennis EA, Quehenberger O, Sharma K

Journal of lipid research12 Mar 2019Cited by 18 (Europe PMC)

PMID30862696 (opens in a new tab)PMCIDPMC6495162 (opens in a new tab)DOI10.1194/jlr.m088690 (opens in a new tab)PepBankPUB-30862696
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Summary

High-fat diet (HFD) causes renal lipotoxicity that is ameliorated with AMP-activated protein kinase (AMPK) activation. Although bioactive eicosanoids increase with HFD and are essential in regulation of renal disease, their role in the inflammatory response to HFD-induced kidney disease and their modulation by AMPK activation remain unexplored. In a mouse model, we explored the effects of HFD on eicosanoid synthesis and the role of AMPK activation in ameliorating these changes. We used targeted lipidomic profiling with quantitative MS to determine PUFA and eicosanoid content in kidneys, urine, and renal arterial and venous circulation. HFD increased phospholipase expression as well as the total and free pro-inflammatory arachidonic acid (AA) and anti-inflammatory DHA in kidneys. Consistent with the parent PUFA levels, the AA- and DHA-derived lipoxygenase (LOX), cytochrome P450, and nonenzymatic degradation (NE) metabolites increased in kidneys with HFD, while EPA-derived LOX and NE metabolites decreased. Conversely, treatment with 5-aminoimidazole-4-carboxamide-1-β-D-furanosyl 5'-monophosphate (AICAR), an AMPK activator, reduced the free AA and DHA content and the DHA-derived metabolites in kidney. Interestingly, kidney and circulating AA, AA metabolites, EPA-derived LOX, and NE metabolites are increased with HFD; whereas, DHA metabolites are increased in kidney in contrast to their decreased circulating levels with HFD. Together, these changes showcase HFD-induced pro- and anti-inflammatory eicosanoid dysregulation and highlight the role of AMPK in correcting HFD-induced dysregulated eicosanoid pathways.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

3 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Mechanism

    In mice fed a high-fat diet, AICAR reduced kidney free arachidonic acid content.

    In plain wordsIn mice fed a high-fat diet, AICAR reduced free arachidonic acid in the kidneys.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseKidney free arachidonic acid
    Study

    mousen: not reported in source

    High-fat diet kidney disease
    Outcome group
    Lipids · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Conversely, treatment with 5-aminoimidazole-4-carboxamide-1-β-D-furanosyl 5'-monophosphate (AICAR), an AMPK activator, reduced the free AA and DHA content and the DHA-derived metabolites in kidney.
    1 context sentence
    Summary · context
    In a mouse model, we explored the effects of HFD on eicosanoid synthesis and the role of AMPK activation in ameliorating these changes.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mice fed a high-fat diet, AICAR reduced kidney free DHA content.

    In plain wordsIn mice fed a high-fat diet, AICAR reduced free DHA in the kidneys.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseKidney free DHA
    Study

    mousen: not reported in source

    High-fat diet kidney disease
    Outcome group
    Lipids · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Conversely, treatment with 5-aminoimidazole-4-carboxamide-1-β-D-furanosyl 5'-monophosphate (AICAR), an AMPK activator, reduced the free AA and DHA content and the DHA-derived metabolites in kidney.
    1 context sentence
    Summary · context
    In a mouse model, we explored the effects of HFD on eicosanoid synthesis and the role of AMPK activation in ameliorating these changes.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In mice fed a high-fat diet, AICAR reduced kidney DHA-derived metabolites.

    In plain wordsIn mice fed a high-fat diet, AICAR reduced DHA-derived substances in the kidneys.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseKidney DHA-derived metabolites
    Study

    mousen: not reported in source

    High-fat diet kidney disease
    Outcome group
    Lipids · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Conversely, treatment with 5-aminoimidazole-4-carboxamide-1-β-D-furanosyl 5'-monophosphate (AICAR), an AMPK activator, reduced the free AA and DHA content and the DHA-derived metabolites in kidney.
    1 context sentence
    Summary · context
    In a mouse model, we explored the effects of HFD on eicosanoid synthesis and the role of AMPK activation in ameliorating these changes.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

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