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Study · In vitro (cells) · 2019

9 results

Lixisenatide enhances mitochondrial biogenesis and function through regulating the CREB/PGC-1α pathway.

Zhao Z, Pu Y

Biochemical and biophysical research communications12 Dec 2018Cited by 29 (Europe PMC)

PMID30553453 (opens in a new tab)DOI10.1016/j.bbrc.2018.11.135 (opens in a new tab)PepBankPUB-30553453
Publisher pagePubMedAsk about this study
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study9

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

  1. 01LabIn vitro (cells)Mechanism

    In HUVECs, lixisenatide significantly increased PGC-1α expression.

    In plain wordsIn cells, lixisenatide significantly increased PGC-1α expression.

    Peptide
    Lixisenatide
    Outcome
    IncreasePGC-1α expression
    Study

    humann: not reported in source

    Human umbilical vein endothelial cells
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In the current study, we found that treatment with lixisenatide significantly increased the expression of PGC-1α, a "molecular switch" of mitochondrial biogenesis in human umbilical vein endothelial cells (HUVECs).
  2. 02LabIn vitro (cells)Mechanism

    In HUVECs, lixisenatide promoted NRF1 expression.

    In plain wordsIn cells, lixisenatide increased NRF1 expression.

    Peptide
    Lixisenatide
    Outcome
    IncreaseNRF1 expression
    Study

    humann: not reported in source

    Human umbilical vein endothelial cells
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Lixisenatide treatment also promoted the expressions of NRF1 and TFAM, which are the target genes of PGC-1α and executors of mitochondrial biogenesis.
    1 context sentence
    Summary · context
    In the current study, we found that treatment with lixisenatide significantly increased the expression of PGC-1α, a "molecular switch" of mitochondrial biogenesis in human umbilical vein endothelial cells (HUVECs).
  3. 03LabIn vitro (cells)Mechanism

    In HUVECs, lixisenatide promoted TFAM expression.

    In plain wordsIn cells, lixisenatide increased TFAM expression.

    Peptide
    Lixisenatide
    Outcome
    IncreaseTFAM expression
    Study

    humann: not reported in source

    Human umbilical vein endothelial cells
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Lixisenatide treatment also promoted the expressions of NRF1 and TFAM, which are the target genes of PGC-1α and executors of mitochondrial biogenesis.
    1 context sentence
    Summary · context
    In the current study, we found that treatment with lixisenatide significantly increased the expression of PGC-1α, a "molecular switch" of mitochondrial biogenesis in human umbilical vein endothelial cells (HUVECs).
  4. 04LabIn vitro (cells)Mechanism

    In HUVECs, lixisenatide increased mtDNA/nDNA, mitochondrial mass, cytochrome B expression, and citrate synthase activity.

    In plain wordsIn cells, lixisenatide increased mtDNA/nDNA, mitochondrial mass, cytochrome B expression, and citrate synthase activity.

    Peptide
    Lixisenatide
    Outcome
    IncreaseMitochondrial biogenesis markers
    Study

    humann: not reported in source

    Human umbilical vein endothelial cells
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Importantly, our results indicate that lixisenatide treatment promoted mitochondrial biogenesis by elevating the ratio of mitochondrial-to-nuclear DNA (mtDNA/nDNA), mitochondrial mass, cytochrome B expression, and citrate synthase activity in HUVECs.
    1 context sentence
    Summary · context
    In the current study, we found that treatment with lixisenatide significantly increased the expression of PGC-1α, a "molecular switch" of mitochondrial biogenesis in human umbilical vein endothelial cells (HUVECs).
  5. 05LabIn vitro (cells)Mechanism

    In HUVECs, lixisenatide increased mitochondrial respiration rate.

    In plain wordsIn cells, lixisenatide increased mitochondrial respiration rate.

    Peptide
    Lixisenatide
    Outcome
    IncreaseMitochondrial respiration rate
    Study

    humann: not reported in source

    Human umbilical vein endothelial cells
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Correspondingly, we found that lixisenatide treatment led to a functional gain and improvement in mitochondria by increasing the mitochondrial respiration rate and ATP generation.
    1 context sentence
    Summary · context
    In the current study, we found that treatment with lixisenatide significantly increased the expression of PGC-1α, a "molecular switch" of mitochondrial biogenesis in human umbilical vein endothelial cells (HUVECs).
  6. 06LabIn vitro (cells)Mechanism

    In HUVECs, lixisenatide increased ATP generation.

    In plain wordsIn cells, lixisenatide increased ATP generation.

    Peptide
    Lixisenatide
    Outcome
    IncreaseATP generation
    Study

    humann: not reported in source

    Human umbilical vein endothelial cells
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Correspondingly, we found that lixisenatide treatment led to a functional gain and improvement in mitochondria by increasing the mitochondrial respiration rate and ATP generation.
    1 context sentence
    Summary · context
    In the current study, we found that treatment with lixisenatide significantly increased the expression of PGC-1α, a "molecular switch" of mitochondrial biogenesis in human umbilical vein endothelial cells (HUVECs).
  7. 07LabIn vitro (cells)Mechanism

    In HUVECs, lixisenatide induced CREB phosphorylation at Ser133.

    In plain wordsIn cells, lixisenatide induced CREB phosphorylation at Ser133.

    Peptide
    Lixisenatide
    Outcome
    IncreaseCREB phosphorylation at Ser133
    Study

    humann: not reported in source

    Human umbilical vein endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, lixisenatide treatment induced the phosphorylation of CREB at Ser133.
    1 context sentence
    Summary · context
    In the current study, we found that treatment with lixisenatide significantly increased the expression of PGC-1α, a "molecular switch" of mitochondrial biogenesis in human umbilical vein endothelial cells (HUVECs).

Studies that did not test the peptide alone2

In this study, Lixisenatide was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Lixisenatide.

  1. 08LabNot a test of Lixisenatide aloneIn vitro (cells)Mechanism

    In HUVECs, H89 blockade of CREB phosphorylation abolished lixisenatide-induced PGC-1α/NRF-1/TFAM activation.

    In plain wordsIn cells, H89 blockade of CREB phosphorylation abolished lixisenatide-induced PGC-1α/NRF-1/TFAM activation.

    Peptide
    Lixisenatide
    Outcome
    DecreaseCREB dependence of PGC-1α/NRF-1/TFAM activation
    Study

    humann: not reported in source

    Human umbilical vein endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Blockage of CREB phosphorylation using its inhibitor H89 abolished the effects of lixisenatide on the activation of PGC-1α/NRF-1/TFAM as well as the increase in mtDNA/nDNA.
    1 context sentence
    Summary · context
    In the current study, we found that treatment with lixisenatide significantly increased the expression of PGC-1α, a "molecular switch" of mitochondrial biogenesis in human umbilical vein endothelial cells (HUVECs).

    In this study, Lixisenatide was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Lixisenatide.

  2. 09LabNot a test of Lixisenatide aloneIn vitro (cells)Mechanism

    In HUVECs, H89 blockade of CREB phosphorylation abolished the lixisenatide-induced increase in mtDNA/nDNA.

    In plain wordsIn cells, H89 blockade of CREB phosphorylation abolished the lixisenatide-induced increase in mtDNA/nDNA.

    Peptide
    Lixisenatide
    Outcome
    DecreaseCREB-dependent mitochondrial DNA increase
    Study

    humann: not reported in source

    Human umbilical vein endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Blockage of CREB phosphorylation using its inhibitor H89 abolished the effects of lixisenatide on the activation of PGC-1α/NRF-1/TFAM as well as the increase in mtDNA/nDNA.
    1 context sentence
    Summary · context
    In the current study, we found that treatment with lixisenatide significantly increased the expression of PGC-1α, a "molecular switch" of mitochondrial biogenesis in human umbilical vein endothelial cells (HUVECs).

    In this study, Lixisenatide was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Lixisenatide.

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

    28 Oct 2026, 02:03 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:36 UTC

    First added · source update from Europe PMC

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Terms as the source lists them.

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