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Study · Animal study (in vivo) · mouse · 2010

7 results

The neurosurvival factor Humanin inhibits beta-cell apoptosis via signal transducer and activator of transcription 3 activation and delays and ameliorates diabetes in nonobese diabetic mice.

Hoang PT, Park P, Cobb LJ, Paharkova-Vatchkova V, Hakimi M, Cohen P, Lee KW

Metabolism: clinical and experimental1 Oct 2009Cited by 121 (Europe PMC)

PMID19800083 (opens in a new tab)PMCIDPMC2932671 (opens in a new tab)DOI10.1016/j.metabol.2009.08.001 (opens in a new tab)PepBankPUB-19800083
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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 study7

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In NOD mice, 6 weeks of humanin treatment normalized glucose tolerance.

    In plain wordsIn mice prone to type 1 diabetes, 6 weeks of humanin brought blood sugar handling back to normal.

    Peptide
    Humanin
    Outcome
    IncreaseGlucose tolerance after 6 weeks
    Study

    mousen: not reported in source

    Nonobese diabetic (NOD) mice
    Outcome group
    Glycemic control · Endocrine and hormones
    Studied dose
    Dose not stated · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Humanin normalized glucose tolerance in NOD mice treated for 6 weeks
    1 context sentence
    Summary · context
    We investigated whether Humanin, a recently described survival factor for neurons, could improve the survival of beta-cells and delay or treat diabetes in the nonobese diabetic (NOD) model.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In NOD mice treated with humanin for 6 weeks, the pancreata showed decreased lymphocyte infiltration and severity.

    In plain wordsIn mice prone to type 1 diabetes, humanin treatment led to fewer immune cells in the pancreas and milder damage.

    Peptide
    Humanin
    Outcome
    DecreasePancreatic lymphocyte infiltration and severity
    Study

    mousen: not reported in source

    Nonobese diabetic (NOD) mice
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Humanin normalized glucose tolerance in NOD mice treated for 6 weeks, and their pancreata revealed decreased lymphocyte infiltration and severity.
    1 context sentence
    Summary · context
    We investigated whether Humanin, a recently described survival factor for neurons, could improve the survival of beta-cells and delay or treat diabetes in the nonobese diabetic (NOD) model.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In NOD mice treated for 20 weeks, humanin delayed or prevented the onset of diabetes.

    In plain wordsIn mice prone to type 1 diabetes, 20 weeks of humanin delayed or prevented the start of diabetes.

    Peptide
    Humanin
    Outcome
    DecreaseOnset of diabetes after 20 weeks
    Study

    mousen: not reported in source

    Nonobese diabetic (NOD) mice
    Outcome group
    Glycemic control · Endocrine and hormones
    Studied dose
    Dose not stated · 20 weeksAs given in this study (mouse).

    Source sentences

    Summary
    In addition, Humanin delayed/prevented the onset of diabetes in NOD mice treated for 20 weeks.
    1 context sentence
    Summary · context
    We investigated whether Humanin, a recently described survival factor for neurons, could improve the survival of beta-cells and delay or treat diabetes in the nonobese diabetic (NOD) model.
  4. 04LabIn vitro (cells)Efficacy outcome

    In NIT-1 beta-cells, humanin reduced apoptosis induced by serum starvation.

    In plain wordsIn cells, humanin reduced the death of insulin-producing cells that were starved of serum.

    Peptide
    Humanin
    Outcome
    DecreaseApoptosis induced by serum starvation
    Study

    n: not reported in source

    NIT-1 beta-cells
    Outcome group
    Cell viability and death · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Humanin reduced apoptosis induced by serum starvation in NIT-1 cells and decreased apoptosis induced by cytokine treatment.
    1 context sentence
    Summary · context
    We investigated whether Humanin, a recently described survival factor for neurons, could improve the survival of beta-cells and delay or treat diabetes in the nonobese diabetic (NOD) model.
  5. 05LabIn vitro (cells)Efficacy outcome

    In NIT-1 beta-cells, humanin decreased apoptosis induced by cytokine treatment.

    In plain wordsIn cells, humanin lowered the death of insulin-producing cells caused by inflammatory cytokines.

    Peptide
    Humanin
    Outcome
    DecreaseCytokine-induced apoptosis
    Study

    n: not reported in source

    NIT-1 beta-cells
    Outcome group
    Cell viability and death · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Humanin reduced apoptosis induced by serum starvation in NIT-1 cells and decreased apoptosis induced by cytokine treatment.
    1 context sentence
    Summary · context
    We investigated whether Humanin, a recently described survival factor for neurons, could improve the survival of beta-cells and delay or treat diabetes in the nonobese diabetic (NOD) model.
  6. 06LabIn vitro (cells)Mechanism

    In beta-cells, humanin induced STAT3 and ERK phosphorylation over a 24-hour time course.

    In plain wordsIn cells, humanin switched on two cell-signalling proteins, STAT3 and ERK, over 24 hours.

    Peptide
    Humanin
    Outcome
    IncreaseSTAT3 and ERK phosphorylation
    Study

    n: not reported in source

    NIT-1 beta-cells
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Humanin induced signal transducer and activator of transcription 3 and extracellular signal-regulated kinase phosphorylation over a 24-hour time course.
    1 context sentence
    Summary · context
    We investigated whether Humanin, a recently described survival factor for neurons, could improve the survival of beta-cells and delay or treat diabetes in the nonobese diabetic (NOD) model.

Studies that did not test the peptide alone1

In this study, Humanin 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 Humanin.

  1. 07LabNot a test of Humanin aloneIn vitro (cells)Mechanism

    Specific inhibition of STAT3 nullified the protective effect of humanin in beta-cells.

    In plain wordsIn cells, blocking STAT3 removed the protection that humanin gave to insulin-producing cells.

    Peptide
    Humanin
    Outcome
    DecreaseHumanin protection after STAT3 inhibition
    Study

    n: not reported in source

    NIT-1 beta-cells
    Outcome group
    Cell viability and death · Endocrine and hormones

    Source sentences

    Summary
    Specific inhibition of signal transducer and activator of transcription 3 resulted in nullifying the protective effect of Humanin.
    1 context sentence
    Summary · context
    We investigated whether Humanin, a recently described survival factor for neurons, could improve the survival of beta-cells and delay or treat diabetes in the nonobese diabetic (NOD) model.

    In this study, Humanin 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 Humanin.

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

    13 Oct 2026, 21:44 UTC

    Study results updated

  2. Version 1

    13 Oct 2026, 16:31 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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