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Study · Animal study (in vivo) · mouse · 2015

10 results

Nonerythropoietic Erythropoietin-Derived Peptide Suppresses Adipogenesis, Inflammation, Obesity and Insulin Resistance.

Liu Y, Luo B, Shi R, Wang J, Liu Z, Liu W, Wang S, Zhang Z

Scientific reports13 Oct 2015Cited by 26 (Europe PMC)

Summary

Erythropoietin (EPO) has been identified as being crucial for obesity modulation; however, its erythropoietic activity may limit its clinical application. EPO-derived Helix B-surface peptide (pHBSP) is nonerythrogenic but has been reported to retain other functions of EPO. The current study aimed to evaluate the effects and potential mechanisms of pHBSP in obesity modulation. We found that pHBSP suppressed adipogenesis, adipokine expression and peroxisome proliferator-activated receptor γ (PPARγ) levels during 3T3-L1 preadipocyte maturation through the EPO receptor (EPOR). In addition, also through EPOR, pHBSP attenuated macrophage inflammatory activation and promoted PPARγ expression. Furthermore, PPARγ deficiency partly ablated the anti-inflammatory activity of pHBSP in macrophages. Correspondingly, pHBSP administration to high-fat diet (HFD)-fed mice significantly improved obesity, insulin resistance (IR) and adipose tissue inflammation without stimulating hematopoiesis. Therefore, pHBSP can significantly protect against obesity and IR partly by inhibiting adipogenesis and inflammation. These findings have therapeutic implications for metabolic disorders, such as obesity and diabetes.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study10

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In high-fat diet-fed mice, pHBSP administration significantly improved obesity.

    In plain wordsIn mice fed a high-fat diet, pHBSP improved obesity.

    Outcome
    DecreaseObesity in HFD-fed mice
    Study

    mousen: not reported in source

    high-fat diet-fed mice
    Outcome group
    Body weight · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Correspondingly, pHBSP administration to high-fat diet (HFD)-fed mice significantly improved obesity, insulin resistance (IR) and adipose tissue inflammation without stimulating hematopoiesis.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In high-fat diet-fed mice, pHBSP administration significantly improved insulin resistance.

    In plain wordsIn mice fed a high-fat diet, pHBSP improved insulin resistance.

    Outcome
    DecreaseInsulin resistance in HFD-fed mice
    Study

    mousen: not reported in source

    high-fat diet-fed mice
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Correspondingly, pHBSP administration to high-fat diet (HFD)-fed mice significantly improved obesity, insulin resistance (IR) and adipose tissue inflammation without stimulating hematopoiesis.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In high-fat diet-fed mice, pHBSP administration significantly improved adipose tissue inflammation.

    In plain wordsIn mice fed a high-fat diet, pHBSP reduced inflammation in fat tissue.

    Outcome
    DecreaseAdipose tissue inflammation in HFD-fed mice
    Study

    mousen: not reported in source

    high-fat diet-fed mice
    Outcome group
    Inflammation markers · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Correspondingly, pHBSP administration to high-fat diet (HFD)-fed mice significantly improved obesity, insulin resistance (IR) and adipose tissue inflammation without stimulating hematopoiesis.
  4. 04AnimalAnimal study (in vivo)Safety outcome

    In high-fat diet-fed mice, pHBSP improved obesity, insulin resistance and adipose inflammation without stimulating hematopoiesis.

    In plain wordsIn mice fed a high-fat diet, pHBSP did not stimulate blood cell production.

    Outcome
    No significant changeHematopoiesis in HFD-fed mice
    Study

    mousen: not reported in source

    high-fat diet-fed mice
    Outcome group
    Adverse events · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    without stimulating hematopoiesis.
    1 context sentence
    Summary · context
    Correspondingly, pHBSP administration to high-fat diet (HFD)-fed mice significantly improved obesity, insulin resistance (IR) and adipose tissue inflammation without stimulating hematopoiesis.
  5. 05LabIn vitro (cells)Efficacy outcome

    In 3T3-L1 preadipocytes, pHBSP suppressed adipogenesis during maturation through the EPO receptor.

    In plain wordsIn fat precursor cells in lab tests, pHBSP reduced fat cell formation.

    Outcome
    DecreaseAdipogenesis in 3T3-L1 preadipocytes (via EPOR)
    Study

    n: not reported in source

    3T3-L1 preadipocytes
    Outcome group
    Body weight · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found that pHBSP suppressed adipogenesis, adipokine expression and peroxisome proliferator-activated receptor γ (PPARγ) levels during 3T3-L1 preadipocyte maturation through the EPO receptor (EPOR).
  6. 06LabIn vitro (cells)Efficacy outcome

    In 3T3-L1 preadipocytes, pHBSP suppressed adipokine expression during maturation through the EPO receptor.

    In plain wordsIn fat precursor cells in lab tests, pHBSP lowered the output of fat-cell signal proteins.

    Outcome
    DecreaseAdipokine expression in 3T3-L1 preadipocytes
    Study

    n: not reported in source

    3T3-L1 preadipocytes
    Outcome group
    Inflammation markers · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found that pHBSP suppressed adipogenesis, adipokine expression and peroxisome proliferator-activated receptor γ (PPARγ) levels during 3T3-L1 preadipocyte maturation through the EPO receptor (EPOR).
  7. 07LabIn vitro (cells)Efficacy outcome

    In 3T3-L1 preadipocytes, pHBSP suppressed PPARγ levels during maturation through the EPO receptor.

    In plain wordsIn fat precursor cells in lab tests, pHBSP lowered PPARγ, a fat-cell growth regulator.

    Outcome
    DecreasePPARγ levels in 3T3-L1 preadipocytes
    Study

    n: not reported in source

    3T3-L1 preadipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found that pHBSP suppressed adipogenesis, adipokine expression and peroxisome proliferator-activated receptor γ (PPARγ) levels during 3T3-L1 preadipocyte maturation through the EPO receptor (EPOR).
  8. 08LabIn vitro (cells)Efficacy outcome

    In macrophages, pHBSP attenuated inflammatory activation through the EPO receptor.

    In plain wordsIn immune cells in lab tests, pHBSP reduced inflammatory activation.

    Outcome
    DecreaseMacrophage inflammatory activation
    Study

    n: not reported in source

    macrophages
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, also through EPOR, pHBSP attenuated macrophage inflammatory activation and promoted PPARγ expression.
  9. 09LabIn vitro (cells)Efficacy outcome

    In macrophages, pHBSP promoted PPARγ expression through the EPO receptor.

    In plain wordsIn immune cells in lab tests, pHBSP raised PPARγ expression.

    Outcome
    IncreasePPARγ expression in macrophages
    Study

    n: not reported in source

    macrophages
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, also through EPOR, pHBSP attenuated macrophage inflammatory activation and promoted PPARγ expression.
  10. 10LabIn vitro (cells)Mechanism

    In macrophages, PPARγ deficiency partly ablated the anti-inflammatory activity of pHBSP.

    In plain wordsIn immune cells in lab tests, removing PPARγ partly stopped pHBSP from reducing inflammation.

    Outcome
    Not applicablePPARγ dependence of anti-inflammatory activity
    Study

    n: not reported in source

    macrophages
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, PPARγ deficiency partly ablated the anti-inflammatory activity of pHBSP in macrophages.

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

    9 Oct 2026, 19:08 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:13 UTC

    First added · source update from Europe PMC

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