Lysine-proline-valine peptide attenuates hepatic lipid accumulation through ROS-dependent regulation of the PPARγ pathway in HepG2 cells.

Lee JY, Lee J, Jung WK, Je JY, Lee SJ

Cytotechnology28 Apr 2026

PMID42064835DOI10.1007/s10616-026-00967-zPepBankPUB-42064835

Publisher page PubMedAsk about this study

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 study8

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

01LabIn vitro (cells)Activity measurement
In HepG2 cells, KPV at 100 µg/mL significantly attenuated oleic acid-induced lipid accumulation.
In plain wordsIn lab tests on liver cells, KPV reduced fat build-up caused by oleic acid.
Peptide
KPV
Outcome
DecreaseOleic acid-induced lipid accumulation
Study
n: not reported in source
HepG2 cells
Comparator
OA-treated cells
Outcome group
Liver fat and liver function · Liver
Studied dose
100 µg/mLAs given in this study.
Source sentences
Summary
Treatment with KPV (100 µg/mL) significantly attenuated OA-induced lipid accumulation and suppressed FAS expression without inducing cytotoxicity.
1 context sentence(design, population, supporting numbers)
Summary · context
This study examined the protective role of Lysine-Proline-Valine (KPV), an endogenous tripeptide derived from α-melanocyte-stimulating hormone, against oleic acid (OA)-induced oxidative damage and lipid accumulation in hepatic epithelial HepG2 cells.
Report a problemFND-4206483501
02LabIn vitro (cells)Mechanism
In HepG2 cells, KPV at 100 µg/mL suppressed fatty acid synthase (FAS) expression.
In plain wordsIn lab tests on liver cells, KPV lowered a fat-making enzyme.
Peptide
KPV
Outcome
DecreaseFatty acid synthase expression
Study
n: not reported in source
HepG2 cells
Outcome group
Fat metabolism and adipogenesis · Liver
Studied dose
100 µg/mLAs given in this study.
Source sentences
Summary
Treatment with KPV (100 µg/mL) significantly attenuated OA-induced lipid accumulation and suppressed FAS expression without inducing cytotoxicity.
1 context sentence(design, population, supporting numbers)
Summary · context
This study examined the protective role of Lysine-Proline-Valine (KPV), an endogenous tripeptide derived from α-melanocyte-stimulating hormone, against oleic acid (OA)-induced oxidative damage and lipid accumulation in hepatic epithelial HepG2 cells.
Report a problemFND-4206483502
03LabIn vitro (cells)Safety outcome
In HepG2 cells, KPV at 100 µg/mL did not induce cytotoxicity.
In plain wordsIn lab tests on liver cells, KPV did not harm the cells.
Peptide
KPV
Outcome
No significant changeCytotoxicity
Study
n: not reported in source
HepG2 cells
Outcome group
Cell viability and death · Liver
Studied dose
100 µg/mLAs given in this study.
Source sentences
Summary
Treatment with KPV (100 µg/mL) significantly attenuated OA-induced lipid accumulation and suppressed FAS expression without inducing cytotoxicity.
1 context sentence(design, population, supporting numbers)
Summary · context
This study examined the protective role of Lysine-Proline-Valine (KPV), an endogenous tripeptide derived from α-melanocyte-stimulating hormone, against oleic acid (OA)-induced oxidative damage and lipid accumulation in hepatic epithelial HepG2 cells.
Report a problemFND-4206483503
04LabIn vitro (cells)Mechanism
In HepG2 cells under lipid load, KPV reduced reactive oxygen species generation.
In plain wordsIn lab tests on liver cells, KPV lowered production of reactive oxygen species.
Peptide
KPV
Outcome
DecreaseReactive oxygen species generation
Study
n: not reported in source
HepG2 cells
Outcome group
Fat metabolism and adipogenesis · Liver
Studied dose
Dose not stated
Source sentences
Summary
Mechanistic analysis revealed that KPV reduced reactive oxygen species generation, thereby preventing activation of extracellular signal-regulated kinase.
1 context sentence(design, population, supporting numbers)
Summary · context
This study examined the protective role of Lysine-Proline-Valine (KPV), an endogenous tripeptide derived from α-melanocyte-stimulating hormone, against oleic acid (OA)-induced oxidative damage and lipid accumulation in hepatic epithelial HepG2 cells.
Report a problemFND-4206483504
05LabIn vitro (cells)Mechanism
In HepG2 cells, KPV prevented activation of extracellular signal-regulated kinase by reducing reactive oxygen species.
In plain wordsIn lab tests on liver cells, KPV blocked activation of the ERK signal.
Peptide
KPV
Outcome
DecreaseERK activation
Study
n: not reported in source
HepG2 cells
Outcome group
Fat metabolism and adipogenesis · Liver
Studied dose
Dose not stated
Source sentences
Summary
Mechanistic analysis revealed that KPV reduced reactive oxygen species generation, thereby preventing activation of extracellular signal-regulated kinase.
1 context sentence(design, population, supporting numbers)
Summary · context
This study examined the protective role of Lysine-Proline-Valine (KPV), an endogenous tripeptide derived from α-melanocyte-stimulating hormone, against oleic acid (OA)-induced oxidative damage and lipid accumulation in hepatic epithelial HepG2 cells.
Report a problemFND-4206483505
06LabIn vitro (cells)Mechanism
In HepG2 cells under hepatic steatosis conditions, KPV downregulated AKT phosphorylation.
In plain wordsIn lab tests on liver cells, KPV lowered AKT phosphorylation.
Peptide
KPV
Outcome
DecreaseAKT phosphorylation
Study
n: not reported in source
HepG2 cells
Outcome group
Fat metabolism and adipogenesis · Liver
Studied dose
Dose not stated
Source sentences
Summary
KPV also downregulated AKT phosphorylation, leading to inhibition of mTORC1 phosphorylation under hepatic steatosis conditions.
1 context sentence(design, population, supporting numbers)
Summary · context
This study examined the protective role of Lysine-Proline-Valine (KPV), an endogenous tripeptide derived from α-melanocyte-stimulating hormone, against oleic acid (OA)-induced oxidative damage and lipid accumulation in hepatic epithelial HepG2 cells.
Report a problemFND-4206483506
07LabIn vitro (cells)Mechanism
In HepG2 cells under hepatic steatosis conditions, KPV led to inhibition of mTORC1 phosphorylation.
In plain wordsIn lab tests on liver cells, KPV lowered mTORC1 phosphorylation.
Peptide
KPV
Outcome
DecreasemTORC1 phosphorylation
Study
n: not reported in source
HepG2 cells
Outcome group
Fat metabolism and adipogenesis · Liver
Studied dose
Dose not stated
Source sentences
Summary
KPV also downregulated AKT phosphorylation, leading to inhibition of mTORC1 phosphorylation under hepatic steatosis conditions.
1 context sentence(design, population, supporting numbers)
Summary · context
This study examined the protective role of Lysine-Proline-Valine (KPV), an endogenous tripeptide derived from α-melanocyte-stimulating hormone, against oleic acid (OA)-induced oxidative damage and lipid accumulation in hepatic epithelial HepG2 cells.
Report a problemFND-4206483507
08LabIn vitro (cells)Mechanism
In HepG2 cells, KPV regulated phosphorylation of PPARγ; the abstract does not give the direction.
In plain wordsIn lab tests on liver cells, KPV changed phosphorylation of the PPARγ protein.
Peptide
KPV
Outcome
Direction not reportedPPARγ phosphorylation
Study
n: not reported in source
HepG2 cells
Outcome group
Fat metabolism and adipogenesis · Liver
Studied dose
Dose not stated
Source sentences
Summary
Furthermore, KPV regulated the phosphorylation of peroxisome proliferator-activated receptor gamma, a key transcription factor in de novo lipogenesis, thereby normalizing FAS expression.
1 context sentence(design, population, supporting numbers)
Summary · context
This study examined the protective role of Lysine-Proline-Valine (KPV), an endogenous tripeptide derived from α-melanocyte-stimulating hormone, against oleic acid (OA)-induced oxidative damage and lipid accumulation in hepatic epithelial HepG2 cells.
Report a problemFND-4206483508

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.

Version 3Current
9 Oct 2026, 18:17 UTC
Study results updated
Version 2
9 Oct 2026, 03:03 UTC
Study data updated · source update from Europe PMC
Version 1
9 Oct 2026, 02:56 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

Publication types

Journal Article

Keywords

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