Skip to content

Study · In vitro (cells) · 2018

3 results

GLP-1 receptor agonists stimulate ANGPTL8 production through the PI3K/Akt pathway in a GLP-1 receptor-dependent manner.

Liu J, Yang K, Xiao W, Le Y, Lang S, Zhang J, Wei R, Yang J, Hong T

Peptides9 Jul 2018Cited by 18 (Europe PMC)

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 study3

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

  1. 01LabIn vitro (cells)Mechanism

    In HepG2 liver cells, liraglutide dose-dependently increased ANGPTL8 expression.

    In plain wordsIn lab-grown human liver cells, liraglutide raised ANGPTL8 production in a dose-dependent way.

    Outcome
    IncreaseANGPTL8 expression in HepG2 cells
    Study

    humann: not reported in source

    HepG2 human liver cell line
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated · 24 hAs given in this study (human).

    Source sentences

    Summary
    exendin-4 or liraglutide dose-dependently upregulated the level of ANGPTL8 expression and secretion in HepG2 cells
    1 context sentence
    Summary · context
    Human liver cell line HepG2 cells were incubated for 24 h with either exendin-4 (a native form of exenatide) or liraglutide in the presence or absence of GLP-1R antagonist exendin (9-39) and PI3K inhibitor LY294002.
  2. 02LabIn vitro (cells)Mechanism

    In HepG2 liver cells, liraglutide dose-dependently increased ANGPTL8 secretion.

    In plain wordsIn lab-grown human liver cells, liraglutide raised ANGPTL8 release in a dose-dependent way.

    Outcome
    IncreaseANGPTL8 secretion in HepG2 cells
    Study

    humann: not reported in source

    HepG2 human liver cell line
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated · 24 hAs given in this study (human).

    Source sentences

    Summary
    exendin-4 or liraglutide dose-dependently upregulated the level of ANGPTL8 expression and secretion in HepG2 cells
    1 context sentence
    Summary · context
    Human liver cell line HepG2 cells were incubated for 24 h with either exendin-4 (a native form of exenatide) or liraglutide in the presence or absence of GLP-1R antagonist exendin (9-39) and PI3K inhibitor LY294002.
  3. 03LabIn vitro (cells)Mechanism

    In HepG2 liver cells, adding exendin (9-39) and LY294002 eliminated the ANGPTL8 upregulation seen with liraglutide.

    In plain wordsIn lab-grown human liver cells, blocking the GLP-1 receptor or PI3K pathway stopped liraglutide from raising ANGPTL8.

    Outcome
    No significant changeANGPTL8 upregulation with GLP-1R antagonist exendin (9-39) and PI3K inhibitor LY294002
    Study

    humann: not reported in source

    HepG2 human liver cell line
    Comparator
    Liraglutide without exendin (9-39) and LY294002
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated · 24 hAs given in this study (human).

    Source sentences

    Summary
    which was eliminated by adding exendin (9-39) and LY294002.
    1 context sentence
    Summary · context
    Human liver cell line HepG2 cells were incubated for 24 h with either exendin-4 (a native form of exenatide) or liraglutide in the presence or absence of GLP-1R antagonist exendin (9-39) and PI3K inhibitor LY294002.

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

    12 Oct 2026, 12:10 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:05 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.