LIM-homeodomain transcription factor Isl-1 mediates kisspeptin's effect on insulin secretion in mice.

Chen J, Fu R, Cui Y, Pan J, Li Y, Zhang X, Evans SM, Cui S, Liu J

Molecular endocrinology (Baltimore, Md.)23 Jun 2014Cited by 12 (Europe PMC)

PMID24956377PMCIDPMC5414806DOI10.1210/me.2013-1410PepBankPUB-24956377

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

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

01AnimalAnimal study (in vivo)Mechanism
In mice, kisspeptin‑54 inhibited Isl-1 expression in vivo.
In plain wordsIn mice, kisspeptin‑54 lowered Isl-1, a protein found in insulin-making cells.
Peptide
Kisspeptin-54 (metastin)
Outcome
DecreaseIsl-1 expression
Study
mousen: not reported in source
mice in vivo
Outcome group
Receptor activity and mechanism · Endocrine and hormones
Studied dose
Dose not stated
Source sentences
Summary
Both in vitro and in vivo results demonstrate that kisspeptin-54 (KISS-54) inhibits Isl-1 expression and insulin secretion and both the in vivo and in vitro effects of KISS-54 on insulin gene expression and secretion are abolished when an Isl-1-inducible knockout model is used.
1 context sentence(design, population, supporting numbers)
Summary · context
Our results demonstrate that Isl-1 and GPR54 are coexpressed in mouse pancreatic islet β-cells and NIT cells.
Report a problemFND-2495637701
02AnimalAnimal study (in vivo)Efficacy outcome
In mice, kisspeptin‑54 inhibited insulin secretion in vivo.
In plain wordsIn mice, kisspeptin‑54 reduced insulin release.
Peptide
Kisspeptin-54 (metastin)
Outcome
DecreaseInsulin secretion
Study
mousen: not reported in source
mice in vivo
Outcome group
Glycemic control · Endocrine and hormones
Studied dose
Dose not stated
Source sentences
Summary
Both in vitro and in vivo results demonstrate that kisspeptin-54 (KISS-54) inhibits Isl-1 expression and insulin secretion and both the in vivo and in vitro effects of KISS-54 on insulin gene expression and secretion are abolished when an Isl-1-inducible knockout model is used.
1 context sentence(design, population, supporting numbers)
Summary · context
Our results demonstrate that Isl-1 and GPR54 are coexpressed in mouse pancreatic islet β-cells and NIT cells.
Report a problemFND-2495637702
03LabIn vitro (cells)Mechanism
In mouse islet and NIT cells, kisspeptin‑54 inhibited Isl-1 expression in vitro.
In plain wordsIn cells, kisspeptin‑54 lowered Isl-1, a protein found in insulin-making cells.
Peptide
Kisspeptin-54 (metastin)
Outcome
DecreaseIsl-1 expression
Study
mousen: not reported in source
NIT cells and mouse pancreatic islet cells
Outcome group
Receptor activity and mechanism · Endocrine and hormones
Studied dose
Dose not stated
Source sentences
Summary
Both in vitro and in vivo results demonstrate that kisspeptin-54 (KISS-54) inhibits Isl-1 expression and insulin secretion and both the in vivo and in vitro effects of KISS-54 on insulin gene expression and secretion are abolished when an Isl-1-inducible knockout model is used.
1 context sentence(design, population, supporting numbers)
Summary · context
Our results demonstrate that Isl-1 and GPR54 are coexpressed in mouse pancreatic islet β-cells and NIT cells.
Report a problemFND-2495637703
04LabIn vitro (cells)Efficacy outcome
In mouse islet and NIT cells, kisspeptin‑54 inhibited insulin secretion in vitro.
In plain wordsIn cells, kisspeptin‑54 reduced insulin release.
Peptide
Kisspeptin-54 (metastin)
Outcome
DecreaseInsulin secretion
Study
mousen: not reported in source
NIT cells and mouse pancreatic islet cells
Outcome group
Glycemic control · Endocrine and hormones
Studied dose
Dose not stated
Source sentences
Summary
Both in vitro and in vivo results demonstrate that kisspeptin-54 (KISS-54) inhibits Isl-1 expression and insulin secretion and both the in vivo and in vitro effects of KISS-54 on insulin gene expression and secretion are abolished when an Isl-1-inducible knockout model is used.
1 context sentence(design, population, supporting numbers)
Summary · context
Our results demonstrate that Isl-1 and GPR54 are coexpressed in mouse pancreatic islet β-cells and NIT cells.
Report a problemFND-2495637704
05LabIn vitro (cells)Mechanism
The direct action of kisspeptin‑54 on insulin secretion was mediated by Isl-1.
In plain wordsIn mouse cells, kisspeptin‑54 acted on insulin release through Isl-1.
Peptide
Kisspeptin-54 (metastin)
Outcome
Not applicableIsl-1 mediation of direct KISS-54 action on insulin secretion
Study
mousen: not reported in source
mouse islet and NIT cells
Outcome group
Receptor activity and mechanism · Endocrine and hormones
Studied dose
Dose not stated
Source sentences
Summary
Moreover, our results demonstrate that the direct action of KISS-54 on insulin secretion is mediated by Isl-1.
1 context sentence(design, population, supporting numbers)
Summary · context
Our results demonstrate that Isl-1 and GPR54 are coexpressed in mouse pancreatic islet β-cells and NIT cells.
Report a problemFND-2495637706
06LabIn vitro (cells)Mechanism
Kisspeptin‑54 influenced Isl-1 expression and insulin secretion through the protein kinase C-ERK1/2 pathway.
In plain wordsIn mouse cells, kisspeptin‑54 changed Isl-1 and insulin release through the protein kinase C-ERK1/2 pathway.
Peptide
Kisspeptin-54 (metastin)
Outcome
Not applicableProtein kinase C-ERK1/2 pathway mediating KISS-54 effect on Isl-1 and insulin secretion
Study
mousen: not reported in source
mouse islet and NIT cells
Outcome group
Receptor activity and mechanism · Endocrine and hormones
Studied dose
Dose not stated
Source sentences
Summary
Our results further show that KISS-54 influences Isl-1 expression and insulin secretion through the protein kinase C-ERK1/2 pathway.
1 context sentence(design, population, supporting numbers)
Summary · context
Our results demonstrate that Isl-1 and GPR54 are coexpressed in mouse pancreatic islet β-cells and NIT cells.
Report a problemFND-2495637707

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

07LabEndogenous levelIn vitro (cells)Mechanism
Insulin regulated kisspeptin expression and secretion through a Janus kinase-phosphatidylinositol 3-kinase pathway feedback loop.
In plain wordsIn mouse cells, insulin affected the body's own kisspeptin through a feedback loop.
Peptide
Kisspeptin-54 (metastin)
Outcome
Direction not reportedInsulin feedback on kisspeptin expression and secretion
Study
mousen: not reported in source
mouse islet and NIT cells
Outcome group
Receptor activity and mechanism · Endocrine and hormones
Source sentences
Summary
Conversely, insulin has a feedback loop via the Janus kinase-phosphatidylinositol 3-kinase pathway regulating kisspeptin expression and secretion.
This result measures the body's own Kisspeptin-54 (metastin). Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-2495637709

Studies that did not test the peptide alone2

In this study, Kisspeptin-54 (metastin) 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 Kisspeptin-54 (metastin).

08AnimalNot a test of Kisspeptin-54 (metastin) aloneAnimal study (in vivo)Mechanism
In an Isl-1 inducible knockout model, the in vivo and in vitro effects of kisspeptin‑54 on insulin gene expression and secretion were abolished.
In plain wordsIn mice and cells lacking Isl-1, the effects of kisspeptin‑54 on insulin were no longer seen.
Peptide
Kisspeptin-54 (metastin)
Outcome
Not applicableKISS-54 effect on insulin gene expression and secretion in Isl-1 knockout
Study
mousen: not reported in source
Isl-1 inducible knockout mice and cells
Outcome group
Glycemic control · Endocrine and hormones
Source sentences
Summary
Both in vitro and in vivo results demonstrate that kisspeptin-54 (KISS-54) inhibits Isl-1 expression and insulin secretion and both the in vivo and in vitro effects of KISS-54 on insulin gene expression and secretion are abolished when an Isl-1-inducible knockout model is used.
1 context sentence(design, population, supporting numbers)
Summary · context
Our results demonstrate that Isl-1 and GPR54 are coexpressed in mouse pancreatic islet β-cells and NIT cells.
In this study, Kisspeptin-54 (metastin) 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 Kisspeptin-54 (metastin).
Report a problemFND-2495637705
09LabNot a test of Kisspeptin-54 (metastin) aloneIn vitro (cells)Mechanism
Isl-1 and GPR54 were coexpressed in mouse pancreatic islet beta-cells and NIT cells.
In plain wordsIn mouse cells, Isl-1 and the kisspeptin receptor GPR54 were found in the same insulin-making cells.
Peptide
Kisspeptin-54 (metastin)
Outcome
Not applicableIsl-1 and GPR54 coexpression
Study
mousen: not reported in source
mouse islet and NIT cells
Outcome group
Receptor activity and mechanism · Endocrine and hormones
Source sentences
Summary
Our results demonstrate that Isl-1 and GPR54 are coexpressed in mouse pancreatic islet β-cells and NIT cells.
In this study, Kisspeptin-54 (metastin) 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 Kisspeptin-54 (metastin).
Report a problemFND-2495637708

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 2Current
13 Oct 2026, 21:44 UTC
Study results updated
Version 1
13 Oct 2026, 16:31 UTC
First added · source update from Europe PMC

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