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Study · In vitro (cells) · 2018

3 results

Kisspeptin Receptor GPR54 Promotes Adipocyte Differentiation and Fat Accumulation in Mice.

Wang T, Cui X, Xie L, Xing R, You P, Zhao Y, Yang Y, Xu Y, Zeng L, Chen H, Liu M

Frontiers in physiology13 Mar 2018Cited by 15 (Europe PMC)

PMID29593567 (opens in a new tab)PMCIDPMC5859022 (opens in a new tab)DOI10.3389/fphys.2018.00209 (opens in a new tab)PepBankPUB-29593567
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Summary

GPR54, Kisspeptin-1 receptor (KISS1R), a member of rhodopsin family, plays a critical role in puberty development and has been proposed to be involved in regulation of energy metabolism. This study aims to explore the function of GPR54 in adipogenesis, lipid metabolism, and obesity in addition to its effect through hormones. Results showed that when fed a high-fat diet, the weight growth of castrated or ovariectomized Gpr54-/- mice was significantly slower than that of WT control, together with a lower triglyceride concentration. The ratio of white adipose tissue was lower, and average size of adipocytes was smaller in Gpr54-/- mice. Meanwhile, there were less adipose tissue macrophages (ATMs), especially pro-inflammatory macrophages. Expression of inflammatory related genes also indicated that inflammatory response caused by obesity was not as drastic in Gpr54-/- mice as in WT mice. Liver triglyceride in Gpr54-/- mice was reduced, especially in female mice. On the other hand, oil drop formation was accelerated when hepatocytes were stimulated by kisspeptin-10 (Kp-10). Primary mesenchymal stem cells (MSCs) of Gpr54-/- mice were less likely to differentiate into adipocytes. When stimulated by Kp-10, 3T3-L1 cell differentiation into adipocytes was accelerated and triglyceride synthesis was significantly promoted. These data indicated that GPR54 could affect obesity development by promoting adipocyte differentiation and triglyceride accumulation. To further elucidate the mechanism, genes related to lipid metabolism were analyzed. The expression of genes involved in lipid synthesis including PPARγ, ACC1, ADIPO, and FAS was significantly changed in Gpr54-/- mice. Among them PPARγ which also participate in adipocyte differentiation displayed a marked reduction. Moreover, phosphorylation of ERK, which involved in GPR54 signaling, was significantly decreased in Gpr54-/- mice, suggesting that GPR54 may promote lipid synthesis and obesity development by activating MAP kinase pathway. Therefore, in addition to the involvement in hormone regulation, our study demonstrated that GPR54 directly participates in obesity development by promoting adipocyte differentiation and fat accumulation. This provided evidence of involvement of GPR54 in lipid metabolism, and revealed new potentials for the identification and development of novel drug targets for metabolic diseases.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In hepatocytes, stimulation with kisspeptin‑10 accelerated oil drop formation.

    In plain wordsIn lab-grown liver cells, kisspeptin‑10 sped up the build-up of fat droplets.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseOil drop formation in hepatocytes
    Study

    n: not reported in source

    Hepatocytes
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    On the other hand, oil drop formation was accelerated when hepatocytes were stimulated by kisspeptin-10 (Kp-10).
  2. 02LabIn vitro (cells)Efficacy outcome

    In 3T3-L1 cells, stimulation with kisspeptin‑10 accelerated differentiation into adipocytes.

    In plain wordsIn lab-grown fat precursor cells, kisspeptin‑10 sped up their change into fat cells.

    Peptide
    Kisspeptin-10
    Outcome
    Increase3T3-L1 differentiation into adipocytes
    Study

    n: not reported in source

    3T3-L1 cells
    Outcome group
    Lipids · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    When stimulated by Kp-10, 3T3-L1 cell differentiation into adipocytes was accelerated and triglyceride synthesis was significantly promoted.
  3. 03LabIn vitro (cells)Efficacy outcome

    In 3T3-L1 cells, stimulation with kisspeptin‑10 significantly promoted triglyceride synthesis.

    In plain wordsIn lab-grown fat precursor cells, kisspeptin‑10 increased the making of triglyceride fats.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseTriglyceride synthesis in 3T3-L1 cells
    Study

    n: not reported in source

    3T3-L1 cells
    Outcome group
    Lipids · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    When stimulated by Kp-10, 3T3-L1 cell differentiation into adipocytes was accelerated and triglyceride synthesis was significantly promoted.

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

    10 Oct 2026, 09:43 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:04 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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