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Study · Animal study (in vivo) · zebrafish · 2021

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Depletion of Alpha-Melanocyte-Stimulating Hormone Induces Insatiable Appetite and Gains in Energy Reserves and Body Weight in Zebrafish.

Hsieh YW, Tsai YW, Lai HH, Lai CY, Lin CY, Her GM

Biomedicines2 Aug 2021Cited by 12 (Europe PMC)

PMID34440144 (opens in a new tab)PMCIDPMC8392443 (opens in a new tab)DOI10.3390/biomedicines9080941 (opens in a new tab)PepBankPUB-34440144
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Summary

The functions of anorexigenic neurons secreting proopiomelanocortin (POMC)/alpha-melanocyte-stimulating hormone (α-MSH) of the melanocortin system in the hypothalamus in vertebrates are energy homeostasis, food intake, and body weight regulation. However, the mechanisms remain elusive. This article reports on zebrafish that have been genetically engineered to produce α-MSH mutants, α-MSH-7aa and α-MSH-8aa, selectively lacking 7 and 8 amino acids within the α-MSH region, but retaining most of the other normal melanocortin-signaling (Pomc-derived) peptides. The α-MSH mutants exhibited hyperphagic phenotypes leading to body weight gain, as observed in human patients and mammalian models. The actions of several genes regulating appetite in zebrafish are similar to those in mammals when analyzed using gene expression analysis. These include four selected orexigenic genes: Promelanin-concentrating hormone (pmch), agouti-related protein 2 (agrp2), neuropeptide Y (npy), and hypothalamic hypocretin/orexin (hcrt). We also study five selected anorexigenic genes: Brain-derived neurotrophic factor (bdnf), single-minded homolog 1-a (sim1a), corticotropin-releasing hormone b (crhb), thyrotropin-releasing hormone (trh), and prohormone convertase 2 (pcsk2). The orexigenic actions of α-MSH mutants are rescued completely after hindbrain ventricle injection with a synthetic analog of α-MSH and a melanocortin receptor agonist, Melanotan II. We evaluate the adverse effects of MSH depletion on energy balance using the Alamar Blue metabolic rate assay. Our results show that α-MSH is a key regulator of POMC signaling in appetite regulation and energy expenditure, suggesting that it might be a potential therapeutic target for treating human obesity.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In alpha-MSH mutant zebrafish, hindbrain ventricle injection of melanotan II completely rescued the orexigenic actions of the mutants.

    In plain wordsIn zebrafish lacking part of alpha-MSH, melanotan II injected into the hindbrain fully reversed their increased drive to eat.

    Peptide
    Melanotan II
    Outcome
    DecreaseOrexigenic (hyperphagic) action of alpha-MSH mutants
    Study

    zebrafishn: not reported in source

    alpha-MSH mutant zebrafish (alpha-MSH -7aa and -8aa)
    Outcome group
    Appetite and food intake · Metabolic and weight
    Studied dose
    Dose not stated · hindbrain ventricle injectionAs given in this study (zebrafish).

    Source sentences

    Summary
    The orexigenic actions of α-MSH mutants are rescued completely after hindbrain ventricle injection with a synthetic analog of α-MSH and a melanocortin receptor agonist, Melanotan II.
    1 context sentence
    Summary · context
    This article reports on zebrafish that have been genetically engineered to produce α-MSH mutants, α-MSH-7aa and α-MSH-8aa, selectively lacking 7 and 8 amino acids within the α-MSH region, but retaining most of the other normal melanocortin-signaling (Pomc-derived) peptides.

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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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