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Study · Not a test of the peptide alone · 2018

3 results

The stimulatory G protein Gsα is required in melanocortin 4 receptor-expressing cells for normal energy balance, thermogenesis, and glucose metabolism.

Podyma B, Sun H, Wilson EA, Carlson B, Pritikin E, Gavrilova O, Weinstein LS, Chen M

The Journal of biological chemistry24 May 2018Cited by 38 (Europe PMC)

PMID29794140 (opens in a new tab)PMCIDPMC6052205 (opens in a new tab)DOI10.1074/jbc.ra118.003450 (opens in a new tab)PepBankPUB-29794140
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Summary

Central melanocortin 4 receptors (MC4Rs) stimulate energy expenditure and inhibit food intake. MC4Rs activate the G protein Gsα, but whether Gsα mediates all MC4R actions has not been established. Individuals with Albright hereditary osteodystrophy (AHO), who have heterozygous Gsα-inactivating mutations, only develop obesity when the Gsα mutation is present on the maternal allele because of tissue-specific genomic imprinting. Furthermore, evidence in mice implicates Gsα imprinting within the central nervous system (CNS) in this disorder. In this study, we examined the effects of Gsα in MC4R-expressing cells on metabolic regulation. Mice with homozygous Gsα deficiency in MC4R-expressing cells (MC4RGsKO) developed significant obesity with increased food intake and decreased energy expenditure, along with impaired insulin sensitivity and cold-induced thermogenesis. Moreover, the ability of the MC4R agonist melanotan-II (MTII) to stimulate energy expenditure and to inhibit food intake was impaired in MC4RGsKO mice. MTII failed to stimulate the secretion of the anorexigenic hormone peptide YY (PYY) from enteroendocrine L cells, a physiological response mediated by MC4R-Gsα signaling, even though baseline PYY levels were elevated in these mice. In Gsα heterozygotes, mild obesity and reduced energy expenditure were present only in mice with a Gsα deletion on the maternal allele in MC4R-expressing cells, whereas food intake was unaffected. These results demonstrate that Gsα signaling in MC4R-expressing cells is required for controlling energy balance, thermogenesis, and peripheral glucose metabolism. They further indicate that Gsα imprinting in MC4R-expressing cells contributes to obesity in Gsα knockout mice and probably in individuals with Albright hereditary osteodystrophy as well.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone3

In this study, Melanotan II 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 Melanotan II.

  1. 01AnimalNot a test of Melanotan II aloneAnimal study (in vivo)Efficacy outcome

    In mice lacking Gs-alpha in MC4R-expressing cells, the ability of MTII to stimulate energy expenditure was impaired.

    In plain wordsIn mice lacking this protein in MC4R cells, MTII was less able to raise energy use.

    Peptide
    Melanotan II
    Outcome
    DecreaseMTII-stimulated energy expenditure in MC4RGsKO mice
    Study

    mousen: not reported in source

    MC4RGsKO mice (Gs-alpha deficiency in MC4R-expressing cells)
    Outcome group
    Energy expenditure and thermogenesis · Metabolic and weight

    Source sentences

    Summary
    Moreover, the ability of the MC4R agonist melanotan-II (MTII) to stimulate energy expenditure and to inhibit food intake was impaired in MC4RGsKO mice.

    In this study, Melanotan II 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 Melanotan II.

  2. 02AnimalNot a test of Melanotan II aloneAnimal study (in vivo)Efficacy outcome

    In mice lacking Gs-alpha in MC4R-expressing cells, the ability of MTII to inhibit food intake was impaired.

    In plain wordsIn mice lacking this protein in MC4R cells, MTII was less able to lower food intake.

    Peptide
    Melanotan II
    Outcome
    DecreaseMTII-inhibited food intake in MC4RGsKO mice
    Study

    mousen: not reported in source

    MC4RGsKO mice (Gs-alpha deficiency in MC4R-expressing cells)
    Outcome group
    Appetite and food intake · Metabolic and weight

    Source sentences

    Summary
    Moreover, the ability of the MC4R agonist melanotan-II (MTII) to stimulate energy expenditure and to inhibit food intake was impaired in MC4RGsKO mice.

    In this study, Melanotan II 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 Melanotan II.

  3. 03AnimalNot a test of Melanotan II aloneAnimal study (in vivo)Efficacy outcome

    In MC4RGsKO mice, MTII failed to stimulate secretion of peptide YY from enteroendocrine L cells, although baseline PYY levels were elevated.

    In plain wordsIn mice lacking this protein in MC4R cells, MTII did not trigger release of the appetite hormone PYY.

    Peptide
    Melanotan II
    Outcome
    DecreaseMTII-stimulated PYY secretion in MC4RGsKO mice
    Study

    mousen: not reported in source

    MC4RGsKO mice (Gs-alpha deficiency in MC4R-expressing cells)
    Outcome group
    Hormone levels · Endocrine and hormones

    Source sentences

    Summary
    MTII failed to stimulate the secretion of the anorexigenic hormone peptide YY (PYY) from enteroendocrine L cells, a physiological response mediated by MC4R-Gsα signaling, even though baseline PYY levels were elevated in these mice.

    In this study, Melanotan II 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 Melanotan II.

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

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