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Study · Animal study (in vivo) · mouse · 2006

4 results

Sim1 haploinsufficiency impairs melanocortin-mediated anorexia and activation of paraventricular nucleus neurons.

Kublaoui BM, Holder JL Jr, Gemelli T, Zinn AR

Molecular endocrinology (Baltimore, Md.)25 May 2006Cited by 90 (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 study4

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In Sim1 heterozygous mice, MTII suppressed feeding to a blunted degree.

    In plain wordsIn mice with one working copy of the Sim1 gene, Melanotan II reduced eating less strongly than it did in normal mice.

    Outcome
    DecreaseMTII-induced suppression of feeding in Sim1 heterozygous mice
    Study

    mousen: not reported in source

    Sim1 heterozygous and wild-type mice
    Comparator
    Wild-type mice
    Outcome group
    Appetite and food intake · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In response to the melanocortin agonist melanotan-2 (MTII) they exhibit a blunted suppression of feeding
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In Sim1 heterozygous mice, MTII increased energy expenditure normally.

    In plain wordsIn mice with one working copy of the Sim1 gene, Melanotan II raised energy use as usual.

    Outcome
    IncreaseMTII-induced energy expenditure in Sim1 heterozygous mice
    Study

    mousen: not reported in source

    Sim1 heterozygous and wild-type mice
    Comparator
    Wild-type mice
    Outcome group
    Energy expenditure and thermogenesis · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    yet increase their energy expenditure normally.
  3. 03AnimalAnimal study (in vivo)Mechanism

    Sim1 heterozygous mice failed to activate paraventricular nucleus neurons in response to MTII at a dose that induced robust c-Fos expression in wild-type mice.

    In plain wordsIn mice with one working copy of the Sim1 gene, Melanotan II did not switch on brain cells that it activated in normal mice.

    Outcome
    No significant changeMTII-induced c-Fos activation of PVN neurons in Sim1 heterozygous mice
    Study

    mousen: not reported in source

    Sim1 heterozygous and wild-type mice
    Comparator
    Wild-type mice
    Outcome group
    Brain and neuronal activity · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    They also fail to activate PVN neurons in response to the drug at a dose that induces robust c-Fos expression in a subset of Sim1 PVN neurons in wild-type mice.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In mice, MTII treatment induced hypothalamic Sim1 gene expression.

    In plain wordsIn mice, Melanotan II raised activity of the Sim1 gene in the hypothalamus.

    Outcome
    IncreaseHypothalamic Sim1 gene expression
    Study

    mousen: not reported in source

    Outcome group
    Brain and neuronal activity · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Hypothalamic Sim1 gene expression is induced by leptin and MTII treatment.

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

    9 Oct 2026, 18:17 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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