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Study · Animal study (in vivo) · mouse · 2010

4 results

The nutritional induction of COUP-TFII gene expression in ventromedial hypothalamic neurons is mediated by the melanocortin pathway.

Sabra-Makke L, Tourrel-Cuzin C, Denis RG, Moldes M, Pégorier JP, Luquet S, Vasseur-Cognet M, Bossard P

PloS one18 Oct 2010Cited by 7 (Europe PMC)

Summary

BackgroundThe nuclear receptor chicken ovalbumin upstream promoter transcription factor II (COUP-TFII) is an important coordinator of glucose homeostasis. We report, for the first time, a unique differential regulation of its expression by the nutritional status in the mouse hypothalamus compared to peripheral tissues.Methodology/principal findingsUsing hyperinsulinemic-euglycemic clamps and insulinopenic mice, we show that insulin upregulates its expression in the hypothalamus. Immunofluorescence studies demonstrate that COUP-TFII gene expression is restricted to a subpopulation of ventromedial hypothalamic neurons expressing the melanocortin receptor. In GT1-7 hypothalamic cells, the MC4-R agonist MTII leads to a dose dependant increase of COUP-TFII gene expression secondarily to a local increase in cAMP concentrations. Transfection experiments, using a COUP-TFII promoter containing a functional cAMP responsive element, suggest a direct transcriptional activation by cAMP. Finally, we show that the fed state or intracerebroventricular injections of MTII in mice induce an increased hypothalamic COUP-TFII expression associated with a decreased hepatic and pancreatic COUP-TFII expression.Conclusions/significanceThese observations strongly suggest that hypothalamic COUP-TFII gene expression could be a central integrator of insulin and melanocortin signaling pathway within the ventromedial hypothalamus. COUP-TFII could play a crucial role in brain integration of circulating signal of hunger and satiety involved in energy balance regulation.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

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)Mechanism

    In mice, intracerebroventricular injection of MTII increased hypothalamic COUP-TFII expression.

    In plain wordsIn mice, MTII injected into the brain raised COUP-TFII gene activity in the hypothalamus.

    Outcome
    IncreaseHypothalamic COUP-TFII expression
    Study

    mousen: not reported in source

    Mice
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated · intracerebroventricularAs given in this study (mouse).

    Source sentences

    Summary
    intracerebroventricular injections of MTII in mice induce an increased hypothalamic COUP-TFII expression
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mice, intracerebroventricular injection of MTII was associated with decreased hepatic and pancreatic COUP-TFII expression.

    In plain wordsIn mice, MTII injected into the brain was linked to lower COUP-TFII gene activity in the liver and pancreas.

    Outcome
    DecreaseHepatic and pancreatic COUP-TFII expression
    Study

    mousen: not reported in source

    Mice
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated · intracerebroventricularAs given in this study (mouse).

    Source sentences

    Summary
    intracerebroventricular injections of MTII in mice induce an increased hypothalamic COUP-TFII expression associated with a decreased hepatic and pancreatic COUP-TFII expression.
  3. 03LabIn vitro (cells)Mechanism

    In GT1-7 hypothalamic cells, the MC4-R agonist MTII caused a dose-dependent increase in COUP-TFII gene expression.

    In plain wordsIn cells, the melanocortin drug MTII raised COUP-TFII gene activity, with larger doses raising it more.

    Outcome
    IncreaseCOUP-TFII gene expression
    Study

    n: not reported in source

    GT1-7 hypothalamic cells
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In GT1-7 hypothalamic cells, the MC4-R agonist MTII leads to a dose dependant increase of COUP-TFII gene expression
  4. 04LabIn vitro (cells)Mechanism

    In GT1-7 hypothalamic cells, the rise in COUP-TFII expression after MTII followed a local increase in cAMP concentrations.

    In plain wordsIn cells, the rise in COUP-TFII gene activity after MTII followed a local rise in the signalling molecule cAMP.

    Outcome
    IncreaseLocal cAMP concentration
    Study

    n: not reported in source

    GT1-7 hypothalamic cells
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In GT1-7 hypothalamic cells, the MC4-R agonist MTII leads to a dose dependant increase of COUP-TFII gene expression secondarily to a local increase in cAMP concentrations.

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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