Melanocortinergic modulation of cholecystokinin-induced suppression of feeding through extracellular signal-regulated kinase signaling in rat solitary nucleus.

Sutton GM, Duos B, Patterson LM, Berthoud HR

Endocrinology16 Jun 2005Cited by 120 (Europe PMC)

PMID15961554DOI10.1210/en.2005-0562PepBankPUB-15961554

Publisher page PubMedAsk about this study

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 study6

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

01AnimalAnimal study (in vivo)Mechanism
In rats, fourth ventricular MTII rapidly and dose-dependently increased phosphorylation of ERK1/2 in the solitary nucleus.
In plain wordsIn rats, MTII injected into the fourth brain ventricle quickly raised ERK1/2 activation in a brain-stem area, more at higher doses.
Peptide
Melanotan II
Outcome
IncreaseERK1/2 phosphorylation in the solitary nucleus
Study
ratn: not reported in source
rats with fourth ventricular cannulas
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
Dose not stated · fourth ventricle injectionAs given in this study (rat).
Source sentences
Summary
Using fourth ventricular-cannulated rats and Western blotting of NTS tissue, we show that the MC4R agonist melanotan II (MTII) rapidly and dose-dependently increases phosphorylation of both ERK1/2 and cAMP response element-binding protein (CREB).
Report a problemFND-1596155401
02AnimalAnimal study (in vivo)Mechanism
In rats, fourth ventricular MTII rapidly and dose-dependently increased phosphorylation of CREB in the solitary nucleus.
In plain wordsIn rats, MTII injected into the fourth brain ventricle quickly raised CREB activation in a brain-stem area, more at higher doses.
Peptide
Melanotan II
Outcome
IncreaseCREB phosphorylation in the solitary nucleus
Study
ratn: not reported in source
rats with fourth ventricular cannulas
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
Dose not stated · fourth ventricle injectionAs given in this study (rat).
Source sentences
Summary
Using fourth ventricular-cannulated rats and Western blotting of NTS tissue, we show that the MC4R agonist melanotan II (MTII) rapidly and dose-dependently increases phosphorylation of both ERK1/2 and cAMP response element-binding protein (CREB).
Report a problemFND-1596155402

Studies that did not test the peptide alone4

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.

03AnimalNot a test of Melanotan II aloneAnimal study (in vivo)Mechanism
In rats, sequential fourth ventricular MTII and peripheral CCK, each at submaximal doses, produced an additive increase in pERK1/2.
In plain wordsIn rats, giving MTII and CCK one after the other, each at a low dose, raised ERK1/2 activation additively.
Peptide
Melanotan II
Outcome
IncreasepERK1/2 after sequential MTII and CCK
Study
ratn: not reported in source
rats with fourth ventricular cannulas
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Source sentences
Summary
Sequential administration of fourth ventricular MTII and peripheral CCK at doses that alone produced submaximal stimulation of pERK1/2 produced an additive increase.
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.
Report a problemFND-1596155403
04AnimalNot a test of Melanotan II aloneAnimal study (in vivo)Mechanism
In rats, pretreatment with the MAPK kinase inhibitor U0126 abolished the capacity of MTII to suppress 2-h food intake.
In plain wordsIn rats, the ERK pathway blocker U0126 stopped MTII from lowering food intake over 2 hours.
Peptide
Melanotan II
Outcome
DecreaseMTII suppression of 2-h food intake after MAPK kinase inhibitor U0126
Study
ratn: not reported in source
rats with fourth ventricular cannulas
Comparator
MTII without U0126
Outcome group
Appetite and food intake · Metabolic and weight
Source sentences
Summary
Prior administration of the MAPK kinase inhibitor U0126 abolished the capacity of MTII to suppress 2-h food intake and significantly decreased MTII-induced ERK phosphorylation in the NTS.
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.
Report a problemFND-1596155404
05AnimalNot a test of Melanotan II aloneAnimal study (in vivo)Mechanism
In rats, U0126 significantly decreased MTII-induced ERK phosphorylation in the solitary nucleus.
In plain wordsIn rats, the ERK pathway blocker U0126 lowered the ERK activation that MTII causes in a brain-stem area.
Peptide
Melanotan II
Outcome
DecreaseMTII-induced ERK phosphorylation in the NTS after U0126
Study
ratn: not reported in source
rats with fourth ventricular cannulas
Comparator
MTII without U0126
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Source sentences
Summary
Prior administration of the MAPK kinase inhibitor U0126 abolished the capacity of MTII to suppress 2-h food intake and significantly decreased MTII-induced ERK phosphorylation in the NTS.
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.
Report a problemFND-1596155405
06AnimalNot a test of Melanotan II aloneAnimal study (in vivo)Mechanism
In rats, pretreatment with the cAMP inhibitor cAMP receptor protein-Rp isomer significantly attenuated pERK stimulation induced by MTII.
In plain wordsIn rats, a cAMP blocker weakened the rise in ERK activation that MTII causes.
Peptide
Melanotan II
Outcome
DecreaseMTII-induced pERK after cAMP inhibitor
Study
ratn: not reported in source
rats with fourth ventricular cannulas
Comparator
MTII without cAMP inhibitor
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Source sentences
Summary
Furthermore, pretreatment with the cAMP inhibitor, cAMP receptor protein-Rp isomer, significantly attenuated stimulation of pERK induced by either CCK or MTII.
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.
Report a problemFND-1596155406

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.

Version 2Current
10 Oct 2026, 09:43 UTC
Study results updated
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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MeSH terms

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