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Study breakdown

Prolactin-Releasing Peptide Naturally Reduces Food Intake in Rodents

Animal StudyModerate evidence
The takeaway

Endogenous prolactin-releasing peptide (PrRP) regulated food intake in rodents, with PrRP-deficient mice showing increased body weight and food intake — establishing PrRP as a natural satiety signal beyond its prolactin-releasing function.

Key finding

PrRP-deficient mice showed increased food intake and body weight, while PrRP administration reduced feeding, establishing endogenous prolactin-releasi

What the researchers found

PrRP-deficient mice showed increased food intake and body weight, while PrRP administration reduced feeding, establishing endogenous prolactin-releasing peptide as a novel satiety signal acting through hypothalamic and brainstem appetite circuits.

Why it matters

Relevant for neuropeptides, weight-loss.

How the study worked

animal-study study.

What this study cannot tell us

See abstract.

How to read the evidence

moderate evidence.

When this study was published

Published in 2008.

The bigger picture

Advances peptide research.

Questions still open

  • Further research needed.
  • Clinical translation to evaluate.

Common questions

What was studied?
Prolactin-Releasing Peptide Naturally Reduces Food Intake in Rodents
What was found?
Endogenous prolactin-releasing peptide (PrRP) regulated food intake in rodents, with PrRP-deficient mice showing increased body weight and food intake — establishing PrRP as a natural satiety signal beyond its prolactin-releasing function.

Read the original research

Endogenous prolactin-releasing peptide regulates food intake in rodents.

The Journal of clinical investigation, 118(12), 4014-24

Citation

Takayanagi, Yuki; Matsumoto, Hirokazu; Nakata, Masanori; Mera, Takashi; Fukusumi, Shoji; Hinuma, Shuji; Ueta, Yoichi; Yada, Toshihiko; Leng, Gareth; Onaka, Tatsushi. (2008). Endogenous prolactin-releasing peptide regulates food intake in rodents.. The Journal of clinical investigation, 118(12), 4014-24. https://doi.org/10.1172/JCI34682