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Endogenous prolactin-releasing peptide regulates food intake in rodents
Yuki Takayanagi, … , Gareth Leng, Tatsushi Onaka
Yuki Takayanagi, … , Gareth Leng, Tatsushi Onaka
Published November 3, 2008
Citation Information: J Clin Invest. 2008;118(12):4014-4024. https://doi.org/10.1172/JCI34682.
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Research Article Metabolism Article has an altmetric score of 6

Endogenous prolactin-releasing peptide regulates food intake in rodents

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Abstract

Food intake is regulated by a network of signals that emanate from the gut and the brainstem. The peripheral satiety signal cholecystokinin is released from the gut following food intake and acts on fibers of the vagus nerve, which project to the brainstem and activate neurons that modulate both gastrointestinal function and appetite. In this study, we found that neurons in the nucleus tractus solitarii of the brainstem that express prolactin-releasing peptide (PrRP) are activated rapidly by food ingestion. To further examine the role of this peptide in the control of food intake and energy metabolism, we generated PrRP-deficient mice and found that they displayed late-onset obesity and adiposity, phenotypes that reflected an increase in meal size, hyperphagia, and attenuated responses to the anorexigenic signals cholecystokinin and leptin. Hypothalamic expression of 6 other appetite-regulating peptides remained unchanged in the PrRP-deficient mice. Blockade of endogenous PrRP signaling in WT rats by central injection of PrRP-specific mAb resulted in an increase in food intake, as reflected by an increase in meal size. These data suggest that PrRP relays satiety signals within the brain and that selective disturbance of this system can result in obesity and associated metabolic disorders.

Authors

Yuki Takayanagi, Hirokazu Matsumoto, Masanori Nakata, Takashi Mera, Shoji Fukusumi, Shuji Hinuma, Yoichi Ueta, Toshihiko Yada, Gareth Leng, Tatsushi Onaka

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Figure 3

Energy utilization in PrRP-deficient and WT mice.

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Energy consumption of PrRP-deficient mice.
(A) At the age of 16 weeks, l...
BW (A) and food intake (B) of mice fed standard laboratory chow (STD) or high-fat diet from the age of 12 weeks (at the ages of 10–16 weeks, PrRP-deficient mice fed standard laboratory chow had not yet begun to show obesity). Mice fed a high-fat diet gained BW faster, with a significantly greater gain in PrRP-deficient mice. Food intake was greater in PrRP-deficient mice at ages when they were heavier than WT mice (n = 4). (C) BWs of WT and pair-fed PrRP-deficient mice from 6 to 57 weeks of age. Half of the mice were fed standard laboratory chow or high-fat diet from the age of 12 weeks. The BWs of pair-fed PrRP-deficient mice were not significantly different from those of WT mice (n = 6 or 7). (D) At the age of 39–40 weeks, pair-fed PrRP-deficient mice on standard laboratory chow had glucose tolerance similar to that of WT mice (n = 6 or 7). (E) At the age of 40–41 weeks, pair-fed PrRP-deficient mice on standard laboratory chow showed insulin resistance similar to that of WT mice. (Blood glucose concentrations before insulin administration were set as 100%; n = 6 or 7.) Error bars indicate SEM. ‡P < 0.01, #P < 0.001 versus WT mice; *P < 0.05, **P < 0.01, ***P < 0.001 versus mice fed standard chow.

Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

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Referenced in 5 patents
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