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Gut hormone PYY3-36 physiologically inhibits food intake

Author

Listed:
  • Rachel L. Batterham

    (Imperial College Faculty of Medicine at Hammersmith Campus)

  • Michael A. Cowley

    (Oregon Health and Sciences University
    Oregon Health and Sciences University)

  • Caroline J. Small

    (Imperial College Faculty of Medicine at Hammersmith Campus)

  • Herbert Herzog

    (Garvan Institute of Medical Research)

  • Mark A. Cohen

    (Imperial College Faculty of Medicine at Hammersmith Campus)

  • Catherine L. Dakin

    (Imperial College Faculty of Medicine at Hammersmith Campus)

  • Alison M. Wren

    (Imperial College Faculty of Medicine at Hammersmith Campus)

  • Audrey E. Brynes

    (Imperial College Faculty of Medicine at Hammersmith Campus)

  • Malcolm J. Low

    (Oregon Health and Sciences University)

  • Mohammad A. Ghatei

    (Imperial College Faculty of Medicine at Hammersmith Campus)

  • Roger D. Cone

    (Oregon Health and Sciences University)

  • Stephen R. Bloom

    (Imperial College Faculty of Medicine at Hammersmith Campus)

Abstract

Food intake is regulated by the hypothalamus, including the melanocortin and neuropeptide Y (NPY) systems in the arcuate nucleus1. The NPY Y2 receptor (Y2R), a putative inhibitory presynaptic receptor, is highly expressed on NPY neurons2 in the arcuate nucleus, which is accessible to peripheral hormones3. Peptide YY3-36 (PYY3-36), a Y2R agonist4, is released from the gastrointestinal tract postprandially in proportion to the calorie content of a meal5,6,7. Here we show that peripheral injection of PYY3-36 in rats inhibits food intake and reduces weight gain. PYY3-36 also inhibits food intake in mice but not in Y2r-null mice, which suggests that the anorectic effect requires the Y2R. Peripheral administration of PYY3-36 increases c-Fos immunoreactivity in the arcuate nucleus and decreases hypothalamic Npy messenger RNA. Intra-arcuate injection of PYY3-36 inhibits food intake. PYY3-36 also inhibits electrical activity of NPY nerve terminals, thus activating adjacent pro-opiomelanocortin (POMC) neurons8. In humans, infusion of normal postprandial concentrations of PYY3-36 significantly decreases appetite and reduces food intake by 33% over 24 h. Thus, postprandial elevation of PYY3-36 may act through the arcuate nucleus Y2R to inhibit feeding in a gut–hypothalamic pathway.

Suggested Citation

  • Rachel L. Batterham & Michael A. Cowley & Caroline J. Small & Herbert Herzog & Mark A. Cohen & Catherine L. Dakin & Alison M. Wren & Audrey E. Brynes & Malcolm J. Low & Mohammad A. Ghatei & Roger D. C, 2002. "Gut hormone PYY3-36 physiologically inhibits food intake," Nature, Nature, vol. 418(6898), pages 650-654, August.
    • Handle: RePEc:nat:nature:v:418:y:2002:i:6898:d:10.1038_nature00887
    DOI: 10.1038/nature00887
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    Cited by:

    1. Chung-Chih Liu & Ayub Khan & Nicolas Seban & Nicole Littlejohn & Aayushi Shah & Supriya Srinivasan, 2024. "A homeostatic gut-to-brain insulin antagonist restrains neuronally stimulated fat loss," Nature Communications, Nature, vol. 15(1), pages 1-16, December.
    2. Abbe M. Mhd Jalil & Emilie Combet & Christine A. Edwards & Ada L. Garcia, 2019. "Effect of β-Glucan and Black Tea in a Functional Bread on Short Chain Fatty Acid Production by the Gut Microbiota in a Gut Digestion/Fermentation Model," IJERPH, MDPI, vol. 16(2), pages 1-14, January.
    3. Junjun Gao & Song Zhang & Pan Deng & Zhigang Wu & Bruno Lemaitre & Zongzhao Zhai & Zheng Guo, 2024. "Dietary L-Glu sensing by enteroendocrine cells adjusts food intake via modulating gut PYY/NPF secretion," Nature Communications, Nature, vol. 15(1), pages 1-22, December.

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