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Peer-reviewedCC BYNeurotherapeutics

Intranasal neuropeptide Y suppresses food intake, reduces sucrose preference and increases circulating corticosterone in obese mice

  • Maike Haag1
  • Karolina Herceg2
  • Chi Kin Ip3
  • Angela Jačan4
  • Florian Reichmann2
  • Herbert Herzog5
  • Andreas Meinitzer6
  • Peter Holzer2
  • Ahmed M. Hassan7
  • Aitak Farzi2
7 affiliations
  1. 1Otto Loewi Research Center, Division of Pharmacology, Medical University of Graz, Graz, Austria; Department of Internal Medicine, Division of Angiology, Medical University of Graz, Graz, Austria
  2. 2Otto Loewi Research Center, Division of Pharmacology, Medical University of Graz, Graz, Austria
  3. 3School of Clinical Medicine, St. Vincent's Clinical School, UNSW Medicine & Health, UNSW Sydney, Sydney, NSW, 2010, Australia
  4. 4Otto Loewi Research Center, Division of Pharmacology, Medical University of Graz, Graz, Austria; CBmed GmbH-Center for Biomarker Research in Medicine, Graz, Austria
  5. 5School of Clinical Medicine, St. Vincent's Clinical School, UNSW Medicine & Health, UNSW Sydney, Sydney, NSW, 2010, Australia; Eating Disorder Research Program, St. Vincent's Centre for Applied Medical Research, 405 Liverpool Street, Darlinghurst, Sydney, NSW, 2010, Australia
  6. 6Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Graz, Austria
  7. 7Otto Loewi Research Center, Division of Pharmacology, Medical University of Graz, Graz, Austria; Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Graz, Austria; Corresponding author
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Abstract

Obesity is associated with an increased risk of psychiatric disorders and altered reward processing. Neuropeptide Y (NPY) links metabolic state, reward-driven behavior, and emotional processing. We therefore tested whether intranasal (i.n.) NPY modifies high-fat diet (HFD)-induced behavioral alterations. Male C57BL/6J mice were fed HFD (48% kcal fat) or control diet for 8 weeks and assessed for anxiety-like behavior using the light/dark box test (LDT), self-care behavior using the splash test, and sucrose-directed ingestive behavior using sucrose intake and sucrose preference (SP). A separate cohort of control- and HFD-fed mice received i.n. NPY or vehicle, followed by assessment of SP and ingestive behavior after 3, 24 and 48 h. Neuroendocrine and inflammatory parameters were measured in blood, brain, and colon. HFD reduced sucrose-directed ingestive behavior, reflected by reduced sucrose intake and SP, without significantly affecting anxiety-like behavior in the LDT or self-care behavior in the splash test. HFD reduced hypothalamic Npy mRNA and peptide levels as well as circulating corticosterone, while the evaluated inflammation-related markers remained unchanged. I.n. NPY had no effect after 24 or 48 h but reduced sucrose intake and SP, and increased circulating corticosterone 3 h after administration specifically in HFD-fed animals. In contrast, i.n. NPY reduced food intake and body weight after 3 h, independent of diet. Because these effects were consistent with neuropeptide Y receptor Y2 (NPY2R)-mediated actions, we tested i.n. NPY in HFD-fed Npy2r -deficient mice. In these mice, i.n. NPY did not affect sucrose intake, SP, food intake, or corticosterone, consistent with a potential involvement of NPY2R.

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Cite

BibTeXRIS
BibTeX
@article{haag2026intranasal,
  title = {{Intranasal neuropeptide Y suppresses food intake, reduces sucrose preference and increases circulating corticosterone in obese mice}},
  author = {Maike Haag and Karolina Herceg and Chi Kin Ip and Angela Jačan and Florian Reichmann and Herbert Herzog and Andreas Meinitzer and Peter Holzer and Ahmed M. Hassan and Aitak Farzi},
  journal = {Neurotherapeutics},
  year = {2026},
  month = oct,
  doi = {10.1016/j.neurot.2026.e01100},
  url = {https://doi.org/10.1016/j.neurot.2026.e01100},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Intranasal neuropeptide Y suppresses food intake, reduces sucrose preference and increases circulating corticosterone in obese mice
AU  - Maike Haag
AU  - Karolina Herceg
AU  - Chi Kin Ip
AU  - Angela Jačan
AU  - Florian Reichmann
AU  - Herbert Herzog
AU  - Andreas Meinitzer
AU  - Peter Holzer
AU  - Ahmed M. Hassan
AU  - Aitak Farzi
PY  - 2026
DA  - 2026/10/22
JO  - Neurotherapeutics
DO  - 10.1016/j.neurot.2026.e01100
UR  - https://doi.org/10.1016/j.neurot.2026.e01100
AB  - Obesity is associated with an increased risk of psychiatric disorders and altered reward processing. Neuropeptide Y (NPY) links metabolic state, reward-driven behavior, and emotional processing. We therefore tested whether intranasal (i.n.) NPY modifies high-fat diet (HFD)-induced behavioral alterations. Male C57BL/6J mice were fed HFD (48% kcal fat) or control diet for 8 weeks and assessed for anxiety-like behavior using the light/dark box test (LDT), self-care behavior using the splash test, and sucrose-directed ingestive behavior using sucrose intake and sucrose preference (SP). A separate cohort of control- and HFD-fed mice received i.n. NPY or vehicle, followed by assessment of SP and ingestive behavior after 3, 24 and 48 h. Neuroendocrine and inflammatory parameters were measured in blood, brain, and colon. HFD reduced sucrose-directed ingestive behavior, reflected by reduced sucrose intake and SP, without significantly affecting anxiety-like behavior in the LDT or self-care behavior in the splash test. HFD reduced hypothalamic Npy mRNA and peptide levels as well as circulating corticosterone, while the evaluated inflammation-related markers remained unchanged. I.n. NPY had no effect after 24 or 48 h but reduced sucrose intake and SP, and increased circulating corticosterone 3 h after administration specifically in HFD-fed animals. In contrast, i.n. NPY reduced food intake and body weight after 3 h, independent of diet. Because these effects were consistent with neuropeptide Y receptor Y2 (NPY2R)-mediated actions, we tested i.n. NPY in HFD-fed Npy2r -deficient mice. In these mice, i.n. NPY did not affect sucrose intake, SP, food intake, or corticosterone, consistent with a potential involvement of NPY2R.
SN  - 1878-7479
SN  - 1933-7213
ER  -