Integrating Chronophysiological and Bioinformatic Perspectives on Nesfatin-1, Circadian Feeding Rhythms, and Cortisol Regulation
- 1Faculty of Medicine and Health Sciences, Universiti Sains Islam Malaysia (USIM), Nilai 71800, Negeri Sembilan, Malaysia
- 2Institute of Medical Science Technology, Universiti Kuala Lumpur, Kajang 43000, Selangor, Malaysia
- 3College of Medicine and Health Sciences, Sultan Qaboos University, Muscat 123, Oman
Abstract
Nesfatin-1, a peptide derived from nucleobindin-2, regulates feeding, stress, and sleep–wake processes. To date, the available information suggests that nesfatin-1 is involved in stress regulation and colocalises with substances that influence cortisol, but the circadian interplay between nesfatin-1 and cortisol remains poorly defined. This review integrates biological timing, tissue-specific actions of the hypothalamic–pituitary–adrenal axis, and circadian misalignment, and is supported by in silico protein-association analysis. A structured database search retained relevant studies published from January 2006 to March 2026; heterogeneity necessitated narrative synthesis. Rodent experiments support effects of central NUCB2/nesfatin-1 on feeding and HPA-axis activation. Murine corticotroph experiments report increased POMC abundance, whereas an H295R human adrenocortical carcinoma-cell study reports reduced cortisol content and stimulated release. These findings concern different experimental systems and do not demonstrate coordinated central–adrenal regulation in vivo. The network analysis identified NPY and POMC as prominent nodes within the predefined candidate network, with enrichment of feeding- and HPA-axis-related pathways. Given the biologically targeted selection of input genes, these findings are interpreted as hypothesis-generating associations rather than independent confirmation of a regulatory mechanism. Within the literature examined in this review, direct evidence characterising the 24 h temporal profile of nesfatin-1 in humans, its phase relationship with cortisol, and potential alterations during circadian misalignment was not identified. This apparent evidence gap warrants further investigation through controlled, time-resolved human studies.
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BibTeX
@article{juliana2026integrating,
title = {{Integrating Chronophysiological and Bioinformatic Perspectives on Nesfatin-1, Circadian Feeding Rhythms, and Cortisol Regulation}},
author = {Norsham Juliana and Izuddin Fahmy Abu and Sahar Azmani and Srijit Das and Nazefah Abdul Hamid and Amirah Azzeri and Mohd Hafiz Jaafar and Sofwatul Mokhtarah Maluin and Marjanu Hikmah Elias},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = nov,
doi = {10.3390/ijms27219942},
url = {https://www.mdpi.com/1422-0067/27/21/9942},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Integrating Chronophysiological and Bioinformatic Perspectives on Nesfatin-1, Circadian Feeding Rhythms, and Cortisol Regulation
AU - Norsham Juliana
AU - Izuddin Fahmy Abu
AU - Sahar Azmani
AU - Srijit Das
AU - Nazefah Abdul Hamid
AU - Amirah Azzeri
AU - Mohd Hafiz Jaafar
AU - Sofwatul Mokhtarah Maluin
AU - Marjanu Hikmah Elias
PY - 2026
DA - 2026/11/06
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219942
UR - https://www.mdpi.com/1422-0067/27/21/9942
AB - Nesfatin-1, a peptide derived from nucleobindin-2, regulates feeding, stress, and sleep–wake processes. To date, the available information suggests that nesfatin-1 is involved in stress regulation and colocalises with substances that influence cortisol, but the circadian interplay between nesfatin-1 and cortisol remains poorly defined. This review integrates biological timing, tissue-specific actions of the hypothalamic–pituitary–adrenal axis, and circadian misalignment, and is supported by in silico protein-association analysis. A structured database search retained relevant studies published from January 2006 to March 2026; heterogeneity necessitated narrative synthesis. Rodent experiments support effects of central NUCB2/nesfatin-1 on feeding and HPA-axis activation. Murine corticotroph experiments report increased POMC abundance, whereas an H295R human adrenocortical carcinoma-cell study reports reduced cortisol content and stimulated release. These findings concern different experimental systems and do not demonstrate coordinated central–adrenal regulation in vivo. The network analysis identified NPY and POMC as prominent nodes within the predefined candidate network, with enrichment of feeding- and HPA-axis-related pathways. Given the biologically targeted selection of input genes, these findings are interpreted as hypothesis-generating associations rather than independent confirmation of a regulatory mechanism. Within the literature examined in this review, direct evidence characterising the 24 h temporal profile of nesfatin-1 in humans, its phase relationship with cortisol, and potential alterations during circadian misalignment was not identified. This apparent evidence gap warrants further investigation through controlled, time-resolved human studies.
SN - 1422-0067
ER -