Central and peripheral neuroendocrine peptides and signalling in appetite regulation: considerations for obesity pharmacotherapy
Abstract
Summary: Appetite and satiety are mediated by complex neuroendocrine signalling pathways involving over 40 hormones, neuropeptides, enzymes, other chemical messengers and their receptors. Research efforts continue to expand understanding of the role of signalling molecules between central hypothalamic nuclei and peripheral enteroendocrine cells; and discoveries of novel networks and messengers provide new biological insights on how to manipulate appetite–satiety pathways. Despite the vast array of peptides that are potentially useful for anti‐obesity drug development, only four classes of agents are approved: (i) catecholamine stimulants; (ii) serotonin and noradrenaline reuptake inhibitors; (iii) lipase inhibitors; and (iv) more recently cannabinoid‐1 receptor antagonists. Clinical effects of these drugs confer modest improvements, and side effects negatively impact long‐term treatment course. This paper suggests single target pharmacological interventions are possibly hampered by the myriad of alternate orexigenic peptidic signals that drive hyperphagia, hence a multiple target model or combination treatment approach is proposed to offer greater therapeutic potential in modulating appetite and managing weight.
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Several neurotransmitters, hormones, and neuropeptides involved in homeostatic regulation of food intake have been implicated in the rewarding effects of food and drugs.
“Several neurotransmitters, including DA, cannabinoids, opioids, gamma-aminobutyric acid (GABA) and serotonin, as well as hormones and neuropeptides involved in homeostatic regulation of food intake, such as insulin, orexin, leptin, ghrelin, PYY, glucagon-like peptide-1 (GLP-1) have been implicated in the rewarding effects of food and drugs (Tables 1 and 2) (18–21).”
From Obesity and addiction: Neurobiological overlaps (2013) · cites this paper as [18]
Several neurotransmitters, including DA, cannabinoids, opioids and serotonin, as well as hormones and neuropeptides involved in homeostatic regulation of food intake such as insulin, orexin, leptin and ghrelin, have been implicated in the rewarding effects of food.
“Several neurotransmitters, including DA, cannabinoids, opioids and serotonin, as well as hormones and neuropetides involved in homeostatic regulation of food intake, such as insulin, orexin, leptin and ghrelin, have been implicated in the rewarding effects of food (Atkinson 2008;Cason et al 2010;Cota et al 2006).”
From Food and Drug Reward: Overlapping Circuits in Human Obesity and Addiction (2011) · cites this paper as Atkinson 2008
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Reward, dopamine and the control of food intake: implications for obesity
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- Authors
- Atkinson, T. J.
- Corresponding author
- Atkinson, T. J.
- Venue
- Obesity Reviews
- Publisher
- Wiley
- Published
- 2007-10-23
- Volume
- 9
- Issue
- 2
- Pages
- 108-120
- ISSN
- 1467-7881 (ISSN-L)
- 1467-789X
- OpenAlex
- W2154971062
- Cited by
- 49
- References
- 102
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 2 · 2022: 5 · 2021: 2 · 2020: 3 · 2019: 4 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 1 · 2013: 2 · 2012: 5
- FWCI
- 0.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Obesity Reviews (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Pharmacology › Pharmacology and Obesity Treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- appetite regulation, satiety, neuroendocrine signalling, neuropeptides, hypothalamus, enteroendocrine cells, obesity pharmacotherapy, anti-obesity drugs, serotonin-norepinephrine reuptake inhibitors, lipase inhibitors, cannabinoid-1 receptor antagonist, combination therapy, hyperphagia
- MeSH terms
- Appetite Regulation, Humans, Neurosecretory Systems, Obesity, Signal Transduction, Anti-Obesity Agents
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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