ArticleDiabetes, obesity & metabolism2022
Growth differentiation factor 15 (GDF15) and semaglutide inhibit food intake and body weight through largely distinct, additive mechanisms.
Article in Diabetes, obesity & metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 43 citations in OpenAlex.
- Circulating total and intact GDF-15 levels are not altered in response to weight loss induced by liraglutide or lorcaserin treatment in humans with obesity.Metabolism: clinical and experimental · 2022Trial
- Chronic semaglutide alters ingestive behavior without impairing taste function in mice.Molecular metabolism · 2026Article
- A rapid review of the effects of GLP-1 receptor agonists on opioid and stimulant use-related outcomes.Drug and alcohol dependence reports · 2026Review
- Insulin and Incretin Receptor Agonists Reciprocally Alter Their Blood-Brain Barrier Permeabilities.International journal of molecular sciences · 2026Article
- GLP-1 at the Metabolic-Cognitive Interface: Reward, Affect, and Memory.Comprehensive physiology · 2026Review
- Chronic semaglutide treatment enhances the incentive motivational value of a small food reward and associated cue in male and female rats.Psychopharmacology · 2026Article
- Taking back control: The experience of adults using semaglutide and tirzepatide for obesity treatment - A qualitative study.Obesity pillars · 2026Article
- Peptide-based therapeutics targeting GPCRs: recent applications in the treatment of metabolic disorders.Frontiers in pharmacology · 2026Review
- GDF15 as a sentinel of metabolic integrity: a narrative review of stress signaling, multisystem pathophysiology, and therapeutic potential.Frontiers in endocrinology · 2026Review
- A melanocortin 4- and glucagon-like peptide 1 receptor multiple agonist for the treatment of diabetes and obesity.Metabolism: clinical and experimental · 2026Article
- The estrous cycle moderates the food and body weight suppressive effects of glucagon-like peptide-1 receptor agonism.Diabetes, obesity & metabolism · 2026Article
- Integrating micro-needle jet injection and sustained GLP-1 therapy with structured feeding: a comprehensive strategy for obesity management.Drug delivery · 2025Article
- Metabolic Messenger: growth differentiation factor 15.Nature metabolism · 2025Review
- Relevance of GDF15 as a biomarker for clinical outcomes after bariatric surgery.The Journal of endocrinology · 2025Article
- Growth Differentiation Factor 15 Induces Gastric Fundus Contraction Involving Cholinergic Excitation: Morphofunctional Evidence in Rodent Models.Journal of cellular and molecular medicine · 2025Article
- Changes in food preferences and ingestive behaviors after glucagon-like peptide-1 analog treatment: techniques and opportunities.International journal of obesity (2005) · 2025Review
- Central mechanisms of emesis: A role for GDF15.Neurogastroenterology and motility · 2025Review
- Effects of semaglutide on metabolism and gut microbiota in high-fat diet-induced obese mice.Frontiers in pharmacology · 2025Article
- Brainstem BDNF neurons are downstream of GFRAL/GLP1R signalling.Nature communications · 2024Article
- Superior metabolic improvement of polycystic ovary syndrome traits after GLP1-based multi-agonist therapy.Nature communications · 2024Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
aimsTo evaluate whether the potent hypophagic and weight-suppressive effects of growth differentiation factor-15 (GDF15) and semaglutide combined would be a more efficacious antiobesity treatment than either treatment alone by examining whether the neural and behavioural mechanisms contributing to their anorectic effects were common or disparate. MATERIALS/
methodsThree mechanisms were investigated to determine how GDF15 and semaglutide induce anorexia: the potentiation of the intake suppression by gastrointestinal satiation signals; the reduction in motivation to feed; and the induction of visceral malaise. We then compared the effects of short-term, combined GDF15 and semaglutide treatment on weight loss to the individual treatments. Rat pharmaco-behavioural experiments assessed whether GDF15 or semaglutide added to the satiating effects of orally gavaged food and exogenous cholecystokinin (CCK). A progressive ratio operant paradigm was used to examine whether GDF15 or semaglutide reduced feeding motivation. Pica behaviour (ie, kaolin intake) and conditioned affective food aversion testing were used to evaluate visceral malaise. Additionally, fibre photometry studies were conducted in agouti-related protein (AgRP)-Cre mice to examine whether GDF15 or semaglutide, alone or in combination with CCK, modulate calcium signalling in hypothalamic AgRP neurons.
resultsSemaglutide reduced food intake by amplifying the feeding-inhibitory effect of CCK or ingested food, inhibited the activity of AgRP neurons when combined with CCK, reduced feeding motivation and induced malaise. GDF15 induced visceral malaise but, strikingly, did not affect feeding motivation, the satiating effect of ingested food or CCK signal processing. Combined GDF15 and semaglutide treatment produced greater food intake and body weight suppression than did either treatment alone, without enhancing malaise.
conclusionsGDF15 and semaglutide reduce food intake and body weight through largely distinct processes that produce greater weight loss and feeding suppression when combined.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.