ArticlePeptides2016
Metabolic responses to xenin-25 are altered in humans with Roux-en-Y gastric bypass surgery.
Article in Peptides, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02204813 (To Define the Role of GLP-1 for Improving Glucose Homeostasis in Humans Following Gastric Bypass Surgery), which is not on this map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
To Define the Role of GLP-1 for Improving Glucose Homeostasis in Humans Following Gastric Bypass Surgery
Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Peptide YY in Type 2 Diabetes: A Complementary Gut Hormone with Therapeutic Potential Beyond GLP-1.Nutrients · 2025Review
- Xenin-Derived Peptides: Multifaceted Regulators and Therapeutic Innovations in Metabolic Diseases.Drug design, development and therapy · 2025Review
- A novel neurotensin/xenin fusion peptide enhances β-cell function and exhibits antidiabetic efficacy in high-fat fed mice.Bioscience reports · 2021Article
- Role of the Autonomic Nervous System in Mechanism of Energy and Glucose Regulation Post Bariatric Surgery.Frontiers in neuroscience · 2021Review
- Article
- Luminal chemosensing in the gastroduodenal mucosa.Current opinion in gastroenterology · 2017Review
- Xenin Augments Duodenal Anion Secretion via Activation of Afferent Neural Pathways.The Journal of pharmacology and experimental therapeutics · 2017Article
- An enzymatically stable GIP/xenin hybrid peptide restores GIP sensitivity, enhances beta cell function and improves glucose homeostasis in high-fat-fed mice.Diabetologia · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Xenin-25 (Xen) is a neurotensin-related peptide secreted by a subset of enteroendocrine cells located in the proximal small intestine. Many effects of Xen are mediated by neurotensin receptor-1 on neurons. In healthy humans with normal glucose tolerance (NGT), Xen administration causes diarrhea and inhibits postprandial glucagon-like peptide-1 (GLP-1) release but not insulin secretion. This study determines (i) if Xen has similar effects in humans with Roux-en-Y gastric bypass (RYGB) and (ii) whether neural pathways potentially mediate effects of Xen on glucose homeostasis. Eight females with RYGB and no history of type 2 diabetes received infusions with 0, 4 or 12pmol Xen/kg/min with liquid meals on separate occasions. Plasma glucose and gastrointestinal hormone levels were measured and insulin secretion rates calculated. Pancreatic polypeptide and neuropeptide Y levels were surrogate markers for parasympathetic input to islets and sympathetic tone, respectively. Responses were compared to those in well-matched non-surgical participants with NGT from our earlier study. Xen similarly increased pancreatic polypeptide and neuropeptide Y responses in patients with and without RYGB. In contrast, the ability of Xen to inhibit GLP-1 release and cause diarrhea was severely blunted in patients with RYGB. With RYGB, Xen had no statistically significant effect on glucose, insulin secretory, GLP-1, glucose-dependent insulinotropic peptide, and glucagon responses. However, insulin and glucose-dependent insulinotropic peptide secretion preceded GLP-1 release suggesting circulating GLP-1 does not mediate exaggerated insulin release after RYGB. Thus, Xen has unmasked neural circuits to the distal gut that inhibit GLP-1 secretion, cause diarrhea, and are altered by RYGB.
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Registered trials
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.