ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2014
Impaired enteroendocrine development in intestinal-specific Islet1 mouse mutants causes impaired glucose homeostasis.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Pooled it
- Type 2 diabetes is associated with impaired jejunal enteroendocrine GLP-1 cell lineage in human obesity.International journal of obesity (2005) · 2021Trial
- Article
- Efficient control of enterochromaffin versus islet differentiation from human pluripotent stem cell-derived pancreatic progenitors.Nature communications · 2026Article
- Intestinal epithelial cells in health and disease.Tissue barriers · 2026Review
- Identification of intestinal enteroendocrine cell subtypes and their associated hormones in zebrafish.PLoS biology · 2025Article
- ETV1 is a key regulator of enteroendocrine PYY production.Disease models & mechanisms · 2025Article
- Unraveling enteroendocrine cell lineage dynamics and associated gene regulatory networks during intestinal development.Biology open · 2025Article
- Enteroendocrine cell differentiation: Implications for human disease.Molecular and cellular endocrinology · 2025Review
- RISING STARS: Endocrine regulation of metabolic homeostasis via the intestine and gut microbiome.The Journal of endocrinology · 2023Review
- Enteroendocrine cell regulation of the gut-brain axis.Frontiers in neuroscience · 2023Review
- Enteroendocrine System and Gut Barrier in Metabolic Disorders.International journal of molecular sciences · 2022Review
- Synergistic effects of ISL1 and KDM6B on non-alcoholic fatty liver disease through the regulation of SNAI1.Molecular medicine (Cambridge, Mass.) · 2022Article
- Article
- Intestinal Neurod1 expression impairs paneth cell differentiation and promotes enteroendocrine lineage specification.Scientific reports · 2019Article
- Rfx6 promotes the differentiation of peptide-secreting enteroendocrine cells while repressing genetic programs controlling serotonin production.Molecular metabolism · 2019Article
- Sox4 Promotes Atoh1-Independent Intestinal Secretory Differentiation Toward Tuft and Enteroendocrine Fates.Gastroenterology · 2018Article
- Distribution and hormonal characterization of primary murine L cells throughout the gastrointestinal tract.Journal of diabetes investigation · 2018Article
- Enteroendocrine cells-sensory sentinels of the intestinal environment and orchestrators of mucosal immunity.Mucosal immunology · 2018Review
- The novel enterochromaffin marker Lmx1a regulates serotonin biosynthesis in enteroendocrine cell lineages downstream of Nkx2.2.Development (Cambridge, England) · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Enteroendocrine cells secrete over a dozen different hormones responsible for coordinating digestion, absorption, metabolism, and gut motility. Loss of enteroendocrine cells is a known cause of severe congenital diarrhea. Furthermore, enteroendocrine cells regulate glucose metabolism, with the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) playing critical roles in stimulating insulin release by pancreatic β-cells. Islet1 (Isl1) is a LIM-homeodomain transcription factor expressed specifically in an array of intestinal endocrine cells, including incretin-expressing cells. To examine the impact of intestinal Isl1 on glycemic control, we set out to explore the role of intestinal Isl1 in hormone cell specification and organismal physiology. Mice with intestinal epithelial-specific ablation of Isl1 were obtained by crossing Villin-Cre transgenic animals with mice harboring a Isl1(loxP) allele (Isl1(int) model). Gene ablation of Isl1 in the intestine results in loss of GLP-1, GIP, cholecystokinin (CCK), and somatostatin-expressing cells and an increase in 5-HT (serotonin)-producing cells, while the chromogranin A population was unchanged. This dramatic change in hormonal milieu results in animals with lipid malabsorption and females smaller than their littermate controls. Interestingly, when challenged with oral, not intraperitoneal glucose, the Isl-1 intestinal-deficient animals (Isl1(int)) display impaired glucose tolerance, indicating loss of the incretin effect. Thus the Isl1(int) model confirms that intestinal biology is essential for organism physiology in glycemic control and susceptibility to diabetes.
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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.