{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T23:39:59Z","timestamp":1791329999099,"version":"4.3.1"},"reference-count":50,"publisher":"American Diabetes Association","issue":"8","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2015,8,1]]},"abstract":"<jats:p>Intestine contributes to energy homeostasis through the absorption, metabolism, and transfer of nutrients to the organism. We demonstrated previously that hepatocyte nuclear receptor-4\u03b1 (HNF-4\u03b1) controls intestinal epithelium homeostasis and intestinal absorption of dietary lipids. HNF-4\u03b3, the other HNF-4 form highly expressed in intestine, is much less studied. In HNF-4\u03b3 knockout mice, we detect an exaggerated insulin peak and improvement in glucose tolerance during oral but not intraperitoneal glucose tolerance tests, highlighting the involvement of intestine. Moreover, the enteroendocrine L-type cell lineage is modified, as assessed by the increased expression of transcription factors Isl1, Foxa1\/2, and Hnf4a, leading to an increase of both GLP-1\u2013positive cell number and basal and stimulated GLP-1 plasma levels potentiating the glucose-stimulated insulin secretion. Using the GLP-1 antagonist exendin (9-39), we demonstrate a direct effect of GLP-1 on improved glucose tolerance. GLP-1 exerts a trophic effect on pancreatic \u03b2-cells, and we report an increase of the \u03b2-cell fraction correlated with an augmented number of proliferative islet cells and with resistance to streptozotocin-induced diabetes. In conclusion, the loss of HNF-4\u03b3 improves glucose homeostasis through a modulation of the enteroendocrine cell lineage.<\/jats:p>","DOI":"10.2337\/db14-0993","type":"journal-article","created":{"date-parts":[[2015,4,1]],"date-time":"2015-04-01T12:45:24Z","timestamp":1427892324000},"page":"2744-2756","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":29,"title":["Glucose Tolerance Is Improved in Mice Invalidated for the Nuclear Receptor HNF-4\u03b3: A Critical Role for Enteroendocrine Cell Lineage"],"prefix":"10.2337","volume":"64","author":[{"given":"Floriane","family":"Baraille","sequence":"first","affiliation":[{"name":"Sorbonne Universit\u00e9s, Universit\u00e9 Pierre et Marie Curie, UMR_S 1138, Centre de Recherche des Cordeliers, Paris, France"},{"name":"INSERM, UMR_S 1138, Centre de Recherche des Cordeliers, Paris, France"},{"name":"Universit\u00e9 Paris Descartes, Sorbonne Paris Cit\u00e9, UMR_S 1138, Centre de 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