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Annieke C G van Baar, Andrei Prodan, Camilla D Wahlgren, Steen S Poulsen, Filip K Knop, Albert K Groen, Jacques J Bergman, Max Nieuwdorp, and Evgeni Levin

Introduction The small intestinal mucosa orchestrates a complex response to a range of internal and external stimuli. A pivotal role is played by enteroendocrine cells, whose dysfunction has been linked to metabolic diseases such as obesity

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Emmi Naskali, Katja Dettmer, Peter J Oefner, Pedro A B Pereira, Kai Krohn, Petri Auvinen, Annamari Ranki, and Nicolas Kluger

directed against aromatic l -amino acid decarboxylase (or DOPA decarboxylase, AADC) and tryptophan hydroxylase (TPH) are commonly found in APECED patients ( 7 , 8 , 9 ) and their presence has been associated with the lack of entero-endocrine (EE) cells

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Monia Cito, Silvia Pellegrini, Lorenzo Piemonti, and Valeria Sordi

‘neoislets’ below the crypt base that were able to secrete insulin in a glucose-dependent manner and ameliorate hyperglycemia in diabetic mice ( 79 ). Recently, Zhou’s group showed that antral enteroendocrine cells also were able to generate functional

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L Ahlkvist, K Brown, and B Ahrén

-protein-coupled receptor 119 (GPR119). This receptor is expressed in gut enteroendocrine cells (5) , whereby activation has been shown to result in increased release of GLP1 (6, 7) . GPR119 protein is also localized to islet β-cells (6) , and consequently, GPR119

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Jens F Rehfeld

steps catalyzed by enzymes that have been reviewed in detail elsewhere ( 62 , 65 , 66 , 67 ). After release of the CCK peptides from enteroendocrine I-cells to blood the plasma pattern changes, because the longer molecular forms (CCK-58, -33 and -22

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Julia Modesto Vicente, Junia Carolina Santos-Silva, Caio Jordão Teixeira, Dailson Nogueira de Souza, Jean Franciesco Vettorazzi, Fabiola Sales Furtuoso, Isabel Gouveia Adabo, Fabio Takeo Sato, Marco Aurélio Ramirez Vinolo, Everardo Magalhães Carneiro, Silvana Bordin, and Gabriel Forato Anhê

both neurotransmitters released during the cephalic phase of insulin release or incretins such as glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP) released by enteroendocrine cells in response to food transit ( 26 ). Human islets are

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Gaëtan Prévost, Marie Picot, Marie-Anne Le Solliec, Arnaud Arabo, Hind Berrahmoune, Mouna El Mehdi, Saloua Cherifi, Alexandre Benani, Emmanuelle Nédélec, Françoise Gobet, Valéry Brunel, Jérôme Leprince, Hervé Lefebvre, Youssef Anouar, and Nicolas Chartrel

lipid metabolism . Bioscience Reports 2018 38 . ( ) 30177523 34 Gribble FM Reimann F . Function and mechanisms of enteroendocrine cells and gut hormones in metabolism . Nature Reviews Endocrinology 2019

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Lin Ji, Huan-Tong Wu, Xiao-Yan Qin, and Rongfeng Lan

peptide hormones, it is likely that alterations in the maturation of other peptides may be responsible for the infertility of Cpe fat /Cpe fat mice. Gastrointestinal deficits Enteroendocrine cells (EEC) maintain the intestinal barrier by

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Sara Storvall, Helena Leijon, Eeva Ryhänen, Johanna Louhimo, Caj Haglund, Camilla Schalin-Jäntti, and Johanna Arola

Langerhans’ islet cells and enteroendocrine cells stained positive appropriate to the SST antibody used, while the surrounding tissue remained negative. Thus, one can assume that the staining we have observed is, in fact, valid also regarding the nuclear

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Jukka Koffert, Henri Honka, Jarmo Teuho, Saila Kauhanen, Saija Hurme, Riitta Parkkola, Vesa Oikonen, Andrea Mari, Andreas Lindqvist, Nils Wierup, Leif Groop, and Pirjo Nuutila

incretin hormones GIP and GLP-1 are released from the enteroendocrine cells of the fore- and hindgut, respectively, upon chyme and bile salt contact with the mucosa, resulting in a potentiation of glucose-stimulated insulin secretion (GSIS) and control of