title: Gluten-Free Diet Only during Pregnancy Efficiently Prevents Diabetes in NOD Mouse Offspring.
abstract: Studies have documented that the pathogenesis of autoimmune diabetes is influenced by the intake of gluten. Aims. To investigate the importance of gluten exposure during pregnancy and the subsequent development of autoimmune diabetes in offspring. Methods. Nonobese diabetic mice were divided into 7 groups to receive combinations of gluten-free and standard diet before, during, or after pregnancy. Diabetes incidence in offspring was followed in each group (n = 16-27) for 310 days. Insulitis score and intestinal expression of T-cell transcription factors (RT-QPCR) were evaluated in animals from the different diet groups. Results. If mothers were fed a gluten-free diet only during pregnancy, the development of autoimmune diabetes in offspring was almost completely prevented with an incidence reduction from 62.5% in gluten-consuming mice to 8.3% (p < 0.0001) in the gluten-free group. The islets of Langerhans were less infiltrated (p < 0.001) and the intestinal expression of RORγt (Th17) (p < 0.0001) reduced in mice whose mothers were Gluten-free during pregnancy. Conclusion. A gluten-free diet exclusively during pregnancy efficiently prevents autoimmune diabetes development in offspring and reduces insulitis and intestinal expression of RORγt (Th17).
authors.affiliation: The Bartholin Institute, Rigshospitalet, 2200 Copenhagen, Denmark.
authors.forename: Julie C
authors.identifier: 0000-0003-2618-6301
authors.initials: JC
authors.lastname: Antvorskov
authors.affiliation: The Bartholin Institute, Rigshospitalet, 2200 Copenhagen, Denmark.
authors.forename: Knud
authors.identifier: 0000-0002-5093-2901
authors.initials: K
authors.lastname: Josefsen
authors.affiliation: The Bartholin Institute, Rigshospitalet, 2200 Copenhagen, Denmark.
authors.forename: Martin
authors.identifier: 0000-0003-4088-5862
authors.initials: M
authors.lastname: Haupt-Jorgensen
authors.affiliation: The Bartholin Institute, Rigshospitalet, 2200 Copenhagen, Denmark; Laboratory of Specific Cellular Immunity, Institute of Microbiology ASCR, 54922 Prague, Czech Republic.
authors.forename: Petra
authors.identifier: 0000-0001-5261-6091
authors.initials: P
authors.lastname: Fundova
authors.affiliation: The Bartholin Institute, Rigshospitalet, 2200 Copenhagen, Denmark; Laboratory of Specific Cellular Immunity, Institute of Microbiology ASCR, 54922 Prague, Czech Republic.
authors.forename: David P
authors.identifier: 0000-0001-8327-6931
authors.initials: DP
authors.lastname: Funda
authors.affiliation: The Bartholin Institute, Rigshospitalet, 2200 Copenhagen, Denmark.
authors.forename: Karsten
authors.identifier: 0000-0002-0126-7423
authors.initials: K
authors.lastname: Buschard
mesh_terms: D000818:Animals; D003922:Diabetes Mellitus, Type 1 / Q000178:diet therapy* / Q000276:immunology / Q000517:prevention & control; D055050:Diet, Gluten-Free / Q000379:methods*; D005260:Female; D007413:Intestinal Mucosa / Q000378:metabolism; D007515:Islets of Langerhans / Q000276:immunology / Q000473:pathology; D051379:Mice; D016688:Mice, Inbred NOD; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics; D010195:Pancreatitis / Q000276:immunology / Q000473:pathology; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000178:diet therapy*; D012333:RNA, Messenger / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051820:TCF Transcription Factors / Q000235:genetics
chemical_list: D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D012333:RNA, Messenger; D051820:TCF Transcription Factors