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Nicole G Barra Department of Biochemistry and Biomedical Sciences, Department of Biochemistry and Biomedical Sciences, Farncombe Family Digestive Health Research Institute, Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada

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Fernando F Anhê Department of Biochemistry and Biomedical Sciences, Department of Biochemistry and Biomedical Sciences, Farncombe Family Digestive Health Research Institute, Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada

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Joseph F Cavallari Department of Biochemistry and Biomedical Sciences, Department of Biochemistry and Biomedical Sciences, Farncombe Family Digestive Health Research Institute, Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada

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Anita M Singh Department of Biochemistry and Biomedical Sciences, Department of Biochemistry and Biomedical Sciences, Farncombe Family Digestive Health Research Institute, Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada

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Darryl Y Chan Department of Biochemistry and Biomedical Sciences, Department of Biochemistry and Biomedical Sciences, Farncombe Family Digestive Health Research Institute, Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada

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Jonathan D Schertzer Department of Biochemistry and Biomedical Sciences, Department of Biochemistry and Biomedical Sciences, Farncombe Family Digestive Health Research Institute, Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada

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excess status linked to T2DM Supplementation:  ↓BW, adiposity, liver weight  ↑blood thyroid hormone (TSH, TT3, FT3, FT4) High I dose:  Pancreatic destruction, hyperglycemia  Impair beta cell insulin secretion, apoptosis Selenium (Se) Male: 55 µg

Article Type:
Review Article
Collections:
Gut microbiome special collection, Top-cited articles of 2023
DOI:
https://doi.org/10.1530/JOE-21-0081
Volume/Issue:
Volume 250: Issue 2
Free access
Marion Régnier UCLouvain, Université Catholique de Louvain, WELBIO – Walloon Excellence in Life Sciences and BIOtechnology, Louvain Drug Research Institute, Metabolism and Nutrition Research Group, Brussels, Belgium

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Matthias Van Hul UCLouvain, Université Catholique de Louvain, WELBIO – Walloon Excellence in Life Sciences and BIOtechnology, Louvain Drug Research Institute, Metabolism and Nutrition Research Group, Brussels, Belgium

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Claude Knauf Université Paul Sabatier, Toulouse III, INSERM U1220, Institut de Recherche en Santé Digestive (IRSD), CHU Purpan, Place du Docteur Baylac, Toulouse Cedex 3, France
European Associated Laboratory (EAL) ‘NeuroMicrobiota’, Brussels/Toulouse, Belgium

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Patrice D Cani UCLouvain, Université Catholique de Louvain, WELBIO – Walloon Excellence in Life Sciences and BIOtechnology, Louvain Drug Research Institute, Metabolism and Nutrition Research Group, Brussels, Belgium
European Associated Laboratory (EAL) ‘NeuroMicrobiota’, Brussels/Toulouse, Belgium

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intestinal homeostasis (gut microbiota composition and gut barrier function) directly or indirectly (via microbial-produced metabolites) disturbs the production and secretion of gut endocrine hormones, thereby triggering metabolic diseases ( Fig. 2 ). The

Article Type:
Review Article
Collections:
Gut microbiome special collection, Top-cited articles of 2023
DOI:
https://doi.org/10.1530/JOE-20-0473
Volume/Issue:
Volume 248: Issue 2
Free access