Duodenal L cell density correlates with features of metabolic syndrome and plasma metabolites. Issue 5 (May 2018)

• Record Type: Journal Article
• Authors: van Baar, Annieke C G; Prodan, Andrei; Wahlgren, Camilla D; Poulsen, Steen S; Knop, Filip K; Groen, Albert K; Bergman, Jacques J; Nieuwdorp, Max; Levin, Evgeni
• Is Part Of: Endocrine connections. Volume 7:Issue 5(2018)
• Page Start: 673
• Page End: 680
• Publication Date: 2018-05
• Subjects: metabolic syndrome -- incretins -- enteroendocrine cells -- plasma metabolites -- machine-learning methodology; Endocrinology -- Periodicals; 616.4005
• DOI: 10.1530/EC-18-0094
• Languages: English
• ISSNs: 2049-3614

Abstract

Abstract : Background: Enteroendocrine cells are essential for the regulation of glucose metabolism, but it is unknown whether they are associated with clinical features of metabolic syndrome (MetS) and fasting plasma metabolites. Objective: We aimed to identify fasting plasma metabolites that associate with duodenal L cell, K cell and delta cell densities in subjects with MetS with ranging levels of insulin resistance. Research design and methods: In this cross-sectional study, we evaluated L, K and delta cell density in duodenal biopsies from treatment-naïve males with MetS using machine-learning methodology. Results: We identified specific clinical biomarkers and plasma metabolites associated with L cell and delta cell density. L cell density was associated with increased plasma metabolite levels including symmetrical dimethylarginine, 3-aminoisobutyric acid, kynurenine and glycine. In turn, these L cell-linked fasting plasma metabolites correlated with clinical features of MetS. Conclusions: Our results indicate a link between duodenal L cells, plasma metabolites and clinical characteristics of MetS. We conclude that duodenal L cells associate with plasma metabolites that have been implicated in human glucose metabolism homeostasis. Disentangling the causal relation between L cells and these metabolites might help to improve the (small intestinal-driven) pathophysiology behind insulin resistance in human obesity.