Baker's yeast (1→3)-β-D-glucan Influences Insulin Sensitivity in Mice with Humanized Obese Diabetic Microbiome in High-Fat Diet-Induced Obesity. (2020)

• Record Type: Journal Article
• Authors: Mitchelson, Kathleen A. J.; de Marco Castro, Elena; Hueston, Cara M.; Lynch, Gina M.; Keogh, Elaine A.; Tran, Tam T.T.; Vlckova, Klara; Roche, Helen M.; O'Toole, Paul W.
• Is Part Of: Proceedings of the Nutrition Society. Volume 79(2020)Supplement OCE2
• Publication Date: 2020
• Subjects: Nutrition -- Congresses; 612.30993
• DOI: 10.1017/S0029665120005765
• Languages: English
• ISSNs: 0029-6651

Abstract

Abstract : Abstract: Introduction: β-glucans are naturally occurring polysaccharides which have isoform specific immunomodulatory and metabolic properties (1 ) . Certain yeast (1→3)-β-D-glucan isoforms improve cholesterol (2 ), glucose (3 ) and lipid homeostasis (4 ) . Feeding (1→3)-β-D-glucan alters the microbiome of high-fat diet (HFD) induced obese (DIO)/type 2 diabetic (T2D) mice (5 ) . Here we investigated the potential impact of baker's yeast (1→3)-β-D-glucan in mice humanized with gut microbiomes from either obese healthy versus obese diabetic subjects on immune-metabolism within the context of high-fat feeding. Methods: C57Bl/6J male mice received an antibiotic cocktail of Ampicillin, Metronidazole, Vancomycin, Imipenem and Ciprofloxacin HCl in their drinking water for 6 weeks to diminish the endogenous gut microbiota. Mice were inoculated with microbiota samples obtained from obese healthy (OBH) or diabetic (OBD) humans twice daily for 3 days by oral dosing. Mice were fed a low-fat diet (LFD) (10% kcal) for 4 weeks followed by HFD (45% kcal) with/without baker's yeast (1→3)-β-D-glucan (βG), for 9 weeks. Weight, feed intake, glucose tolerance (1.5g/kg), insulin tolerance (0.5U/kg), hepatic and skeletal lipid levels were examined. Tissue specific molecular markers of metabolism and inflammation, and gut microbiome analysis are being determined to compliment the phenotypic data. Results: OBH mice were more glucose tolerant and insulin sensitive than OBD mice, despite equal weight gain and adipose tissue mass. Fasting HOMA-IR, attributable to higher insulin concentrations, was higher in OBD compared to OBH mice. βG supplementation reduced HOMA-IR in OBD mice (P < 0.0611). Hepatic triacylglycerol (TAG) and cholesterol levels were also higher in OBD mice, which were prevented by βG supplementation. Hepatic proteomic, caecal microbiomic and metabolomic analysis is on-going in order to ascertain the impact of the OBD versus OBH dysbosis with/without βG supplementation with specific attention on immune-metabolism.