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The effects of obesity microbiota produced metabolites on colorectal carcinogenesis in murine models

ABSTRACT: Obesity is a risk factor for colorectal cancer (CRC). We aim to study the effects and mechanisms of gut microbiota of obese subjects in contributing to CRC progression. Conventional AOM-treated and ApcMin/+ mice receiving feces from obese individuals showed significantly increased colon tumor formation compared with those receiving feces from control subjects. AOM-treated mice receiving feces from obese (OB-M) exhibited microbiota dysbiosis with enriched potential pathobionts Erysipelotrichaceae bacterium GAM147, Turicibacter sp. H121, Mucinivorans hirudinis, and depleted symbionts Bacteroides vulgatus, Faecalibaculum rodentium, Bifidobacterium spp. and Lactobacillus delbrueckii. The OB-M group also showed altered gut metabolites including elevated phenylacetic acid, and depleted genipin. Moreover, OB-M group showed impaired intestinal barrier function and significant upregulation of pro-inflammatory cytokines and activation of oncogenic Wnt signaling pathway. In conclusion, gut microbiota from obese individuals promotes colorectal carcinogenesis. Microbiota modulation in obese individuals may provide new insight into obesity-driven CRC prevention and therapy.

ORGANISM(S): Mouse Mus Musculus

TISSUE(S): Feces

DISEASE(S): Cancer

SUBMITTER: Xing Kang

PROVIDER: ST002193 | MetabolomicsWorkbench | Wed May 18 00:00:00 BST 2022

REPOSITORIES: MetabolomicsWorkbench

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Project description:The expression of adipogenic genes is decreased in obesity and diabetes mellitus ; Samuel T. Nadler*, Jonathan P. Stoehr*, Kathryn L. Schueler*, Gene Tanimoto, Brian S. Yandell, and Alan D. Attie*,Â§ ; Departments of * Biochemistry, and Statistics and Horticulture, University of Wisconsin, Madison, WI, 53706; and Affymetrix, Inc., Santa Clara, CA 95051 ; Communicated by Neal L. First, University of Wisconsin, Madison, WI, July 13, 2000 (received for review April 3, 2000) ; Obesity is strongly correlated with type 2 diabetes mellitus, a common disorder of glucose and lipid metabolism. Although adipocytes are critical in obesity, their role in diabetes has only recently been appreciated. We conducted studies by using DNA microarrays to identify differences in gene expression in adipose tissue from lean, obese, and obese-diabetic mice. The expression level of over 11,000 transcripts was analyzed, and 214 transcripts showed significant differences between lean and obese mice. Surprisingly, the expression of genes normally associated with adipocyte differentiation were down-regulated in obesity. Not all obese individuals will become diabetic; many remain normoglycemic despite profound obesity. Understanding the transition to obesity with concomitant diabetes will provide important clues to the pathogenesis of type 2 diabetes. Therefore, we examined the levels of gene expression in adipose tissue from five groups of obese mice with varying degrees of hyperglycemia, and we identified 88 genes whose expression strongly correlated with diabetes severity. This group included many genes that are known to be involved in signal transduction and energy metabolism as well as genes not previously examined in the context of diabetes. Our data show that a decrease in expression of genes normally involved in adipogenesis is associated with obesity, and we further identify genes important for subsequent development of type 2 diabetes mellitus. Experiment Overall Design: For obesity study, lean samples include C57BL/6J lean, (C57BL/6J X BTBR) F1 and BTBR lean, obese sampples incluse C57BL/6J-ob/ob, (C57BL/6J X BTBR) F2-ob/ob and BTBR-ob/ob. All samples are subjected to Mu11K A and B arrays. Experiment Overall Design: For diabetes study, B6-ob/ob, (C57BL/6J X BTBR) F2-ob/ob low glucose, (C57BL/6J X BTBR) F2-ob/ob medium glucose, (C57BL/6J X BTBR) F2-ob/ob high glucose, and BTBR-ob/ob samples were analyzed for genes whose expression levels changes correlated with the plasma glucose levels in these mice. All samples are subjected to Mu11K A and B arrays.

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The effects of obesity microbiota produced metabolites on colorectal carcinogenesis in murine models

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