Yasaman Ghorbani1,2, Katherine J P Schwenger2, Johane P Allard3,4,5,6,7. 1. Institute of Medical Science, University of Toronto, Toronto, ON, Canada. 2. Toronto General Hospital, University Health Network, Toronto, Canada. 3. Institute of Medical Science, University of Toronto, Toronto, ON, Canada. Johane.allard@uhn.on.ca. 4. Toronto General Hospital, University Health Network, Toronto, Canada. Johane.allard@uhn.on.ca. 5. Department of Nutritional Sciences, University of Toronto, Toronto, Canada. Johane.allard@uhn.on.ca. 6. Department of Medicine, University of Toronto, Toronto, Canada. Johane.allard@uhn.on.ca. 7. Department of Medicine, Division of Gastroenterology, Toronto General Hospital, 585 University Avenue, 9N-973, Toronto, ON, M5G 2N2, Canada. Johane.allard@uhn.on.ca.
Abstract
PURPOSE: Increasing evidence suggests that the intestinal microbiome (IM) and bacterial metabolites may influence glucose homeostasis, energy expenditure and the intestinal barrier integrity and lead to the presence of systemic low-grade inflammation, all of which can contribute to insulin resistance (IR) and type 2 diabetes (T2D). The purpose of this review is to explore the role of the IM and bacterial metabolites in the pathogenesis and treatment of these conditions. RESULTS: This review summarizes research focused on how to modulate the IM through diet, prebiotics, probiotics, synbiotics and fecal microbiota transplant in order to treat IR and T2D. CONCLUSION: There is an abundance of evidence suggesting a role for IM in the pathogenesis of IR and T2D based on reviewed studies using various methods to modulate IM and metabolites. However, the results are inconsistent. Future research should further assess this relationship.
PURPOSE: Increasing evidence suggests that the intestinal microbiome (IM) and bacterial metabolites may influence glucose homeostasis, energy expenditure and the intestinal barrier integrity and lead to the presence of systemic low-grade inflammation, all of which can contribute to insulin resistance (IR) and type 2 diabetes (T2D). The purpose of this review is to explore the role of the IM and bacterial metabolites in the pathogenesis and treatment of these conditions. RESULTS: This review summarizes research focused on how to modulate the IM through diet, prebiotics, probiotics, synbiotics and fecal microbiota transplant in order to treat IR and T2D. CONCLUSION: There is an abundance of evidence suggesting a role for IM in the pathogenesis of IR and T2D based on reviewed studies using various methods to modulate IM and metabolites. However, the results are inconsistent. Future research should further assess this relationship.
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