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1-Kestose supplementation mitigates the progressive deterioration of glucose metabolism in type 2 diabetes OLETF rats.
- Source :
-
Scientific reports [Sci Rep] 2020 Sep 24; Vol. 10 (1), pp. 15674. Date of Electronic Publication: 2020 Sep 24. - Publication Year :
- 2020
-
Abstract
- The fructooligosaccharide 1-kestose cannot be hydrolyzed by gastrointestinal enzymes, and is instead fermented by the gut microbiota. Previous studies suggest that 1-kestose promotes increases in butyrate concentrations in vitro and in the ceca of rats. Low levels of butyrate-producing microbiota are frequently observed in the gut of patients and experimental animals with type 2 diabetes (T2D). However, little is known about the role of 1-kestose in increasing the butyrate-producing microbiota and improving the metabolic conditions in type 2 diabetic animals. Here, we demonstrate that supplementation with 1-kestose suppressed the development of diabetes in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, possibly through improved glucose tolerance. We showed that the cecal contents of rats fed 1-kestose were high in butyrate and harbored a higher proportion of the butyrate-producing genus Anaerostipes compared to rats fed a control diet. These findings illustrate how 1-kestose modifications to the gut microbiota impact glucose metabolism of T2D, and provide a potential preventative strategy to control glucose metabolism associated with dysregulated insulin secretion.
- Subjects :
- Animals
Body Weight drug effects
C-Peptide blood
Cecum drug effects
Cecum microbiology
Cecum pathology
Diabetes Mellitus, Type 2 microbiology
Diabetes Mellitus, Type 2 pathology
Disease Models, Animal
Drinking drug effects
Fasting blood
Gastrointestinal Microbiome drug effects
Insulin blood
Organ Size drug effects
Rats
Blood Glucose metabolism
Diabetes Mellitus, Type 2 blood
Disease Progression
Glucose metabolism
Trisaccharides pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 2045-2322
- Volume :
- 10
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Scientific reports
- Publication Type :
- Academic Journal
- Accession number :
- 32973311
- Full Text :
- https://doi.org/10.1038/s41598-020-72773-2