1-kestose and Disease-Models--Animal

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.

Topics: Animals; Blood Glucose; Body Weight; C-Peptide; Cecum; Diabetes Mellitus, Type 2; Disease Models, Animal; Disease Progression; Drinking; Fasting; Gastrointestinal Microbiome; Glucose; Insulin; Organ Size; Rats; Trisaccharides

Atopic dermatitis (AD) is recently increasing among populations, but the underlying mechanisms remain controversial. Interactions between the gut microbiota and mucosal immunity are considered to be a crucial etiology. Fructooligosaccharide (FOS), prebiotics have been reported as activators of the gut microbiota.. The aim of this study was to investigate the effects of kestose, the smallest FOS and FOS on atopic dermatitis in mice.. An AD mouse model was developed by (ovalbumin) epidermal sensitization using BALB/c mice. Kestose (1%, 5%, and 10%) or FOS (5%, positive control) was orally administered throughout the study.. In comparison with the values observed for the control AD mice, transepidermal water loss (TEWL), clinical score, and skin inflammation on histopathology were significantly decreased by the oral administration of kestose. Total IgE, thymic stromal lymphopoietin (TSLP) in skin, and IL-4 were also suppressed by this administration. In addition, the population of CD4. These findings suggest that kestose activates the gut immune system to induce the tolerance against allergic skin inflammations in AD.

Topics: Animals; CD4-Positive T-Lymphocytes; Dermatitis, Atopic; Disease Models, Animal; Epidermis; Female; Food Hypersensitivity; Gastrointestinal Microbiome; Humans; Immune Tolerance; Immunity, Mucosal; Intestinal Mucosa; Mice; Mice, Inbred BALB C; Ovalbumin; Trisaccharides