Ric intake of Fut2-/mice to create it equal towards the caloric intake of WT mice for the duration of Western diet feeding for 20 weeks. Calorie-restricted Fut2-/mice were totally protected from characteristics from the metabolic syndrome as evidenced by reduce physique μ Opioid Receptor/MOR Source weight and brown adipose tissue, enhanced insulin sensitivity, and reduced levels of plasma cholesterol and leptin than Fut2-/- mice with unrestricted access to a Western diet plan (Figures 4A and 5A). There was no difference in fecal lipid content throughout Western diet plan feeding, indicating that Fut2-/- mice have similar levels of intestinal lipid absorption (Figure 5B). We compared the metabolic rates of WT and Fut2-/- mice on various diets, and no distinction was found in controlZhou et alCellular and Molecular Gastroenterology and Hepatology Vol. 12, No.Intestinal Fucosylation in SteatohepatitisFigure 3. Intestinal a1-2-fucosylation in manage and Western diet plan ed mice. Fut2-/- and WT littermates were fed with either a control diet program or a Western diet regime for 20 weeks. To facilitate fecal microbiota transfer we performed co-housing by feeding WT and Fut2-/- mice inside 1 cage given that weaning, and these mice were offered a Western diet plan. Representative images of colon tissues with immunohistochemistry staining for a1-2-fucosylated glycans (with Ulex Europaeus Agglutinin I) are shown. Experiments had been performed in n six from 2 experiments.diet plan ed mice. In Western diet ed mice, oxygen consumption (VO2) and carbon dioxide production (VCO2) rate had been slightly larger in Fut2-/- compared with WT mice (Figure 6A). Western eating plan ed Fut2-/- mice had a greater respiratory exchange ratio, power expenditure, and more vertical activity compared with WT mice (Figures 4F and 6A). These variations were far more obvious throughout the dark cycles (Figure 6A) compared with the light cycles (Figure 6B), that is consistent with enhanced nocturnal activity of mice. In line with improved power expenditure, Western eating plan ed Fut2-/- mice generated additional heat, with a considerably greater core physique p38β drug temperature (Figure 4G). An enhanced protein amount of uncoupling protein 1 (Ucp1) in brown adipose tissue (Figure 4H) indicates augmented nonshivering thermogenesis in Western diet program ed Fut2-/mice compared with WT mice. Taken together, Futdeficiency increases power expenditure and thermogenesis in brown adipose tissue, which could possibly contribute to protection from Western diet program nduced obesity.Fut2 Deficiency Attenuates Western Diet regime nduced SteatohepatitisTo assess the role of Fut2 for the development of steatohepatitis, we investigated parameters of liver injury, steatosis, inflammation, and fibrosis. Western diet nduced liver injury as assessed by levels of ALT (Figure 7A) and hepatic steatosis as evaluated by liver weight, hepatic triglycerides, and H E staining (Figure 7B and C) had been reduced in Western diet program ed Fut2-/- mice compared with WT mice. Hepatic expression of inflammatory genes for example Tnfa and Ccl2 (Figure 7D), and genes associated with fibrosis like ActaFigure 2. (See prior web page). Western diet program feeding reduces intestinal a1-2-fucosylation in mice. WT C57BL/6 mice were fed with either manage diet program and standard water (manage eating plan groups) or Western diet program combined with glucose (18.9 g/L) and fructose (23.1 g/L) in drinking water (Western diet groups) for 20 weeks. (A) Expression of Fut2 mRNA in ileum and colon tissue. (B) Expression of Fut4 mRNA in ileum and colon tissue. (C) Expression of Fut8 mRNA in ileum and colon tissue. (D) Representative photos of colon.