Maternal obesity induces gut inflammation and impairs gut epithelial barrier function in nonobese diabetic mice |
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| Institution: | 1. School of Food Science, Washington State University, Pullman, WA 99164, USA;2. Department of Animal Science, University of Wyoming, Laramie, WY 82071, USA;3. Department of Animal Science, Washington State University, Pullman, WA 99164, USA;4. School of Food Science, University of Idaho, Moscow, ID 83844, USA;1. Department of Medicine, University of Florida, Gainesville, FL, United States;2. Department of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, United States;3. Department of Pharmaceutical Outcomes and Policy, University of Florida, Gainesville, FL, United States;4. Department of Medicine, Cleveland Clinic Foundation, Cleveland, OH, United States;5. Department of Medicine, Jefferson University Hospital/Christiana Care Health System, Newark, DE, United States;6. Department of Medicine, University of Iowa Carver College of Medicine, Iowa City, IA, United States;1. Department of Anatomy, Donders Institute for Brain, Cognition, and Behaviour, Radboud university medical center, Nijmegen, The Netherlands;2. Department of Geriatrics, Donders Institute for Brain, Cognition, and Behaviour, Radboud university medical center, Nijmegen, The Netherlands;3. Department of Radiology, Donders Institute for Brain, Cognition, and Behaviour, Radboud university medical centerr, Nijmegen, The Netherlands;4. Laboratory Medicine, University Medical Center Groningen, Groningen, The Netherlands;5. Mead Johnson Pediatric Nutrition Institute, Nijmegen/Evansville, The Netherlands/IN, USA;6. Department of Cognitive Neuroscience, Donders Institute for Brain, Cognition, and Behaviour, Radboud university medical center, Nijmegen, The Netherlands;1. Exercise Cell Biology Lab, Faculty of Applied Sciences, University of Campinas, Limeira, Brazil;2. Laboratory of Nutritional Genomics, Faculty of Applied Sciences, University of Campinas, Limeira, Brazil;3. Motricity Sciences, Institute of Biosciences, São Paulo State University Julio de Mesquita Filho, Rio Claro, SP, Brazil;4. Multidisciplinary Laboratory of Food and Health, Faculty of Applied Sciences, University of Campinas, Limeira, Brazil;5. School of Physical Education and Sport of Ribeirão Preto, University of São Paulo (USP), Ribeirão Preto, São Paulo, Brazil;6. Postgraduate Program in Rehabilitation and Functional Performance, Ribeirão Preto Medical School, USP, Ribeirão Preto, São Paulo, Brazil;7. Laboratory of Molecular Biology of Exercise, Faculty of Applied Sciences, University of Campinas, Limeira, Brazil |
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| Abstract: | Impairment of gut epithelial barrier function is a key predisposing factor for inflammatory bowel disease, type 1 diabetes (T1D) and related autoimmune diseases. We hypothesized that maternal obesity induces gut inflammation and impairs epithelial barrier function in the offspring of nonobese diabetic (NOD) mice. Four-week-old female NOD/ShiLtJ mice were fed with a control diet (CON; 10% energy from fat) or a high-fat diet (HFD; 60% energy from fat) for 8 weeks to induce obesity and then mated. During pregnancy and lactation, mice were maintained in their respective diets. After weaning, all offspring were fed the CON diet. At 16 weeks of age, female offspring were subjected to in vivo intestinal permeability test, and then ileum was sampled for biochemical analyses. Inflammasome mediators, activated caspase-1 and mature forms of interleukin (IL)-1β and IL-18 were enhanced in offspring of obese mothers, which was associated with elevated serum tumor necrosis factor α level and inflammatory mediators. Consistently, abundance of oxidative stress markers including catalase, peroxiredoxin-4 and superoxide dismutase 1 was heightened in offspring ileum (P<.05). Furthermore, offspring from obese mothers had a higher intestinal permeability. Morphologically, maternal obesity reduced villi/crypt ratio in the ileum of offspring gut. In conclusion, maternal obesity induced inflammation and impaired gut barrier function in offspring of NOD mice. The enhanced gut permeability in HFD offspring might predispose them to the development of T1D and other gut permeability-associated diseases. |
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