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Maternal high‐fat diet consumption enhances offspring susceptibility to DSS‐induced colitis in mice
Objective Maternal high‐fat diet (HFD) may alter the offspring intestinal immune system, thereby enhancing susceptibility toward inflammatory bowel disease. The objective of the current study was to investigate the impact of maternal HFD on offspring intestinal health using a mouse model of dextran...
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Published in: | Obesity (Silver Spring, Md.) Md.), 2017-05, Vol.25 (5), p.901-908 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Objective
Maternal high‐fat diet (HFD) may alter the offspring intestinal immune system, thereby enhancing susceptibility toward inflammatory bowel disease. The objective of the current study was to investigate the impact of maternal HFD on offspring intestinal health using a mouse model of dextran sulfate sodium (DSS)‐induced colitis.
Methods
Dams were provided with either HFD (60%) or control diet. After weaning, female offspring from both groups were kept on 45% HFD. At 14 weeks of age, offspring were subjected to 2.5% DSS in drinking water for 5 days, followed by 5 days of recovery.
Results
Offspring from maternal HFD had higher body weight gain before DSS induction and had higher liver and fat weights with increased adipocyte size at necropsy. When subjected to DSS treatment, HFD offspring had accelerated body weight loss and exaggerated disease activity index. HFD offspring had an elevated histopathological score and interleukin (IL)‐1β, IL‐6, and IL‐17 expression with upregulated NF‐κB signaling. Maternal HFD resulted in enhanced neutrophil infiltration associated with elevated expression of monocyte chemoattractant protein‐1. Furthermore, maternal HFD suppressed AMP‐activated protein kinase activity and decreased sirtuin 1 and p53 protein contents in offspring gut.
Conclusions
Maternal HFD consumption predisposes offspring to a higher susceptibility to develop inflammatory bowel disease. |
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ISSN: | 1930-7381 1930-739X |
DOI: | 10.1002/oby.21816 |