Maternal high-fat diet consumption enhances offspring susceptibility to DSS-induced colitis in mice.

Abstract

Objective:Maternal high fat diet (HFD) may alter the offspring intestinal immune system thereby enhancing susceptibility towards inflammatory bowel disease. The objective of current study was to investigate the impact of maternal HFD on offspring intestinal health using a mouse model of dextran sodium sulfate (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 elevated histopathological score, interleukin (IL)-1β, IL-6, and IL-17 expression with up-regulated NF-κB signaling. Maternal HFD resulted in enhanced neutrophil infiltration associated with elevated expression of monocyte chemoattractant protein-1 (MCP-1). Furthermore, maternal HFD suppressed AMP activated protein (AMPK) activity, and decreased sirtuin 1 (SIRT1) and p53 protein contents in offspring gut.Conclusion:Maternal HFD consumption predisposes offspring to a higher susceptibility of inflammatory bowel disease development.