Abstract
With the epidemic of human obesity, dietary fats have increasingly become a focal point of biomedical research. Epidemiological studies indicate that high-fat diets (HFDs), especially those rich in long-chain saturated fatty acids (e.g., Western Diet, National Health Examination survey; NHANES ‘What We Eat in America’ report) have multi-organ pro-inflammatory effects. Experimental studies have confirmed some of these disease associations, and have begun to elaborate mechanisms of disease induction. However, many of the observed effects from epidemiological studies appear to be an over-simplification of the mechanistic complexity that depends on dynamic interactions between the host, the particular fatty acid, and the rather personalized genetics and variability of the gut microbiota. Of interest, experimental studies have shown that certain saturated fats (e.g., lauric and myristic fatty acid-rich coconut oil) could exert the opposite effect; that is, desirable anti-inflammatory and protective mechanisms promoting gut health by unanticipated pathways. Owing to the experimental advantages of laboratory animals for the study of mechanisms under well-controlled dietary settings, we focus this review on the current understanding of how dietary fatty acids impact intestinal biology. We center this discussion on studies from mice and rats, with validation in cell culture systems or human studies. We provide a scoping overview of the most studied diseases mechanisms associated with the induction or prevention of Inflammatory Bowel Disease in rodent models relevant to Crohn’s Disease and Ulcerative Colitis after feeding either high-fat diet (HFD) or feed containing specific fatty acid or other target dietary molecule. Finally, we provide a general outlook on areas that have been largely or scarcely studied, and assess the effects of HFDs on acute and chronic forms of intestinal inflammation.
Highlights
Many regions of the world are currently affected by an epidemic of obesity and chronic inflammatory disease in humans, which has been, in part, attributed to excessive dietary fat intake [1]
Various rodent models have an increased susceptibility to chronic intestinal inflammation, which worsens with highfat diet (HFD) [11, 12], by immunological mechanisms that resemble human inflammatory bowel disease (IBD) pathogenesis (e.g., cytokines IL-1b and TNFa, monocyte chemoattractant protein-1 (MCP1), and keratinocyte-derived chemokines) [12]
This study was based on a scoping review of published evidence conducted by our group to assess the effects of dietary fats on IBDs in laboratory rodents, and the mechanisms associated with the observed clinical effects on the animal gut
Summary
Many regions of the world are currently affected by an epidemic of obesity and chronic inflammatory disease in humans, which has been, in part, attributed to excessive dietary fat intake [1]. In the United States, a ‘Western’ diet which is characteristically high in fat, saturated fats, symbolizes the link between increased availability of fast food diets and public health risk for inflammatory diseases [1,2,3]. Various rodent models have an increased susceptibility to chronic intestinal inflammation, which worsens with HFDs [11, 12], by immunological mechanisms that resemble human IBD pathogenesis (e.g., cytokines IL-1b and TNFa, monocyte chemoattractant protein-1 (MCP1), and keratinocyte-derived chemokines) [12]. This review seeks to summarize proposed mechanisms of disease modulation by dietary FAs, with the ultimate objective to compile peerreviewed evidence on the mechanisms that could trigger divergent pro- and anti-inflammatory responses
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