Trans Fatty Acid Intake Induces Intestinal Inflammation and Impaired Glucose Tolerance

Front Immunol. 2021 Apr 29;12:669672. doi: 10.3389/fimmu.2021.669672. eCollection 2021.

Abstract

Background and aims: Many nutritional and epidemiological studies have shown that high consumption of trans fatty acids can cause several adverse effects on human health, including cardiovascular disease, diabetes, and cancer. In the present study, we investigated the effect of trans fatty acids on innate immunity in the gut by observing mice fed with a diet high in trans fatty acids, which have been reported to cause dysbiosis.

Methods: We used C57BL6/J mice and fed them with normal diet (ND) or high-fat, high-sucrose diet (HFHSD) or high-trans fatty acid, high-sucrose diet (HTHSD) for 12 weeks. 16S rRNA gene sequencing was performed on the mice stool samples, in addition to flow cytometry, real-time PCR, and lipidomics analysis of the mice serum and liver samples. RAW264.7 cells were used for the in vitro studies.

Results: Mice fed with HTHSD displayed significantly higher blood glucose levels and advanced fatty liver and intestinal inflammation, as compared to mice fed with HFHSD. Furthermore, compared to mice fed with HFHSD, mice fed with HTHSD displayed a significant elevation in the expression of CD36 in the small intestine, along with a reduction in the expression of IL-22. Furthermore, there was a significant increase in the populations of ILC1s and T-bet-positive ILC3s in the lamina propria in mice fed with HTHSD. Finally, the relative abundance of the family Desulfovibrionaceae, which belongs to the phylum Proteobacteria, was significantly higher in mice fed with HFHSD or HTHSD, than in mice fed with ND; between the HFHSD and HTHSD groups, the abundance was slightly higher in the HTHSD group.

Conclusions: This study revealed that compared to saturated fatty acid intake, trans fatty acid intake significantly exacerbated metabolic diseases such as diabetes and fatty liver.

Keywords: ILC; gut microbiota; innate lymphoid cells; small intestine; trans fatty acid.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Glucose / drug effects*
  • Blood Glucose / metabolism
  • CD36 Antigens / metabolism
  • Diet, High-Fat / adverse effects*
  • Dietary Sucrose / toxicity
  • Dysbiosis
  • Enteritis / chemically induced*
  • Enteritis / immunology
  • Enteritis / metabolism
  • Enteritis / microbiology
  • Gastrointestinal Microbiome / drug effects
  • Glucose Intolerance / blood
  • Glucose Intolerance / chemically induced*
  • Glucose Intolerance / immunology
  • Immunity, Innate / drug effects*
  • Interleukins / metabolism
  • Intestine, Small / drug effects*
  • Intestine, Small / immunology
  • Intestine, Small / metabolism
  • Intestine, Small / microbiology
  • Liver / drug effects
  • Liver / immunology
  • Liver / metabolism
  • Lymphocytes / drug effects*
  • Lymphocytes / immunology
  • Lymphocytes / metabolism
  • Macrophages / drug effects
  • Macrophages / immunology
  • Macrophages / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Non-alcoholic Fatty Liver Disease / chemically induced
  • Non-alcoholic Fatty Liver Disease / immunology
  • Non-alcoholic Fatty Liver Disease / metabolism
  • RAW 264.7 Cells
  • Trans Fatty Acids / toxicity*

Substances

  • Blood Glucose
  • CD36 Antigens
  • Cd36 protein, mouse
  • Dietary Sucrose
  • Interleukins
  • Trans Fatty Acids
  • interleukin-22

Associated data

  • figshare/10.6084/m9.figshare.14370035.v1