Published online Mar 20, 2024. doi: 10.5662/wjm.v14.i1.89723
Peer-review started: November 10, 2023
First decision: December 17, 2023
Revised: December 26, 2023
Accepted: February 18, 2024
Article in press: February 18, 2024
Published online: March 20, 2024
Processing time: 117 Days and 20.5 Hours
Excessive saturated fat intake compromises the integrity of the intestinal mucosa, leading to low-grade inflammation, impaired mucosal integrity, and increased intestinal permeability, resulting in the migration of lipopolysaccharide (LPS) to other tissues.
To evaluate the chronic effects (at 10 and 16 wk) of a high-fat diet (HFD) (with 50% energy as fat) on the phylogenetic gut microbiota distribution and intestinal barrier structure and protection in C57BL/6 mice.
Forty adult male mice were divided into four nutritional groups, where the letters refer to the type of diet (control and HFD or HF) and the numbers refer to the period (in weeks) of diet administration: Control diet for 10 wk, HFD for 10 wk, control diet for 16 wk, and HFD for 16 wk. After sacrifice, biochemical, molecular, and stereological analyses were performed.
The HF groups were overweight, had gut dysbiosis, had a progressive decrease in occludin immunostaining, and had increased LPS concentrations. Dietary progression reduced the number of goblet cells per large intestine area and Mucin2 expression in the HF16 group, consistent with a completely disarranged intestinal ultrastructure after 16 wk of HFD intake.
Chronic HFD intake causes overweight, gut dysbiosis, and morphological and functional alterations of the intestinal barrier after 10 or 16 wk. Time-dependent reductions in goblet cell numerical density and mucus production have emerged as targets for countering obesity-driven intestinal damage.
Core Tip: There is great interest in the scientific community in the impact of unhealthy eating habits, such as excess saturated fatty acid intake, on the gut microbiota composition and metabolic disease onset. Here, we evaluated the progressive changes in the intestinal structural barrier and gut microbiota composition in mice fed a high-fat diet (HFD) for 10 or 16 wk. HFD administration resulted in gut dysbiosis, compensatory enhancement of goblet cell numerical density, and increased Mucin2 expression after 10 wk. Continuous feeding reduced the goblet cell number and the expression of Mucin2 and occludin, consistent with the impaired tight junction ultrastructure in the chronically obese HFD-fed mice after 16 wk.