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
There is great interest in the scientific community in the role of gut dysbiosis in obesity and metabolic impairments. However, there is little evidence in the literature on the progressive impact of a high-fat diet (HFD) on mouse intestinal barrier structure and microbiota composition.
Recently, different dietary models and durations of diet administration have yielded controversial results regarding the QA (goblet cells), mucus layer, and microbiota composition in mice with diet-induced obesity. Considering the importance of understanding the progressive changes in intestinal structure and microbiota composition that occur during obesity onset, we examined these changes after 10 or 16 wk of HFD feeding to establish tools to characterize obesity-related intestinal impairments.
We further studied the chronic effects (at 10 and 16 wk) of an HFD (with 50% energy as fat) on the phylogenetic gut microbiota distribution and intestinal barrier structure and protection in C57BL/6 mice. The study considered the mouse model, diet composition, and duration of intervention that were most prevalent in the literature.
Mice were fed ad libitum, and food intake and body mass gain were monitored during the experiment. Intestinal samples were subjected to light and electron microscopy, and plasma lipopolysaccharide concentrations were determined through ELISA. After 16S rRNA gene amplification by qPCR was performed on the frozen cecal feces to determine the phylogenetic microbiota distribution, the ileum samples were subjected to qPCR analysis for Occludin expression.
Our results confirmed that body mass increased gradually with HFD feeding without altering food intake. Dysbiosis in the HFD model involved an increase in Firmicutes and a decrease in Bacteroidetes concomitant with an increase in plasma lipopolysaccharide concentrations, so-called endotoxemia. The original findings were compensatory goblet cell hyperplasia and increased Mucin2 expression in the tenth week, followed by a drastic reduction in both parameters after 16 wk of HFD feeding. These structural alterations were consistent with the progressive damage to the intestinal ultrastructure in obese mice.
Chronic HFD intake causes gut dysbiosis and endotoxemia, with time-dependent overweight, and morphological and functional alterations of the intestinal barrier after 10 or 16 wk. We identified QA (goblet cells) and mucin expression as viable tools to address the progressive damage caused by obesity in the intestine.
The evaluation of QA (goblet cells), functionality, and ultrastructure has led to the identification of potential targets for addressing the impact of excessive saturated fatty acid intake on the intestine.