Prior High Fiber Intake Impinges on the Cellular Responses of Mesenteric Adipose and Intestinal Tissues to Subsequent High Fat Feeding [16s rRNA-seq]
Obesity, characterized by its chronic, recurrent and progressive nature, has become one of the most serious public health problems. As living standards improve, plant-based diet composed of whole grain and vegetable is gradually replaced by high-fat food of animal origin in daily life. The resulting increase in caloric intake is one of the major causes of obesity. In white adipose tissue, excessive calorie intake promotes adipocyte hypertrophy and hyperplasia, increases immune cell infiltration around dysfunctional adipocytes and causes rearrangement of adipocyte subpopulations. In intestinal tissue, obesity development is associated with activation of the gut microbiota to process indigestible dietary polysaccharides into short-chain fatty acid (SCFA) for intestinal absorption. At the cellular level, a high-fat/high-sugar diet induces excessive proliferation and differentiation of intestinal stem cells, leading to onset of intestinal maladaptation and obesity development. In addition, several studies have shown that a high-fat diet (HFD) can affect the enteric nervous system in multiple aspects, including neuronal density, expression of glial cell marker proteins, and ganglion size. A recent study shows that enteric glial cells play a key role in maintaining the homeostasis of the intestinal stem cell niche. Overall design: We collected fecal samples from the two diet groups at the three time points for 16S sequencing to compare the temporal dynamics of the gut microbiome.