Discussion
Experimental bariatric surgery was performed to prevent weight gain. Studies in animals have shown that groups of rats or mice often gain weight over the observation period of a study36, and we consider this model to be efficient for experimental gastric restriction. Not only was weight gain prevented in the restrict group, but weight was lost in 10 days; a total of 4% of the initial weight. The control and sham groups gained weight over the 10-day study period; 11% and 5.2%, respectively, of the initial weight gained.
Regarding the inflammatory cells, polymorphonuclear cells were enhanced in all groups compared to lymphomononuclear cells, which was significant between the groups, showing inflammation compared to the control group but not different from the sham group. This inflammatory response probably occurred due to the presence of the phytobezoar, which may also have contributed to a decrease in the supply of nutrients to the intestines. To evaluate the evolution of this inflammatory response, it may be necessary to increase the time of exposure to the phytobezoar.
Experimental studies have shown a reduction in height of the colonic glands in the colonic mucosa devoid of the fecal stream26. The authors suggest that a lack of SCFA supply and the oxidative stress in the colonic mucosa without a fecal stream are the main factors associated with colonic gland atrophy. In this study, we found that after 10 days of gastric restriction, the height of the crypts in general decreased compared to the sham and control groups. This has also occurred in experimental models of diversion colitis, where food restriction due to a phytobezoar probably led to the atrophy of the colonic glands. Interestingly, no differences were seen in the number of goblet cells. Controversies exist regarding the population of cells in colonic segments devoid of the fecal stream37,38. It is possible that the different results found in relation to the goblet cell population in the colonic mucosa restricting the regular supply of SCFAs may be related to the different exclusion times adopted in the experiment durations of different studies22.
The major function of intestinal goblet cells is the formation of mucus layers, which represent the first line of defense in the colonic epithelium22,27. Intestinal mucus layers secreted by goblet cells are rich in mucins, which provide the frontline defense of the host against endogenous and exogenous irritants and microbial attachment and invasion, but allow the transport of nutrients24,25. In most intestinal infections, the induction of goblet cells and mucin synthesis and secretion occur frequently during the acute phase. However, chronic infection results in the depletion of goblet cells24,25,39. Neutral mucins were enhanced even though their goblet cells did not increase, although the height of the crypt became higher. Neutral mucins represent the main subtype of mucins in the right colon, and the content of this type of mucins usually undergoes minor modifications in the colonic mucosa without a regular supply of feces22. SCFAs are crucial for intestinal health because they serve as the major energy substrates for colonocytes and have anti-inflammatory and anti-carcinogenic properties40. Furthermore, under germfree conditions, neutral mucins in the colon are higher41. The proportions between neutral and acid mucins in rats also occur in men and are usually constant in the colonic mucosa42,43. However, the tissue content of acidic mucins can be modified with food restriction, which should influence how the nourishment of the colonic mucosa interferes with the production and absorption of SCFAs22,44. This feature may be associated with intestinal barrier dysfunction24,25,39,40,45,46. The tissue content of total acid mucins was not increased. The proportion between sulfomucins and sialomucins is usually constant in the mucosa of normal colon tissue, but may undergo changes in various illnesses41,46.
One study showed that in the colonic mucosa without a fecal stream, the tissue content of sialomucins decreased, and this reduction was related to the time of fecal exclusion27 . Gastric restriction substantially reduces the supply of fibers to the colon, thereby reducing the production of SCFAs26. This lower supply of SCFAs to the colonic mucosa, the main substrate for epithelial cells, causes less mucin production, as demonstrated by studies that measured the glycoprotein content in the colonic mucosa devoid of a fecal stream22,27. In this study, it is possible that we did not find modifications in the tissue content of sialomucins because a phytobezoar does not completely prevent the passage of SCFAs into the colon, thus maintaining a content of sialomucins similar to that of the sham group. Additionally, under germfree conditions, the ratio of neutral to acidic mucins in the colon is higher, and sulfomucins appear to increase at the expense of sialylated mucins48,-51. Similar to other authors who studied the tissue content of sialomucins in the colonic mucosa devoid of a fecal stream, we also found a lower expression of sialomucins and no difference in sulfomucins. It is likely that due to the incomplete absence of food, the acid mucins were not reshaped, but the goblet cells that express the sulfomucins were enhanced. This phenomenon could be triggered by the food restriction at the time. In general, trophism is conserved with the enhancement of neutral mucins. Collagen was enhanced in the restrict group, probably due to the inflammatory process triggered by gastric restriction.
To the best of our knowledge, no studies have quantified the expression patterns of acid and neutral mucins in an experimental model with gastric restriction.
Epithelial integrity, mucus production, and the presence and equilibrium of commensal bacteria interfere directly with the immunity of the intestinal barrier. The gastrointestinal epithelium is protected by a layer of mucus containing glycoprotein mucins secreted against the attack of digestive fluids, microorganisms, and toxins52. The integrity of the protective mucus layer is ensured by the rapid and massive secretion of goblet cells. Intestinal inflammation and injury result from a defective mucosal barrier, abnormal commensal bacteria, and defective host innate and adaptive immunitye53,54.
Overweight and obesity have reached epidemic levels in the United States and worldwide, affecting nearly three-fourths of adults in the United States55-57. Childhood obesity is one of the most serious global public health challenges of the 21st century, affecting every country in the world. In just 40 years, the number of school-age children and adolescents with obesity has risen more than 10-fold, from 11 million to 124 million (2016 estimates) (NCD Risk Factor Collaboration [NCD-RisC] 2017). In addition, in this same population, an estimated 216 million were classified as overweight but not obese in 2016 (NCD Risk Factor Collaboration [NCD-RisC] 2017).
The condition also affects younger children, with over 38 million children under the age of 5 living with overweight or obesity in 201758. Bariatric surgery is considered for patients with severe obesity57. This study contributes to assessing the impact of weight loss strategies and to the effectiveness and safety of gastric restriction therapy, which has been increasing worldwide.