Nutrients handling after bariatric surgery, the role of gastrointestinal adaptation

Abstract

Bariatric surgery determines a rearrangement of the gastrointestinal tract that influences nutrient handling and plays a role in the metabolic changes observed after surgery. Most of the changes depend on the accelerated gastric emptying observed in Roux-en-Y gastric bypass (RYGB) and, to a lesser extent, in sleeve gastrectomy (SG). The rapid delivery of meal into the jejunum, particularly after RYGB, contributes to the prompt appearance of glucose in peripheral circulation. Glucose increase is the principal determinant of GLP-1 increase with the consequent stimulation of insulin secretion, the latter balanced by a paradoxical glucagon increase that stimulates EGP to prevent hypoglycaemia. Protein digestion and amino acid absorption appear accelerated after RYGB but not after SG. After RYGB, the adaptation of the gut to the new condition participates to the metabolic change. The intestinal transit is delayed, the gut microbioma is changed, the epithelium becomes hypertrophic and increases the expression of glucose transporter and of the number of cell secreting hormones. These changes are not observed after SG. After RYGB-less after SG-bile acids (BA) increase, influencing glucose metabolism probably modulating FXR and TGR5 with an effect on insulin sensitivity. Muscle, hepatic and adipose tissue insulin sensitivity improve, and the gut reinforces the recovery of IS by enhancing glucose uptake and through the effect of the BA. The intestinal changes observed after RYGB result in a light malabsorption of lipid but not of carbohydrate and protein. In conclusion, functional and morphological adaptations of the gut after RYGB and SG activate inter-organs cross-talk that modulates the metabolic changes observed after surgery.Level of evidence Level V, narrative literature review.

Keywords: Bariatric surgery; Gastrointestinal adaptation; Glucose disposal; Insulin sensitivity; Nutrients handling; Obesity.

Fig. 1

The table summarizes anatomic and functional changes in gastrointestinal tract after RYGB and SG. ↑: increased; ↓: decreased; ↔ unchanged; n/a: the information is unavailable or not found

Fig. 2

Principal determinants of postmeal plasma glucose profile after RYGB. OrGlu-Ra rate of oral glucose appearance, GLP-1 glucagon like peptide-1, INS plasma insulin, INS/GLUC molar ratio from insulin secretion values and plasma glucagon during the postmeal period, EGP endogenous glucose production. The red line in the lower part of the figure describes the temporal pattern of plasma glucose after glucose ingestion in patients after RYGB. In the upper part of the figure are described the principal determinants of the post meal glucose excursion. The temporal pattern of post meal plasma glucose after RYGB is mainly the result of the altered delivery of the ingested glucose into the systemic circulation, due to an accelerated gastric emptying and increased glucose absorption. The accelerated gastric emptying causes an abnormal increase in the GLP-1 release in response to a meal which contributes to increased insulin secretion. The consequent increase in the insulin to glucagon molar ratio (INS/GLUC) determines the suppression of EGP with the consequent tendency to hypoglycemia observed 2 h after glucose ingestion. After the peak at the first hour after the meal, the INS/GLUC drops rapidly in phase with the reduction of plasma glucose with a consequent increase of EGP that is critical to prevent post prandial hypoglycaemia