**4. Conclusion**

may be attributed to accelerated intestinal transit. Fast transit results in accelerated glucose uptake, which causes increased insulin secretion. Accelerated transport of peptides and lipids gives an unusually large incentive to the secretion of cholecystokinin and stimulation of feedback regulation. In the end, there are abnormally high levels of gastrointestinal hormones and increased production of somatostatin. Excreted somatostatin has an inhibitory effect on GUT hormones, but this further reduces bowel motility and digestive juice production. This entire phenomenon becomes less significant in time due to the adaptation of the intestine [66]. Several studies have shown that the presence of postprandial hyperglycemia following TG reconstruction can indicate an abnormal glucose metabolism, possibly representing intolerance to glucose or diabetes at an early stage [43]. In relation to the type of RP, Schwarz and authors have found significantly higher levels of glucose in a patient with RY reconstruction, when there was no DP preservation in patients with pouch, as opposed to patients undergoing a RP in which DP was preserved. There was no development of pathological glucose tolerance in patients with established DP prevention [43]. Kalmár and authors have published significantly higher levels of postprandial glucose in patients with exclusion of DP RY reconstruction than the control group, thus supporting the hypothesis that the exclusion of DP disrupts homeostasis of glucose more than reconstruction with the preservation of DP [66]. Observing duodenal preservation, the glucose homeostasis disorder was significantly higher

With the standardization of TG performance due to GC, the survival period of operative patients has significantly increased and hence the possibility of postgastrectomy syndrome. The causes of the postgastrectomy syndrome can be hypocaloric food intake, exclusion of duodenal passage, loss of absorption surface, lack of peptic digestion, excessive bacterial colonization, and the occurrence of exocrine and endocrine pancreatic insufficiency [57]. Symptoms related to food intake due to abnormal transit reported in several studies relate to the onset of early and late dumping syndrome, alkaline reflux, pyrosis, loss of appetite, feeling of satiety and fullness, epigastric pain, meteorism, dysphagia, and diarrhea [67]. Schwarz and authors, as well as Zherlov and authors, have shown in their studies that reconstruction in which DP is preserved has a lower incidence of postgastrectomy symptoms [43, 68]. Persistent postprandial discomfort and fullness may be to some extent due to poor receptive adaptation of the proximal part of the small intestine. In addition to poor receptive adaptation of the proximal part of the small intestine, the distal end of the Roux loop can also act as a functional obstruction, which leads to Roux-stasis syndrome, which is characterized by epigastric pain, nausea, and vomiting, and is most likely due to the lack of motor function in the distal region Roux loop [57, 69]. The lack of gastric acid after TG and altered intestinal motility in reconstruction with RY configuration with or without pouch seems to lead to bacterial colonization, which may be one of the main causes of malnutrition after TG. Excessive bacterial growth leads to the formation of damage to the mycelium and decongestion of bile salts. Several mechanisms blame for malabsorption of fat: loss of gastric emulsification of triglycerides, rapid food passage, and

The overall impact of many symptoms after a RP can be summarized in the health quality of life. The quality of life is a multidimensional approach that consists of functional, emotional,

in patients with RY procedure [65].

16 Gastric Cancer - An Update

pancreatic stimulation disorder [63].

TG is widely used as a major surgical treatment for GC. TG results in risk of postgastrectomy syndrome, such as weight loss, dumping syndrome, biliary reflux esophagitis, and a reduction in the quality of life [3, 4]. The ideal RP after TG should replace all lost functions of the stomach, provide an optimal enough reservoir that can accommodate to the size of the meal, prevent reflux, ensure strong propulsion of equal-sized boluses of chyme entering the duodenum, and respond properly to the changing levels of gastrointestinal hormones and neural information [7]. The choice of RP should ensure good digestive function to prevent persistent postgastrectomy syndrome. Preservation of duodenal transit with replacement of the jejunal segment, the so-called physiological route, is now believed to be preferential for postoperative nutritional condition. RP which allow DP should be regarded as a key to physiological reconstruction.
