Stomachs: does the size matter? Aspects of intestinal satiety, gastric satiety, hunger and gluttony

Many surgeons and most laypeople think that there is a strict correlation between the size of the stomach and the size of the meals. The term ‘‘stomach reduction’’ became a synonym for weight loss surgeries, as if by reducing the stomach, all meals would automatically be small. However, there is no strict correlation between the size of this organ and the size of meals. Some morbidly obese patients have previously undergone total gastrectomy! If a simple stomach reduction treated obesity, the absence of a stomach should cause impressive weight loss; however, this principle is not always true. On the other hand, some patients, despite having normal-sized stomachs, feel very satisfied with three spoonfuls of food. How can these phenomena be explained? The stomach is a pouch with a hole. The rate of emptying is even more important than the size of the pouch itself. In addition, a variety of different and complex mechanisms are involved in the initiation and termination of a meal. The rate of gastric emptying to the bowel is very important. It defines the amount of nutrients that may, through absorption, enter the blood stream, thereby altering the blood composition and threatening the homeostasis. A fast and intense nutrient absorption rapidly changes the blood composition (i.e., with elevations in sugars and lipids) and demands a quick and efficient metabolic answer. Some refined and pre-digested elements of the modern diet are free of fiber and completely ready for a fast absorption. These elements have been called high-glycemic index foods, ever since Jenkins (1) defined the concept of the glycemic index in 1980. In the stomach, food is mixed with acidic gastric secretions and proteolytic enzymes. Most microbes ingested with food are killed by acid; therefore, any contamination risk is minimized. Large pieces of food are broken down, and the osmolarity of the content is adjusted. The food and drink that present the right osmolarity will leave the stomach sooner, thereby explaining why one can drink a liter of sweet iced tea more easily and quickly than a liter of pure water. Additionally, the stomach adds the R factor and intrinsic factor to allow vitamin B12 to be absorbed in the ileum. Once these steps are complete, the stomach sends the chyme (i.e., the food mixed with digestive secretions) to the small bowel, where it is immediately admixed with the biliopancreatic juices that lead to near-complete digestion (mammals cannot digest fiber without the bacterial help of fermentation, which occurs in the colon). In the duodenum, the absorption of small particles is initiated promptly, and the chyme keeps moving downwards as the absorption process occurs. Endogenous glucose production is not interrupted at this stage (i.e., the pancreatic a-cells do not suspend glucagon production). Hypoglycemia may kill an animal in minutes, so the proximal bowel does not have the ‘‘authority’’ to give such an extreme order, but it can produce a less powerful one (i.e., the proximal gut secretes glucose-dependent insulinotropic polypeptide, an insulinotropic agent that cannot suppress glucagon and the endogenous production of glucose (2-4)). At this point, satiety is not supposed to occur. For quite obvious reasons, the proximal gut is not the point at which food should trigger intense satiety or initiate the suspension of glucagon production. Nonetheless, when the distal portion of the small bowel receives nutrients (meaning that a significant meal was effectively consumed), the neuroendocrine L cells in the mucosa produce hormones like glucagon-like peptide 1 (GLP-1), oxyntomodulin and polypeptide YY (PYY), which are typical postprandial hormones (5-7). These hormones promote the transition from the fasting state to a postprandial state. In the fasting state, there is hunger, high levels of glucagon, endogenous glucose production, and lipolysis. In the typical postprandial state, an intense production of insulin, blood clearance of glucose and lipids, lipogenesis, and a diminution in the gastric emptying and satiety progressively appear. They are opposite metabolic states. GLP-1 inhibition of gastric emptying indeed outweighs its insulinotropic effects (8). In other words, the distal intestine stops the gastric emptying at a certain point (e.g., when stimulated by nutrients). Therefore, the intestine defines the functional size of the stomach. If we suddenly eat progressively more and more refined food, absorption becomes easier and more intense in the proximal gut, thereby reducing the distal stimulation. As a consequence, there may be deficiencies in the production of distal gut hormones, like GLP-1 and PYY (which happens in obese and type 2 diabetic patients (9,10)), and much food may pass through stomach, regardless of its size. If we do not have the proper stimulation of the distal gut, a simple reduction of the stomach may not work. Indeed, some post-surgical patients left with 30-mL stomach pouches can still eat enough to remain obese or at least to regain most of the lost weight after post-operative adaptation. Email: [email protected] Tel.: 55-11-9137-0930