Koopmans (1981) transplanted an extra stomach and length of intestine into rats and then joined the major arteries and veins of the implants to the recipients’ circulatory systems (see Figure 12.12). Koopmans found that food injected into the transplanted stomach and kept there by a noose around the pyloric sphincter decreased eating in proportion to both its caloric content and volume. Because the transplanted stomach had no functional nerves, the gastrointestinal satiety signal had to be reaching the brain through the blood. And because nutrients are not absorbed from the stomach, the bloodborne satiety signal could not have been a nutrient. It had to be some chemical or chemicals that were released from the stomach in response to the caloric value and volume of the food—which leads us nicely into the next subsection.

The experiments about the role of the gastrointestinal tract being the source of satiety signals , have been great support on the early studies of hunger and stomach contractions.

Explanation:

The re-emerged interest, in the 1980s, in the role of the gastrointestinal tract in eating, resulted in trials such as the described Koopmans´ in 1981, which led to the hunger and satiety peptides deeper study on an   evolutionary perspective , as evidence proved that short chains of amino acids can function as hormones and neurotransmitters. The hypothesis that circulating gut peptides provide the brain, particularly in areas of the hypothalamus involved in energy metabolism, and a dozen or so (e.g., CCK, bombesin, glucagon, alpha-melanocyte-stimulating hormone, and somatostatin) to reduce food intake,  indicating that the neural system that controls eating likely reacts to many different signals, not just to glucose and fat.

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