Protein: Gut Hormones and Satiety

High protein diets show weight loss effect when compared to high fat or high carbohydrate diets. The reason for this is unknown, but protein has satiety inducing effects and this may contribute to its anti-obesogenic effects. The mechanisms by which protein may regulate appetite has been extensively investigated and it appears that the rate of gastric emptying plays an important role. The presence of undigested protein in the duodenum of the small intestine causes stimulation of I cells that in turn stimulate the release of cholecystokinin. Cholecystokinin then causes contraction of the pyloric sphincter and this inhibits the release of chyme from the stomach allowing further digestion of proteins to occur in the acid environment of the stomach. In this way it is ensured that protein digestion is completed in the stomach before the amino acids and peptides are presented to the small intestine for further digestion and absorption. As well as cystokinin, a number of other gut hormones have also been implicated as possible satiety signals following the ingestion of protein.

For example, protein has been shown to cause increases in glucagon-like peptide 1, peptide YY and glucagon following ingestion of protein1. In this study, subjects were fed test meals which varied in their protein and carbohydrate content while the fat content remained constant at 30 % of energy. The protein content of the meals was 14, 25 or 50 % of total energy, with the carbohydrate content decreasing to compensate for energy. Compared to the low protein meal, the medium protein diet increased plasma concentrations of glucagon-like peptide 1, peptide YY and glucagon by 10, 7 and 47 % respectively, while the high protein diet increased plasma concentrations by 20, 14 and 116 %, respectively. The hunger and the prospective consumption of food (assessed by subjective response) decrease in both the medium (15 and 13 %, respectively) and high (25 and 26 %, respectively) protein test meals compared to the controls, suggesting these hormones may be involved in the regulation of satiety.

These results suggest that high protein diets lower hunger and potentially, food intake. They also suggest that glucagon-like peptide 1, peptide YY and glucagon may be involved. However, the effects on these hormones may have been affected by the carbohydrate content of the diet which fell in relation to the protein content. A control were the protein and fat content were varied, but carbohydrate content remained unchanged may have made the results from this study easier to interpret. For example, in the study, the authors admit that the varying carbohydrate content may have masked the ability of protein to stimulate insulin. In addition, the test meals were low in fibre in order to preclude the possible confounding effects of fibre on satiety and gut hormone release. However, testing the satiety effects of protein with refined carbohydrates is problematic because such foods are known to influence gut hormones and satiety and their low fibre content may have enhanced the ability of the carbohydrates to mask the insulinogenic effects of protein.

In addition, there was no change in the plasma concentrations of ghrelin or cholecystokinin, which is unexpected based on their role in hunger stimulation and stomach emptying rates. However, with regard ghrelin, it should be noted that there may be differences in the satiety inducing pathways and appetite stimulating pathways, and they may be mutually exclusive in their activity. Protein may activate the satiety pathway, without the need to decrease the hunger pathway. The authors also detected no change to the ad libitum energy intake following the protein preload meals. However, others have suggested a minimum subject number (25) using a paired design design is necessary in order to detect a 120 kcal difference in energy intake. The subject may therefore have had different ad libitum food intakes in the subsequent pizza mal they were fed, but the study design may have limited the ability to detect significant differences. However, taken as a whole these results support other findings that indicate satiety effects from protein.

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1Belza, A., Ritz, C., Sorensen, M. Q., Holst, J. J., Rehfeld, J. F. and Astrup, A. 2013. Contribution of gastrointeropancreatic appetite hormones to protein-induced satiety. American Journal of Clinical Nutrition. 97: 980-989

About Robert Barrington

Robert Barrington is a writer, nutritionist, lecturer and philosopher.
This entry was posted in Cholecystokinin, Ghrelin, Glucagon, Glucagon-like Peptide 1, Peptide YY, Protein, Satiety. Bookmark the permalink.