Involvement of gastrointestinal hormones in the thermic effect of dietary protein in rats

Background and objectives: Glucagon-like peptide-1 (GLP-1) is a gastrointestinal hormone secreted from enteroendocrine cells after a meal and has various postprandial physiological effects such as inducing satiety and suppressing blood glucose elevation via promoting insulin secretion. Among the three major nutrients, proteins potently stimulate GLP-1 secretion. Protein intake is a potent inducer of diet-induced thermogenesis, an important postprandial physiological effect. However, the involvement of GLP-1 is unknown. In this study, we examined the thermic effects of various nutrients, including dietary proteins, by measuring rectal temperature in rats, and the involvement of gastrointestinal hormones, including GLP-1, in this effect. Methods: Rectal temperatures of rats fasted for 4 hours were measured using a thermocouple thermometer before (0 h) and after an oral administration of nutrients. In other studies, various antagonists were administered intraperitoneally immediately after an oral protein administration, and rectal temperature was measured as above. Each test was performed under awake, normal housing conditions (22°C). Results: Of the energy-producing nutrients (isocaloric carbohydrates, lipids, and proteins), oral administration of protein raised rectal temperature the most. Among five dietary proteins (casein, whey, rice, egg, and soy) examined, soy protein had the highest thermic effect. This rectal temperature increase was attenuated by intraperitoneal administration of a GLP-1 receptor antagonist (exendin-9). In contrast, various receptor antagonist treatments of other representative gastrointestinal hormones, GIP, CCK, and PYY, had no effect. In addition, intraperitoneal administration of propranolol, a nonselective beta-adrenergic receptor blocker, did not affect the rectal temperature increase induced by soy protein administration. Conclusions: These results suggest that soy protein induces postprandial body temperature increase via GLP-1 signaling, independently of brown adipose tissue activation.