Interaction between GLP-1 and CCK-33 in inhibiting food intake and appetite in men

Abstract

. Interaction between GLP-1 and CCK-33 in inhibiting food intake and appetite in men. Am J Physiol Regul Integr Comp Physiol 287: R562-R567, 2004. First published April 22, 2004 10.1152/ajpregu.00599.2003.-Glucagon-like peptide-1 (GLP-1) and CCK-33 were intravenously infused alone or in combination into normal weight men for 60 min before they were served a lunch of ham sandwiches, chocolate mousse, and orange juice. Infusion of GLP-1 (dose: 0.9 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 ) or CCK-33 (dose: 0.2 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 ) each reduced calorie intake of the test meal. However, simultaneous infusion of these peptide doses reduced calorie intake less than the sum of the peptides' individual effects. Infusions of the same doses of GLP-1 plus CCK-33 had neither individual nor interactive effects on meal size or calorie consumption. The combination of GLP-1 plus CCK-33 induced, however, a significant reduction in hunger feelings in the premeal period (P ϭ 0.036 vs. all other treatments). In summary, intravenous infusion of near physiological doses of CCK-33 and GLP-1 produced specific inhibitions of hunger feeling in men; the simultaneous infusion resulted in an infra-additive reduction in calorie consumption, rejecting thereby the hypothesis that the two peptides exert a positive synergistic effect on food intake compared with the effects observed with infusion of individual peptides. In conclusion, CCK and GLP-1 are meal-related satiety signals that are released from the gastrointestinal tract during food intake. glucagon-like peptide; cholecystokininA SERIES OF REMARKABLE DISCOVERIES and the emergence of obesity as major health problem have stimulated research efforts into how the body controls appetite and food intake. The close relationship between the gastrointestinal endocrine system and the brain in regulating food intake and satiety requires a coordinated interplay in which circulating hormones convey information about food intake and appetite to brain pathways that control eating. However, little is known about which physiological signals interact to control human eating. To further explore the role of specific digestive signals, we investigated the potential interaction of two preabsorptive satiety signals, CCK and glucagon-like peptide-1 (GLP-1). Both peptides are two classical gastrointestinal hormones that are released into the circulation in response to meal consumption (14, 17); compelling evidence has accumulated in the past years to document that each participates in the control of appetite in healthy volunteers, but also in patients with obesity or diabetes type II (3,8,11,15,[25][26][27]. As mentioned before, the control of human eating habits is, however, highly complex and our understanding of appetite regulation is far from complete. In many areas our knowledge is only rudimentary. More important, the interactions between individual signals and their integration into the control system have hardly been explored.From studies in animals and humans it is known that individual satiety signals can interact:...

Effects of Combined Oleoyl-Estrone and Rimonabant on Overweight Rats

“…OE or rimonabant did not change circulating ghrelin in spite of decreased food intake. GLP-1 tends to decrease appetite (33), but this signal is also reduced in the rats receiving OE. Cholecystokinin enhances satiety by decreasing gastric emptying (34), a trait in part shared with OE (R. Ferrer-Lorente et al, unpublished results).…”

Mechanisms of gastric emptying disturbances in chronic and acute inflammation of the distal gastrointestinal tract

“…Apart from regulatory effects on the upper gastrointestinal tract, CCK also reduces appetite and food intake via central effects; supraphysiological CCK levels induce nausea (5,6,14,21). Thus excessive CCK release might explain why some patients with CD have severe symptoms of gastroparesis that are refractory to tube feeding (30).…”

Effect of CCK-1 receptor blockade on ghrelin and PYY secretion in men

“…These signals are transmitted from the gut to the brain and become integrated at various centers in the hypothalamus, reflecting the load of nutrients ingested (34). As a group, these peptides are called satiety signals because most create a sensation of fullness and reduce food intake when administered to humans or animals.Cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1), peptide YY (PYY), and ghrelin are examples of gastrointestinal signals that exert various physiological effects in the gastrointestinal tract, including modulation of appetite and satiety (4,17,35). CCK, GLP-1, and PYY exert inhibitory effects (4,10,11,17,22) on food intake and satiety, whereas ghrelin initiates meal ingestion (10, 11).…”

“…CCK, GLP-1, and PYY exert inhibitory effects (4,10,11,17,22) on food intake and satiety, whereas ghrelin initiates meal ingestion (10, 11). CCK, GLP-1, and PYY are stimulated from specialized endocrine cells into the circulation during meals by the presence of food in the intestine; in contrast, ghrelin secretion is increased by fasting and inhibited by meal ingestion.…”