Summary. There are now a large number of experiments demonstrating that peripheral administration of exogenous cholecystokinin or its synthetic analogue, CCK-8, reduces meal size in a number of species. The peptide interacts with other factors which influence satiety, and treatments thought to be effective in eliciting secretion of cholecystokinin have predictable effects on meal size. Cholecystokinin is effective in the genetically obese Zucker rat, obese rats with lesions of the ventromedial hypothalamus, and subdiaphragmatically vagotomized rats. Somatostatin and bombesin are also reasonable candidates for satiety factors. Intraperitoneal naloxone reduces meal size in rats, and beta-endorphin injected intraventricularly causes an increase in meal size of 50% over 30 minutes. We conclude that cholecystokinin and bombesin may interact in weight regulation and control of meal time food intake.Key words: Satiety, CCK, bombesin, somatostatin, beta-endorphin, VIP, meal size, vagotomy, Zucker (Fatty) ratsWe have presented the view [1] that factors which regulate food intake can be separated into two categories, namely those that vary with the adipose mass and which, therefore, carry information regarding the level of adiposity, and those that affect food intake independently of body weight. We reviewed our hypothesis that the amount of insulin acting at the brain, perhaps via the cerebrospinal fluid (CSF), is a key factor in the adiposity-determined regulation of food intake over long intervals. In the present paper, we shall review the evidence that other gastroenteropancreatic peptide hormones affect the size of individual meals and act relatively independently of the size of the adipose mass. In particular, we shall consider certain peptide hormones which are normally secreted in response to ingested foodstuffs. Some of these peptides act to reduce meal size and others act to increase it. This paper is divided into four sections. The first reviews selectively the literature dealing with peptides and satiety, focusing upon the ability of cholecystokinin-pancreozymin (CCK) to reduce meal size. The second section covers other peptides purported to reduce meal size, and focuses upon recent work in our own lab utilizing the hormones somatostatin (SRIF) and bombesin (BB). A third section deals with the possibility that some other peptides, perhaps the endorphins, function as appetite enhancers, thus countering these other peptides. The final section examines some possible interactions of the peptide and meal size system with the insulin body adiposity system discussed in the previous paper [1].
CCK and SatietyBecause of the clinical importance attached to the determination of factors which might regulate appetite and/or the consumption of food, considerable research has been directed to this end. However, until the past fifteen years most of the focus was on psychological factors and nutrients, especially glucose levels [2,3], as major controllers. Although a large number of experiments provided evidence that nutrition...