Cholecystokinin octapeptide decreases intake of solid food in man

Stacher, G; Steinringer, H; Schmierer, G; Schneider, Christa; Winklehner, S.

doi:10.1016/0196-9781(82)90041-9

Cited by 101 publications

(34 citation statements)

References 12 publications

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“…Administration of exogenous CCK to healthy adults increases sensations of fullness and reduces sensations of hunger and subsequent food intake (13,(32)(33)(34). Most reports of CCKinduced satiety involve studies in which CCK is administered in doses that increase plasma CCK concentrations above physiologic postprandial concentrations.…”

Section: Discussionmentioning

confidence: 99%

Effects of age on concentrations of plasma cholecystokinin, glucagon-like peptide 1, and peptide YY and their relation to appetite and pyloric motility

MacIntosh

Andrews

Jones

et al. 1999

The American Journal of Clinical Nutrition

225

140

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Background: Aging is associated with a decrease in appetite and a slowing of gastric emptying. The gastrointestinal hormones cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1), and peptide YY (PYY) may mediate these changes. Objective: We investigated whether aging influenced the secretion of CCK, GLP-1, and PYY and their effects on appetite and pyloric motility. Design: Eight healthy older (65-80 y) and 7 younger (20-34 y) men received isoenergetic (12.1 kJ/min) intraduodenal infusions of lipid and glucose for 120 min on separate days. Plasma CCK, GLP-1, and PYY concentrations were measured. Results: Plasma CCK concentrations were higher in older than in younger subjects (P = 0.004) as a result of higher baseline values (4.7 ± 0.2 compared with 3.2 ± 0.2 pmol/L; P < 0.0001) and a greater rise during lipid infusion (increase from baseline: 7.1 ± 0.5 compared with 5.3 ± 0.6 pmol/L; P = 0.048). Plasma GLP-1 and PYY concentrations were not significantly different between groups. The decrease in hunger during intraduodenal lipid infusion was inversely related to the increase in CCK, GLP-1, and PYY in younger but not older subjects. During intraduodenal lipid infusion, the increase in isolated pyloric pressure wave (IPPW) frequency was positively related to GLP-1 and PYY and the increase in IPPW amplitude was positively related to CCK in older but not younger subjects, whereas the increase in IPPW amplitude and pyloric tone was negatively related to GLP-1 and PYY in younger subjects. Conclusions: Human aging is associated with increased CCK concentrations, which may contribute to the slowing of gastric emptying, mediated by increased pyloric motility. The role of increased plasma CCK concentrations in mediating the agerelated decrease in appetite remains to be established.Am J Clin Nutr 1999;69:999-1006. KEY WORDSCholecystokinin, CCK, glucagon-like peptide 1, GLP-1, peptide YY, PYY, appetite, pylorus, gastric emptying, small intestine, elderly, men, aging INTRODUCTIONAging is associated with a decrease in appetite and food intake (1, 2); additionally, body weight tends to decrease from 65 to 70 y of age (1). This anorexia of aging may predispose the elderly to pathologic weight loss and increased morbidity and mortality (3). The causes of the anorexia of aging are unknown but are likely to be multifactorial.Appetite is controlled by a central system that is responsible for the initiation of eating and that is held in check by a peripheral satiety system, which is activated by the presence of food in the gastrointestinal tract (3). An important mediator of gastrointestinal satiety signals is thought to be the release of gastrointestinal satiety hormones, including cholecystokinin (CCK) (4, 5), bombesin, glucagon, and glucagon-like peptide 1 (GLP-1) (6), induced by interaction of nutrients with receptors in the small intestine (4).Gastric emptying of nutrients is slightly slower in healthy elderly than in young adults (7,8) and there is evidence that this may contribute to increased satiation, perhaps by p...

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Section: Discussionmentioning

confidence: 99%

Effects of age on concentrations of plasma cholecystokinin, glucagon-like peptide 1, and peptide YY and their relation to appetite and pyloric motility

MacIntosh

Andrews

Jones

et al. 1999

The American Journal of Clinical Nutrition

225

140

View full text Add to dashboard Cite

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“…The second is an intestinal factor (luminal CCK-releasing factor) that stimulates CCK release in response to ingestion of protein or fats or in response to protease inhibitors. This coordinate system (Kissileff et al 1981;Stacher et al 1982;Liddle, 1995;Herzig et al 1996;Miyasaka & Funakoshi, 1997;Gibbs & Smith, 1998) can regulate cholecystokinin levels in the gastrointestinal tract. When injected parenterally CCK-8 produces a dose-related reduction in sham-feeding in experimental animals and in lean and obese human subjects (Table 2; Kissileff et al 1981;Stacher et al 1982;Baile & Della-Fera, 1984;Boosalis et al 1992;Smith & Gibbs, 1994;Lieverse et al 1995a;Gibbs & Smith, 1998).…”

Section: Cholecystokininmentioning

confidence: 99%

Afferent signals regulating food intake

2000

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Food intake is a regulated system. Afferent signals provide information to the central nervous system, which is the centre for the control of satiety or food seeking. Such signals can begin even before food is ingested through visual, auditory and olfactory stimuli. One of the recent interesting findings is the demonstration that there are selective fatty acid taste receptors on the tongue of rodents. The suppression of food intake by essential fatty acids infused into the stomach and the suppression of electrical signals in taste buds reflect activation of a K rectifier channel (K 1.5). In animals that become fat eating a high-fat diet the suppression of this current by linoleic acid is less than that in animals that are resistant to obesity induced by dietary fat. Inhibition of fatty acid oxidation with either mercaptoacetate (which blocks acetyl-CoA dehydrogenase) or methylpalmoxirate will increase food intake. When animals have a choice of food, mercaptoacetate stimulates the intake of protein and carbohydrate, but not fat. Afferent gut signals also signal satiety. The first of these gut signals to be identified was cholecystokinin (CCK). When CCK acts on CCK-A receptors in the gastrointestinal tract, food intake is suppressed. These signals are transmitted by the vagus nerve to the nucleus tractus solitarius and thence to higher centres including the lateral parabrachial nucleus, amygdala, and other sites. Rats that lack the CCK-A receptor become obese, but transgenic mice lacking CCK-A receptors do not become obese. CCK inhibits food intake in human subjects. Enterostatin, the pentapeptide produced when pancreatic colipase is cleaved in the gut, has been shown to reduce food intake. This peptide differs in its action from CCK by selectively reducing fat intake. Enterostatin reduces hunger ratings in human subjects. Bombesin and its human analogue, gastrin inhibitory peptide (also gastrin-insulin peptide), reduce food intake in obese and lean subjects. Animals lacking bombesin-3 receptor become obese, suggesting that this peptide may also be important. Circulating glucose concentrations show a dip before the onset of most meals in human subjects and rodents. When the glucose dip is prevented, the next meal is delayed. The dip in glucose is preceded by a rise in insulin, and stimulating insulin release will decrease circulating glucose and lead to food intake. Pyruvate and lactate inhibit food intake differently in animals that become obese compared with lean animals. Leptin released from fat cells is an important peripheral signal from fat stores which modulates food intake. Leptin deficiency or leptin receptor defects produce massive obesity. This peptide signals a variety of central mechanisms by acting on receptors in the arcuate nucleus and hypothalamus. Pancreatic hormones including glucagon, amylin and pancreatic polypeptide reduce food intake. Four pituitary peptides also modify food intake. Vasopressin decreases feeding. In contrast, injections of desacetyl melanocyte-stimulating hormone, growth hormone and prolactin are associated with increased food intake. Finally, there are a group of miscellaneous peptides that modulate feeding. β-Casomorphin, a heptapeptide produced during the hydrolysis of casein, stimulates food intake in experimental animals. In contrast, the other peptides in this group, including calcitonin, apolipoprotein A-IV, the cyclized form of histidyl-proline, several cytokines and thyrotropin-releasing hormone, all decrease food intake. Many of these peptides act on gastrointestinal or hepatic receptors that relay messages to the brain via the afferent vagus nerve. As a group they provide a number of leads for potential drug development.

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“…Although a predominant role of the hypothalamus in satiety control is well recognized, controversy exists about the principal stimuli. Some hormones such as cholecystokinin (CCK) have been found to have satiation properties at supraphysiological blood levels only (4,5), but their endogenous action on satiety is not certain (6,7). Mayer's glucostatic theory (8) has been revisited by various investigators (9,10).…”

Section: Introductionmentioning

confidence: 99%

Relationship Between Hunger‐Satiety Feelings and Various Metabolic Parameters in Women with Obesity During Controlled Weight Loss

Heini¹,

Kirk

Lara-Castro³

et al. 1998

Obesity Research

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HEINl, ADRIAN F., KATHARINE A. KIRK, CRISTINA LARA-CASTRO, ROLAND L. WEINSIER. Relationship between hunger-satiety feelings and various metabolic parameters in women with obesity during controlled weight loss. Obes Res. 1998;6:225-230. Objective: Satiety plays an important role in weight control. The meaning of fasting hormone levels and satiety feelings, and how post-absorptive changes after meals high in carbohydrate regulate appetite remains to be demonstrated. Research Methods and Procedures:Prospective metabolic study with 25 non-diabetic obese women at the Energy Metabolism Research Unit of the Department of Nutrition Sciences, University of Alabama at Birmingham. We analyzed fasting and postprandial ratings of hunger-satiety and values of various metabolic parameters (serum glucose and insulin, plasma cholecystokinin, respiratory quotient) during controlled weight loss. The postprandial measures were assessed following a test meal providing 320 kcal and yielding a food quotient of 0.89. Results.' In the fasting state, there was no correlation between hunger-satiety ratings and any of the measured metabolic parameters. Under postprandial conditions, satiety was positively related to glucose (p = 0.002) and insulin (p =0.002) responses to the test meal. In multivariate analysis including glucose, insulin, cholecystokinin, hungersatiety ratings and respiratory quotient, insulin was the only independent predictor of satiety in the postprandial state. Discussion: These data suggest an association between the endogenous insulin response and feelings of postprandial satiety. Insulin's satiation properties, which could well be mediated by other hormones, may represent a primary factor of food intake regulation after meals relatively high in carbohydrate.

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Cholecystokinin octapeptide decreases intake of solid food in man

Cited by 101 publications

References 12 publications

Effects of age on concentrations of plasma cholecystokinin, glucagon-like peptide 1, and peptide YY and their relation to appetite and pyloric motility

Effects of age on concentrations of plasma cholecystokinin, glucagon-like peptide 1, and peptide YY and their relation to appetite and pyloric motility

Afferent signals regulating food intake

Relationship Between Hunger‐Satiety Feelings and Various Metabolic Parameters in Women with Obesity During Controlled Weight Loss

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