cholecystokinin and Nutrition-Disorders

Aging is associated with a reduction in appetite and food intake, predisposing to protein-energy malnutrition. The causes of this "anorexia of aging" are largely unknown. To investigate possible contributions of enhanced satiating effects of cholecystokinin (CCK) and reduced stimulation of food intake by ghrelin, eight undernourished older women [age, 80.4 +/- 2.6 yr; body mass index (BMI), 16.9 +/- 0.57 kg/m(2)], eight well-nourished older women (age, 77 +/- 0.9 yr; BMI, 23.7 +/- 0.8 kg/m(2)), and eight well-nourished young women (age, 22 +/- 1.3 yr; BMI, 20.5 +/- 0.4 kg/m(2)), in randomized order, ate on 1 d a 280-kCal preload and on the other no preload, 90 min before an ad libitum meal. At baseline the undernourished, but not the well-nourished, older subjects were less hungry (P < 0.05) than young subjects. Before and after the preload, plasma CCK levels were higher (P < 0.05) in the older than young subjects, with no difference between the older groups. Plasma ghrelin concentrations were higher in the undernourished than both well-nourished groups and decreased similarly after the preload in all groups. The preload suppressed food intake in the well-nourished older and young subjects (P < 0.05), but was without effect in the undernourished old. These observations suggest that reduced basal hunger, rather than increased meal-induced satiety, contributes to the anorexia of aging and that changes in CCK and ghrelin are unlikely to be responsible.

Topics: Aged; Aged, 80 and over; Aging; Appetite; Blood Glucose; Cholecystokinin; Dietary Carbohydrates; Dietary Fats; Eating; Energy Metabolism; Female; Gastrointestinal Hormones; Ghrelin; Humans; Nutrition Disorders; Peptide Hormones; Satiety Response

Malnutrition has definitely been related to mortality among dialysis patients. Persistent loss of appetite is one of the major symptoms found in these patients. It is also well recognized that several substances produce anorexia or disorders of the hunger-satiety cycle in several diseases. The aim of this study was to identify the role of anorexigen substances (TNF-alpha and cholecystokinin or CCK) and an orexigen substance (neuropeptide Y or NPY) in anorexia and malnutrition among 55 clinically stable peritoneal dialysis (PD) patients.. High TNF-alpha plasma levels were found in 41 of 42 patients (97.6%) with a mean of 70.5+/-32.3 pg/ml. Patients with anorexia (n=11) or anorexia with nausea or vomiting (n=5) had higher TNF-alpha values than patients without these symptoms (75.9+/-34 vs 52.1 +/-24.5 pg/ml, P<0.05). Eight patients with a prior diagnosis of acid pylori disease showed higher TNF-alpha values (87.2+/-24.3) than 30 unaffected patients (63.6+/-30.5, P<0.05). TNF-alpha showed a significant negative linear correlation with retinol binding protein (RBP) (r=-0.37, n=34, P<0.05), and venous pH (r=-0.4, n=42, P<0.01); also, TNF-alpha values higher than 65 pg/ml were inversely associated with transferrin, cholesterol, blood urea nitrogen (BUN) and CCK. Patients with prealbumin levels lower than 30 mg/dl, a BMI lower than 30 kg/m2, nPCR lower than 1.1 g/kg/day and urea KT/V lower than 2.2 showed higher serum TNF-alpha levels. Patients who had been on CAPD treatment for longer periods showed higher TNF-alpha values. High plasma CCK levels were found in 38 of 45 patients (84%), mean 45.9+/-32.3 pg/ml. Patients with anorexia had no difference in CCK values compared with those without. A direct association was found between CCK levels and some nutritional markers (albumin, fibronectin, triglycerides, folic acid and nPCR in non diabetic patients). Although CCK has a recognized anorectic effect, this direct association might be because of an abnormal stimulation of CCK glucose feedback (trypsin) due to continuous peritoneal glucose absorption. This suggests that CCK could be an immediate food intake marker in PD patients. The NPY plasma levels were normal in 33 patients, high in 6 and low in 11. Patients with anorexia showed lower NPY levels than those without. NPY values greater than 50 pg/ml were directly associated with higher transferrin, prealbumin, RBP, nPCR and urea KT/V values. Importantly, a negative linear correlation between NPY and TNF-alpha was found (r=-0.42, n= 41, P<0.01). There was no significant relationship between residual renal clearance and the serum levels of the three peptides.. In conclusion, our data suggest that high TNF-alpha and low NPY serum levels are associated with anorexia. High TNF-alpha, low CCK and low NPY serum levels are also related to a poor nutritional status. Further research on these circulating substances is required.

Topics: Adult; Aged; Aged, 80 and over; Anorexia; Biomarkers; Cholecystokinin; Cross-Sectional Studies; Female; Humans; Male; Middle Aged; Neuropeptide Y; Nutrition Disorders; Nutritional Status; Peritoneal Dialysis; Protein-Energy Malnutrition; Tumor Necrosis Factor-alpha

1. The development of endogenous cholecystokinin (CCK) effects on food intake was studied in normal and undernourished growing rats of postnatal day 1-22. 2. Food intake was estimated by recording the gain in body weight before weaning. 3. l-phenylalanine, a potent stimulant of endogenous CCK release, suppressed 30 min food intake in normally nourished pups of day 7-15 or more but not of day 1-6 rats. 4. However, l-phenylalanine did not affect 24 hr gain in body weight day 1-6 or more, rat pups. 5. l-phenylalanine neither suppressed 30 min food intake nor affected 24 hr body weight in day 16-19 or 20-22 undernourished rat pups. 6. The study suggests that the endogenous CCK satiety effects appear early in the second week of postnatal life in normally nourished rats, whereas in undernourished rat pups it does not appear till day 20-22.

Topics: Animals; Body Weight; Cholecystokinin; Diet; Eating; Male; Nutrition Disorders; Nutritional Status; Phenylalanine; Rats; Satiety Response

Under certain conditions, exogenously administered cholecystokinin (CCK) or its COOH-terminal octapeptide can terminate feeding and cause behavioral satiety in animals. Furthermore, high concentrations of CCK are normally found in the brains of vertebrate species. It has thus been hypothesized that brain CCK plays a role in the control of appetite. To explore this possibility, a COOH-terminal radioimmunoassay was used to measure concentrations of CCK in the cerebral cortex, hypothalamus, and brain stem of rats and mice after a variety of nutritional manipulations. CCK, mainly in the form of its COOH-terminal octapeptide, was found to appear in rat brain shortly before birth and to increase rapidly in cortex and brain stem throughout the first 5 wk of life. Severe early undernutrition had no effect on the normal pattern of CCK development in rat brain. Adult rats deprived of food for up to 72 h and rats made hyperphagic with highly palatable diets showed no alterations in brain CCK concentrations or distribution of molecular forms of CCK as determined by Sephadex gel filtration of brain extracts. Normal CCK concentrations were also found in the brains of four strains of genetically obese rodents and in the brains of six animals made hyperphagic and obese by surgical or chemical lesioning of the ventromedial hypothalamus. It is concluded that despite extreme variations in the nutritional status of rats and mice, CCK concentrations in major structures of the brain are maintained with remarkable constancy.

Topics: Aging; Animals; Appetite Regulation; Brain Stem; Cerebral Cortex; Cholecystokinin; Feeding Behavior; Female; Food Deprivation; Hypothalamus; Mice; Nutrition Disorders; Nutritional Physiological Phenomena; Obesity; Rats; Satiety Response

Topics: Acetylcholine; Acute Disease; Alcoholism; Antigen-Antibody Reactions; Cholecystokinin; Chronic Disease; Cortisone; Drug Interactions; Female; Humans; Hyperparathyroidism; Male; Nutrition Disorders; Pancreas; Pancreatitis; Radionuclide Imaging

Topics: Amylases; Bicarbonates; Celiac Disease; Cholecystokinin; Diet; Folic Acid Deficiency; Humans; Intestinal Diseases; Intestine, Small; Malabsorption Syndromes; Nutrition Disorders; Pancreas; Protein Deficiency; Secretin; Serum Albumin