Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As pectin delays gastric emptying in normal subjects and satiety may be linked to the rate of gastric emptying, we designed this study to evaluate, in a group of obese subjects, the effect of adding pectin to a meal on gastric emptying, sensation of satiety, and postprandial plasma cholecystokinin and pancreatic polypeptide levels. We studied gastric emptying of solids in 9 adult obese subjects on 2 separate days in a randomized fashion. On day 1, 15 g of pectin was added to the meal, and on day 2 15 g of methylcellulose was added and served as control. Satiety was evaluated by an analogue rating scale. Pectin significantly delayed gastric emptying time [t1/2 = 116 +/- 23 min vs. 71 +/- 17 min observed with methylcellulose (p less than 0.001)]. Pectin also significantly increased subjects' sensation of satiety [98 +/- 7 vs. 74 +/- 17 (p less than 0.001)]. Postprandial release of cholecystokinin and pancreatic polypeptide was not modified by pectin. As pectin induces satiety and delays gastric emptying in obese patients, it may be a useful adjuvant in the treatment of disorders of overeating.
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PMID:Pectin delays gastric emptying and increases satiety in obese subjects. 316 89

Rats with bilateral dorsomedial hypothalamic electrolytic lesions (DMNL rats) are hypophagic, hypodipsic and have reduced linear and ponderal growth when compared to sham operated controls (SCON). Nevertheless, previous studies have shown that DMNL rats eat and drink adequate amounts for their size and have normal body composition. In the present study we investigated meal parameters: meal size, and frequency (both light and dark period), total intake and meal size per metabolic size (body weight 0.75). Compared to SCON, DMNL rats at twelve days post surgery weighed less, were shorter, but had a normal body composition as determined by the Lee Index, and were hypophagic (grams eaten/day). The animals were placed into individual, self-contained feeding modules and given powdered chow. After familiarization to the modules, meal parameters were recorded continuously by a computer for an eight day period. While dark phase meal frequency did not differ significantly between groups, the lesioned rats took more meals during the light period. Over the eight-day measurement period DMNL rats were hypophagic compared to SCON in absolute terms. However, when total intake and meal size were normalized to metabolic size, these two parameters did not differ significantly between groups. Upon refeeding, after a one-day fast, the initial meal size of the normally hypophagic DMNL rats exceeded that of SCON. Rats with DMNL have previously been shown to have deficits in some hypothesized short-term food intake control mechanism (e.g., cholecystokinin, glucose sensing). Thus overeating by the lesioned rats after a fast could possibly result from a specific short term control deficit.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Meal patterns of rats with dorsomedial hypothalamic nuclei lesions or sham operations. 352 Jun 11

Effects of the dietary carbohydrate-to-fat ratio on opiate-stimulated eating and on naloxone-, cholecystokinin- and bombesin-suppressed eating were examined. Rats were fed either a high carbohydrate (cornstarch) diet (68% of energy from carbohydrate and 12% from fat), an intermediate diet (40% carbohydrate and 40% fat) or a high fat (corn oil and lard) diet (3% carbohydrate and 77% fat). Other rats self-selected from the high carbohydrate and high fat diets. Subcutaneous administration of naloxone, an opiate antagonist, generally suppressed intake of the high fat diet to a greater extent than intake of the high carbohydrate diet. Neither cholecystokinin octapeptide nor bombesin (administered intraperitoneally) exerted preferential suppression of fat intake. The opiate agonists ketocyclazocine and butorphanol tartrate administered subcutaneously at 1000 h preferentially, although not exclusively, stimulated intake of the high fat diet in a dose-dependent manner during the 6-h feeding trial. Repeated daily subcutaneous injections of butorphanol tartrate caused rats to consume more than 50% of their daily intake during the 6-h period postinjection; intake during the normal night feeding period was suppressed to maintain total daily intake equal to that of vehicle-injected rats. We conclude that stimulation of the opioid feeding system contributes to the overeating often associated with consumption of a high fat diet.
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PMID:Effects of kappa opiate agonists, cholecystokinin and bombesin on intake of diets varying in carbohydrate-to-fat ratio in rats. 358 53

Obese Zucker rats are less responsive than their lean littermates to the effects of cholecystokinin-octapeptide on satiety and pancreatic growth and exocrine function. We hypothesized that the hyperphagia observed in obese Zucker rats may be caused by a decreased pyloric contractile response to cholecystokinin, resulting in an increased rate of gastric emptying, decreased postprandial gastric distention, and thus decreased satiety. Pyloric muscle strips from six obese Zucker rats and six lean littermates were mounted in separate tissue baths and isometric contraction was measured in response to acetylcholine and cholecystokinin-octapeptide. The dose-response curves for acetylcholine- and cholecystokinin-octapeptide-stimulated pyloric muscle contraction were similar for both the obese and the lean rats. (For cholecystokinin, D50 obese = 4.0 +/- 0.6 nM, D50 lean = 3.4 +/- 0.2 nM; P = 0.16). We conclude that the decreased satiety response to cholecystokinin-octapeptide observed in obese Zucker rats is not secondary to a decreased pyloric responsiveness to cholecystokinin.
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PMID:Role of pylorus in mediating cholecystokinin-stimulated satiety in the Zucker rat. 369 66

During lactation food intake increases greatly without an accompanying large increase in body weight; therefore, this physiological state is an excellent example of non-obese hyperphagia. In the present study, we found that cholecystokinin (CCK-8) decreased food intake in lactating and virgin female rats. However, female rats were more resistant to the effect of CCK on eating following weaning of the pups. Bombesin (BB) suppressed food intake in virgin female rats and in lactating rats during early and mid lactation. Rats were resistant to its satiating effect during late lactation and during the postweaning period. Calcitonin potently suppressed food intake in virgin, lactating and postweaning rats. The present findings suggest that CCK and bombesin decrease food intake more effectively in virgin female rats and during earlier phases of lactation than during late lactation or postweaning.
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PMID:The effect of cholecystokinin, bombesin and calcitonin on food intake in virgin, lactating and postweaning female rats. 379 39

Modulation of feeding by opiates, putative satiety peptides, and dopamine was explored in the Chinese hamster, an animal that develops diabetes mellitus in certain inbred strains. Diabetic hamsters were hyperphagic relative to their nondiabetic controls, but both groups exhibited natural circadian variation in feeding. Starvation provoked hyperphagia of about 1-h duration in both groups. Naloxone and butorphanol had no effects on Chinese hamster feeding. Opiate receptor binding on Chinese hamster brains demonstrated no specific binding of naloxone or ethylketocyclazocine, but IR-dynorphin concentrations were comparable with that in rats. N-allylnormetazocine, a sigma-opiate receptor agonist, appeared to stimulate diabetic hamster feeding. Peptides reputed to have satiety effects in rats were without effect in Chinese hamsters: cholecystokinin, bombesin, somatostatin, and pancreatic polypeptide. Calcitonin limited feeding in both groups but may be nonspecific. Dopaminergic blockade by haloperidol also limited feeding, and diabetic hamsters were more sensitive to this. Although Chinese hamsters clearly can modulate their food intake when diabetic, we conclude that the opiatergic and peptidergic influences on feeding are very different from those in rats and may be of little importance.
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PMID:Feeding systems in Chinese hamsters. 614 21

Cholecystokinin (CCK) secreted from the duodenum during feeding has been shown to elicit satiety and stimulate growth of the pancreas in addition to affecting gastrointestinal function. In previous experiments hyperphagic Zucker obese rats were less sensitive to the effects of CCK on satiety and had a smaller pancreas than normal-weight rats. In the present experiments with hyperphagic lactating Zucker rats, the food intake response to exogenously administered CCK and the size and composition of the pancreas were measured. Food intakes after a 2-h fast were not decreased by 4.0 or 8.0 micrograms/kg CCK-8 during wk 1, 2, or 3 of lactation. However, in the same rats 2 wk after pups were weaned, 4.0 and 8.0 micrograms/kg CCK-8 decreased food intake 32% (2.1 +/- 0.4 vs. 3.1 +/- 0.3 g, paired t = 2.33, P less than 0.03) and 52% (1.5 +/- 0.2 vs. 3.1 +/- 0.5 g, paired t = 3.48, P less than 0.006). On day 18 of lactation, pancreas weight was increased 41% (1.38 +/- 0.05 vs. 0.98 +/- 0.02 g, paired t = 2.68, P less than 0.02) and contents of DNA, RNA, and protein were increased 57, 57, and 73%, respectively. Thus, hyperphagia in lactating female rats was associated with 1) decreased sensitivity to the satiety effect of CCK similar to that in hyperphagic obese rats and 2) hypertrophy of the pancreas in contrast to decreased pancreas size in obese rats.
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PMID:Hyperphagia during lactation: satiety response to CCK and growth of the pancreas. 618 5

The area postrema (AP) is a hindbrain circumventricular organ (CVO) with apparent chemoreceptive function. The AP has demonstrated neural and vascular connections with the nucleus of the solitary tract (SOL), a structure which receives the primary visceral afferents from the oral cavity and gastrointestinal tract. The anatomical structure and connections of the AP suggests a potential role for this CVO in the control of feeding behavior. We have found that rats with surgically produced AP lesions consumed the same amounts of pelleted food ad libitum as control rats. Lesioned and control rats also consumed equal amounts of lab chow after 21 h food deprivation. However, when presented with a preferred food (instant breakfast or cookies), AP-lesioned rats consumed at least double the amount consumed by control rats. It is possible that AP lesions impair sensitivity to satiety cues. However, lesion rats did decrease their instant breakfast intake in response to cholecystokinin injections or gastric preloads. Furthermore, overingestion by AP-lesioned rats occurred only in response to preferred (highly palatable) foods and not in response to lab chow. Lesioned rats rejected quinine-adulterated instant breakfast at the same adulterant concentration as controls. Therefore, the lesioned rats do not suffer from ageusia or from enhanced responsiveness to bitter taste. Rather, the selective overeating by AP-lesioned rats may reflect an enhanced behavioral response to the sensory qualities of normally preferred foods. The close association of the AP with the SOL provides a neuroanatomical avenue by which a putative AP-chemoreceptor could alter the quality or intensity of information arriving via the taste afferents. Such tuning of gustatory mechanisms could be an important component of ingestive control.
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PMID:Ablation of the area postrema causes exaggerated consumption of preferred foods in the rat. 724 78

Rats eat more at night than during the day. This work investigated whether this nocturnal hyperphagia is characterized by increased hunger, decreased postprandial satiety, or both. Rats were presented with liquid food after 3-hr food deprivation at the midpoint of the night or day phase of a 12:12 hr light/dark cycle. Quinine adulteration of food produced equal percentage suppression of first meal size (MS) and of 60-min intakes in the night and the day. This suggests that rats are equally hungry after 3-hr food deprivation in the night and the day. In contrast to apparently equal hunger, rats were less satiated by ingested food after 3 hr of food deprivation at night than during the day. This conclusion is based on the observations that the postprandial intermeal interval (IMI) was significantly shorter at night and that the satiety ratio (IMI/MS) was smaller at night. This nocturnal decrease in the satiating potency of ingested food was demonstrated for two specific preabsorptive satiety mechanisms: (a) the pregastric satiety mechanism(s) stimulated by sham feeding and (b) cholecystokinin, the putative satiety hormone released by food contacting the mucosal surface of the upper small intestine. All the results suggest that the diurnal variation of food intake in rats is primarily the result of diurnal variation in the potency of postprandial satiety mechanisms.
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PMID:Nocturnal hyperphagia in the rat is characterized by decreased postprandial satiety. 736 7

Hyperamylasemia of pancreatic origin has been noted in patients with severe head injury without abdominal trauma or evidence of pancreatitis. Thirty-eight patients with intracranial bleeding of various types were evaluated for elevated pancreatic amylase and lipase enzymes without associated pancreatitis. Twenty-five patients had elevated serum lipase; 17 of 25 also had elevated amylase without pancreatitis. Most lipase elevations occurred earlier than those of amylase. Six clinical variables--mannitol, ceftriaxone, nimodipine, steroids, Glasgow Coma Score, and total parenteral and enteral hyperalimentation--were evaluated to determine relationship to the enzyme elevations. A significant relationship exists between patients not treated with steroids and elevated lipase and amylase enzyme activities. Multivariate analysis revealed a significant interaction between lipase elevation and decreasing Glasgow Coma Score, indicative of increasing severity of intracranial bleeding. Proposed causes of enzyme elevations in intracranial bleeding include vagal stimulation, altered modulation of the central control of pancreatic enzyme release, and release of cholecystokinin from the brain. Physician awareness of the association of intracranial bleeding with the elevation of amylase and lipase without pancreatitis can save the patient needless cost and manipulation.
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PMID:Significance of elevated pancreatic enzymes in intracranial bleeding. 752 51


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