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)

Hypothalamic concentrations of six regulatory peptides having central effects on appetite and/or glucoregulation were measured by radioimmunoassay in spontaneously-diabetic Chinese hamsters and in age- and sex-matched non-diabetic control animals. In the diabetic hamsters, hypothalamic concentrations of somatostatin and neuropeptide Y were significantly reduced by 25-30% below controls. None of the other four peptides examined (bombesin, galanin, neurotensin and vasoactive intestinal peptide) differed significantly between the two groups. Disturbances in neuropeptide Y (the most potent central appetite stimulant yet discovered) and in somatostatin could be related to hyperphagia, an early and possibly primary abnormality of the diabetic syndrome in the Chinese hamster.
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PMID:Reduced hypothalamic somatostatin and neuropeptide Y concentrations in the spontaneously-diabetic Chinese hamster. 290 91

The rapid growth (0.8 +/- 0.3 g/day) of a transplantable insulinoma, which also contained substance P (2.9 +/- 2.3 pmol/g) and gastrin-releasing peptide (3.2 +/- 2.1 pmol/g), resulted in the development of hyperphagia, hyperinsulinaemia and hypoglycaemia in rats (n = 8). After a 14-day growth period, the insulinoma-bearing rats showed an increase (49%; p less than 0.01) in the weight of the small intestine but no significant change in stomach weight compared with control animals. The content (pmol/organ) of somatostatin, substance P, neurokinin A and vasoactive intestinal peptide in the stomachs of the tumour rats was unchanged. A depletion in the content (53% p less than 0.01) and concentration (57%; p less than 0.01) of gastrin-releasing peptide, however, suggested either hypersecretion, possibly mediated through hypoglycaemia-induced vagal stimulation, or inhibition of synthesis. The concentration and content of glucagon-like immunoreactivity (enteroglucagon) in the small intestine of the insulinoma rats increased markedly (47%; p less than 0.01 and 120%; p less than 0.01). This increase is consistent with a proposed role of this peptide as a factor trophic to the intestinal mucosa. No significant changes in the concentrations of somatostatin, substance P, neurokinin A, vasoactive intestinal peptide and gastrin-releasing peptide in the small intestine were observed. However, the increase in gut weight resulted in a greater content of vasoactive intestinal peptide (40%; p less than 0.01) and substance P (37%; p less than 0.05) in the insulinoma rats.
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PMID:Effects of a transplantable insulinoma upon regulatory peptide concentrations in the gastrointestinal tract of the rat. 301 8

Central and lateral hypothalamic concentrations of 10 regulatory peptides were measured by radioimmunoassay in streptozocin-induced diabetic (STZ-D) and matched control rats between 1 day and 14 wk after diabetes induction. After 2 wk, both central and lateral hypothalamic neuropeptide Y (NPY) concentrations in STZ-D rats were consistently higher than those found in control rats, with significant 30-50% increases at 4 wk in the central hypothalamus, and at 6 and 14 wk in both central and lateral hypothalamus. Immunocytochemical studies in 4- and 6-wk STZ-D animals showed the appearance of intensely NPY-positive swollen cell bodies in the supraoptic nucleus and a subjective increase in NPY staining of medial hypothalamic nerve fibers. Central hypothalamic concentrations of three other peptides were significantly greater in STZ-D animals than those in control animals at single points (neurotensin, 1 day; calcitonin gene-related peptide, 2 wk; neurokinin, 4 wk). Hypothalamic concentrations of the other six peptides examined (bombesin, galanin, neuromedin B, substance P, somatostatin, and vasoactive intestinal peptide) did not differ significantly between STZ-D and control groups at any time. However, galanin immunostaining in the supraoptic and magnocellular paraventricular nuclei was strikingly concentrated in a reduced number of distended cell bodies. Hypothalamic peptide changes in STZ-D could be related to metabolic disturbance, changes in energy and water balance, altered pituitary function, or other factors. Persistently elevated concentrations of NPY, a very potent central stimulant of eating and drinking, may mediate the hyperphagia and polydipsia characteristic of STZ-D.
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PMID:Increased hypothalamic neuropeptide Y concentrations in diabetic rat. 328 97

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

The obese hyperglycaemic ob/ob mouse exhibits hyperphagia and other abnormalities of hypothalamic function. We measured hypothalamic concentrations of four peptides implicated in the control of appetite and energy expenditure, neuropeptide-Y (NPY), neurotensin, galanin, and somatostatin, by RIA and their respective mRNAs using semiquantitative Northern blotting. Using lean (+/+) mice as controls, we found unchanged concentrations of NPY, galanin, and somatostatin and a 25% reduction in neurotensin (P < 0.01). Neurotensin mRNA was similarly decreased (by 30%; P < 0.02), while NPY mRNA was increased 3-fold (P < 0.01). Centrally administered neurotensin decreases food intake, whereas NPY potently stimulates food intake. An increase in NPY gene expression together with reductions in neurotensin concentration and mRNA in the hypothalamus may be implicated in the development of hyperphagia and other neuroendocrine abnormalities seen in the ob/ob mouse.
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PMID:Increased neuropeptide-Y messenger ribonucleic acid (mRNA) and decreased neurotensin mRNA in the hypothalamus of the obese (ob/ob) mouse. 768 36

Pancreatic pseudocysts in children are rare. A total of 213 cases have been reported in the literature, the majority secondary to trauma (65%). Treatment options range from conservative, non-operative management to operative drainage. Octreotide acetate, a long-acting analog of somatostatin, is a synthetic peptide with a variety of endocrine and gastrointestinal functions. Octreotide has been successfully used following pancreatic surgery to reduce exocrine function and most recently in the management of adult pancreatic pseudocysts. We report the efficacy of octreotide, as an adjunct to treatment, in two children with pancreatic pseudocyst. Each child was treated conservatively with bowel rest, hyperalimentation, and octreotide acetate (2.5 micrograms/kg SQ QD). Complete resolution of the pseudocysts occurred within 5 weeks. We conclude that octreotide acetate is a safe and potentially effective adjunct in the treatment of pediatric pancreatic pseudocyst, and should be added to the management of pseudocyst before drainage procedures.
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PMID:Conservative management of pediatric pancreatic pseudocyst using octreotide acetate. 788 30

Pancreatic ascites, etiologically related to a leaking pseudocyst or ductal disruption, has been treated medically with hyperalimentation, somatostatin analog, and large-volume paracentesis. Surgery is ultimately required in more than 50% of such patients. Mortality figures in patients with pancreatic ascites approximate 15% to 25% with either treatment modality. We describe 4 patients who were found to have ductal disruptions in conjunction with pancreatic ascites who responded to transpapillary pancreatic duct endoprosthesis placement. There has been no recurrence of ascites in these patients at a mean follow-up of 12 months following stent-retrieval. Further evaluation of endoscopic therapy for pancreatic ascites appears warranted.
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PMID:Endoscopic treatment of pancreatic ascites. 808 56

Diet protein increases whereas carbohydrates decrease urea synthesis. Traditionally, these effects have been explained by changes in substrate supply. Diet protein intake increases whereas carbohydrate decreases blood amino acid concentration. However, glucose also decreases urea synthesis by a hepatic mechanism independent of the decrease in blood amino acid concentration. Whether this is due to an effect of glucose in itself, or whether the fall in glucagon or the rise in insulin is responsible, was not known. This survey deals with the effect of an increase in diet protein intake and of the separate effects of glucose, glucagon and insulin on functional hepatic nitrogen clearance in normal man and in patients with cirrhosis of the liver. The functional hepatic nitrogen clearance is calculated as the slope of the linear regression analysis of alanine-stimulated urea synthesis rate and blood alpha-amino nitrogen concentration, and expresses urea synthesis independent of changes in blood amino acid concentration. In patients with cirrhosis, hepatic nitrogen clearance is reduced in parallel with liver cell mass, despite high glucagon concentration that would normally up-regulate the process. In both healthy subjects and in patients with cirrhosis, an increase in diet protein intake (plus approximately 50 g/day) for 14 days increases hepatic nitrogen clearance by 40%. Thus, in addition to the substrate effect, protein intake increases urea synthesis by an effect in the liver, probably by enzyme formation. What induces this is not clear but high postprandial levels of glucagon may be involved. Although the effect is qualitatively intact in the patients, the response relative to the increase in protein intake is reduced by two-thirds. The effect may be important to control blood amino acid concentration during a high protein diet and may partly explain why patients with cirrhosis usually tolerates protein hyperalimentation without developing hepatic encephalopathy. It is shown that the reduction of hepatic nitrogen clearance by glucose depends on hyperglycaemia, and is accomplished by the additive effects of a direct hormone-independent action of glucose, and indirectly via suppression of glucagon. Insulin is not a direct controller of hepatic nitrogen clearance, but is still considered an important regulator of urea synthesis by its reducing effects on blood amino acid concentration. High experimental glucagon levels overrule the normal suppressive effect of glucose. In contrast, it is shown that the sugar-alcohol xylitol normalises the glucagon induced increase in hepatic nitrogen clearance. During normal glucagon levels xylitol exerts only a very little decrease in hepatic nitrogen clearance. In patients with cirrhosis, glucose does not down-regulate hepatic nitrogen clearance. However, when the spontaneous high glucagon levels are normalised by somatostatin, glucose decreases hepatic nitrogen clearance. This shows that the direct hormone-independent effect of glucose is intact. These findings indicate that the high glucagon levels during spontaneous hormone responses overrule the suppressive effect of glucose. Incomplete glucose suppression of glucagon secretion during alanine infusion contributes to the high glucagon levels. The removal of the high glucagon levels decreases hepatic nitrogen clearance in itself. Thus, the hyperglucagonaemia may be a compensatory mechanism by which the cirrhotic liver to some extent reestablishes its capacity to produce urea. The consequence is the defective down-regulation of hepatic nitrogen clearance by glucose. The reduction in urea synthesis by glucose, i.e. its nitrogen sparing effect, is accomplished by two different mechanisms: A hepatic component (reduction of the hepatic nitrogen clearance) and a peripheral component (reduced substrate availability mediated by the insulin response). This is an extension of former thoughts according to which glucose reduces urea synthesis due solely to
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PMID:Regulation of urea synthesis by diet protein and carbohydrate in normal man and in patients with cirrhosis. Relationship to glucagon and insulin. 923 44

We report herein the case of an 80-year-old woman with insulinoma who was regarded as an unsuitable candidate for immediate surgery due to her advanced age and obesity, for whom octreotide, a long-acting analogue of somatostatin, was used to improve her hypoglycemia and hyperinsulinemia without hyperalimentation. Administering a minimal dose of octreotide for a long period resulted in the improvement of leg edema, weight control, and cardiopulmonary function, and resection of the pancreatic tumor was safely carried out without any complications.
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PMID:The effectiveness of administering a minimal dose of octreotide long-term prior to surgery for insulinoma: report of a case. 1088 68

Obesity and its related disorders are the most prevalent health problems in the Western world. Using the paradigm of fetal programming we developed a rodent model which displays the phenotype of obesity and metabolic disorders commonly observed in human populations. We apply maternal undernutrition throughout gestation, generating a nutrient-deprived intrauterine environment to induce fetal programming. Maternal undernutrition results in fetal growth retardation and in significantly decreased body weight at birth. Programmed offspring develop hyperphagia, obesity, hypertension, hyperleptinemia and hyperinsulinism during adult life and postnatal hypercaloric nutrition amplifies the metabolic abnormalities induced by fetal programming. The adipoinsular axis has been proposed as a primary candidate for linking the status of body fat mass to the function of the pancreatic beta-cells. We therefore investigated the relationship between circulating plasma concentrations of leptin and insulin and immunoreactivity in the endocrine pancreas for leptin and leptin receptor (OB-R) in genetically normal rats that were programmed to become obese during adult life. Virgin Wistar rats were time mated and randomly assigned to receive food either available ad libitum (AD group) or at 30% of the ad libitum available intake (UN group). Offspring from UN mothers were significantly smaller at birth than AD offspring (AD 6.13+/-0.04 g, UN 4.02+/-0.03 g, P<0.001). At weaning, offspring were assigned to one of two diets (a standard control diet or a hypercaloric diet consisting of 30% fat) for the remainder of the study. At the time of death (125 days of age), UN offspring had elevated (P<0.005) fasting plasma insulin (AD control 1.417+/-0.15 ng/ml, UN control 2.493+/-0.33 ng/ml, AD hypercaloric 1.70+/-0.17 ng/ml, UN hypercaloric 2.608+/-0.41 ng/ml) and leptin (AD control 8.8+/-1.6 ng/ml, UN control 14.32+/-1.9 ng/ml, AD hypercaloric 15.11+/-1.8 ng/ml, UN hypercaloric 30.18+/-5.3 ng/ml) concentrations, which were further increased (P<0.05) by postnatal hypercaloric nutrition. The elevated plasma insulin and leptin concentrations were paralleled by increased immunolabeling for leptin in the peripheral cells of the pancreatic islets. Dual immunofluorescence histochemistry for somatostatin and leptin revealed that leptin was co-localized in the pancreatic delta-cells. OB-R immunoreactivity was evenly distributed throughout the pancreatic islets and was not changed by programming nor hypercaloric nutrition. Our data suggest that reduced substrate supply during fetal development can trigger permanent dysregulation of the adipoinsular feedback system leading to hyperleptinemia, hyperinsulinism and compensatory leptin production by pancreatic delta-cells in a further attempt to reduce insulin hypersecretion in the progression to adipogenic diabetes.
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PMID:Dysregulation of the adipoinsular axis -- a mechanism for the pathogenesis of hyperleptinemia and adipogenic diabetes induced by fetal programming. 1147 29


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