Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003123 (anorexia)
 13,794 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The three neuropeptides calcitonin, neurotensin and bombesin can decrease food intake in the rat when injected into the cerebral ventricles or into the paraventricular nucleus of the hypothalamus. The paraventricular nucleus of the hypothalamus is an important site for the integration of visceral and endocrine systems, and has connections with the nucleus of the tractus solitarius which is a major locus for visceral afferents. Since calcitonin, neurotensin and bombesin, or their receptors, have been found to be present in the nucleus of the tractus solitarius, we tested the effects of local infusions of these peptides on food intake. The peptides were microinjected in a 0.25 microliter volume in rats trained to eat for only 3 hours per day. The injections were made in the rostral part of the nucleus and surrounding areas, through the lateral vestibular nuclei, to avoid leakage of the peptides into the cerebrospinal fluid. In the nucleus of the tractus solitarius the three peptides decreased food intake by more than 50%. The peptides were also active in the spinal trigeminal nucleus oralis, and, for calcitonin and bombesin, in the reticular formation under the nucleus of the tractus solitarius. A local diffusion from the point of injection may explain some of these results. Therefore, the area of the nucleus of the tractus solitarius is a nonhypothalamic site where these peptides can act to produce anorexia.
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PMID:Anorectic effect of calcitonin, neurotensin and bombesin infused in the area of the rostral part of the nucleus of the tractus solitarius in the rat. 322 51

Three cases of bladder carcinomas associated with hypercalcemia were presented. Case 1: A 43-year-old male was diagnosed as having bladder carcinoma 2 years ago and treated in another hospital by partial cystectomy with uretero-vesiconeostomy of the left side. On March 6, 1985, in our clinic, he received a total cystectomy with an ileal conduit for urinary bladder carcinoma. A 5-month post-operative clinical examination showed recurrence of the carcinoma with elevated serum Ca level (15.6 mg/dl). He was treated with eel-calcitonin, predonine, indomethacin, and furosemide, but died on August 23, 1985. Autopsy disclosed carcinoma of the urinary bladder (transitional cell cancer much greater than squamous cell cancer). Case 2: A 51-year-old male was diagnosed as having transitional carcinoma of the urinary bladder and was treated in our clinic by total cystectomy with cutaneous ureterostomy. Three months after the operation, he was readmitted with complaints of anorexia and disturbances of consciousness. His serum Ca level was elevated (17 mg/dl), and clinical examination showed recurrence of the carcinoma; bone scan revealed no metastasis. He was treated by radiotherapy with eel-calcitonin, predonine, indomethacin, and furosemide, but died on October 22, 1985. Autopsy disclosed carcinoma of the urinary bladder (squamous cell cancer). Case 3: A 72-year-old male was diagnosed as having a large urinary bladder tumor. An IVP showed a left non-functioning kidney. On admission, he complained of anorexia and confusion. His serum Ca level was elevated (13.8 mg/dl); bone scan revealed no metastasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bladder carcinoma associated with hypercalcemia: report of 3 cases]. 328 51

Early satiety may play a role in the anorexia of aging. The effects of the peripheral satiety agents cholecystokinin (CCK), bombesin, glucagon, and calcitonin were studied in 8 and 25 month old mice. During normal feeding behavior, the older mice consumed more than their younger counterparts, however, when food deprived, the younger consumed more. All peptides inhibited food intake over the first hour after administration in young and old mice. CCK, bombesin, and calcitonin suppressed feeding in 25 month old mice to a greater extent than in 8 month old mice. However, CCK demonstrated the greatest age-related suppression of food intake. CCK has a potential role to play in the pathogenesis of the anorexia of aging.
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PMID:Effect of gastrointestinal peptides on ingestion in old and young mice. 337 33

Intracerebroventricular (i.c.v.) injection of 19 pmol/rat or more of salmon calcitonin (sCT) or iodinated sCT suppressed spontaneous intake of food and water in a dose-dependent manner. Tail-whipping was a peculiar behavior which concomitantly developed, but no analgesia ensued from the doses tested (up to 62 pmol/rat). It was examined how the rise and fall pattern of these behavioral effects would correlate with the dispositional pattern of 125I-sCT. When the radioactive peptide was injected in anorectic doses via the i.c.v. route, the radioactivity was found to distribute throughout the brain, but not uniformly. In rats which showed a marked anorexia and tail-whipping behavior, distribution occurred in such a manner that it could be interpreted to reflect the regional and subcellular distribution pattern of sCT-specific binding sites. Even 3 hr after injection, the hypothalamus, the smallest region, retained the highest radioactivity corresponding to about 1% of the dose and at least one half of which was identified as the intact iodo-sCT. To be noted is the finding that sCT injected centrally will quickly enter the systemic circulation and peripherally induced long-lasting hypocalcemia, since the anorectic dose of sCT is considerably higher than the dose needed for the peripheral effect. It is concluded that most of the sCT after i.c.v. injection leaks into the systemic circulation, but the rest is retained rather selectively around the receptor in hypothalamic nuclei for a long time, leading to day-long suppression of feeding and drinking behavior.
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PMID:Intracerebroventricular injection of 125I-salmon calcitonin in rats: fate, anorexia and hypocalcemia. 399 41

Salmon calcitonin (sCT, 2 and 20 U/kg), porcine calcitonin (pCT, 20 and 40 U/kg) and human calcitonin (hCT, 20 and 40 U/kg) were injected subcutaneously to rats trained to eat their food during two hours each day. Food intake and serum Ca++ concentrations were determined at the end of 2h-feeding period. A long lasting anorectic effect was observed for 20 U/kg of sCT with a parallelism between hypocalcaemia and anorexia in the first 8 hours after treatment; on the contrary, rats continued to eat less than controls in the following hours when their serum Ca++ concentrations had risen to normal or even higher levels. As regards pCT and hCT, it was shown that these peptides reduced significantly meal size only for 1-2 hours when serum Ca++ levels were at their lowest levels for these peptides.
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PMID:Relationships between hypocalcaemic and anorectic effect of calcitonin in the rat. 401 45

In a total of 277 patients with advanced breast cancer treated between July 1977 and November 1983 at Cancer Institute Hospital, there were 26 cases (9.4%) showing hypercalcemia (Ca greater than or equal to 11.0 mg/dl). All these patients had bone metastasis examined by either X-ray films or bone scintigram during clinical course of the disease and confirmed at the time of autopsy, thus an overall incidence of hypercalcemia in 149 patients with bone metastasis was 17.4%. Major clinical signs due to hypercalcemia were gastrointestinal symptoms such as anorexia, nausea and vomiting, renal dysfunction and neurological symptoms but there was no definitive correlation in between clinical signs and values of serum calcium. Among various treatments performed, a combination of hydration, steroids and calcitonin was the most effective. Mean survival time from the diagnosis of hypercalcemia was 288 + days for responders, and 28.8 days for non-responders (p less than 0.001). Seven patients expired due to hypercalcemia and were died suddenly, while others died of renal failures.
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PMID:[Hypercalcemia in breast cancer]. 674 68

The anorectic potency of salmon, porcine and human calcitonins (sCT, pCT and hCT, respectively) and two sCT-fragments were compared in rats. Intraventricular injections of sCT (0.062 and 0.031 nmole/animal) significantly reduced the normal feeding and body weight. The effect appeared to be dose-dependent, reversible and lasted longer than 6 hr. No anorexia ensued, however, on injections of mammalian hormones though tested in relatively high doses (pCT: up to 3.7 nmole, hCT: 3.7 nmole). The C-terminal fragments of sCT, sCT (10-32) and sCT (22-32) were also found to be devoid of anorectic activity; but when administered with sCT, the longer fragment (1.2 nmole) significantly decreased the effect of sCT and even the shorter one (18 nmole) tended to act as an antagonist. This property was not recorded with pCT and hCT in the doses examined. On the one hand, these results indicate a novel specificity of the anorectic receptor in rat brain; and on the other hand, they seem to strongly argue against the hypothesis that in mammals thyroidal calcitonin secreted postprandially might participate in the regulation of subsequent feeding, unless the presence of the sCT-like molecule can be detected in mammals. All the more because detection of such a molecule must await development of a specific assay, the antagonistic property of the sCT fragment found herein would have use for clarifying the physiological significance of the anorectic receptor which is possibly in the hypothalamus.
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PMID:Calcitonin-induced anorexia in rats: a structure-activity study by intraventricular injections. 716 57

The purpose of this study was to compare the localization in the brain of calcitonin-induced anorexia to the distribution of calcitonin binding sites (as described by others). We, thus, performed an extensive mapping of brain structures to determine those involved in calcitonin-induced anorexia. A significant anorexia is found after injection of calcitonin (15 ng in 0.3 microliters) into several brain areas. Forebrain: lateral septum, lateral part of the anterior commissure, and bed nucleus of the stria terminalis; hypothalamus: floor of the anterior part of the hypothalamus, paraventricular nucleus and adjacent perifornical area; thalamus: nucleus reuniens, an area internal to the mamillo-thalamic tract, and medial geniculate body; other areas: amygdala, lateral hippocampus, and central gray. No significant effect is found in the following areas: forebrain: nucleus accumbens, striatum, and medial septum; hypothalamus: lateral, ventro-medial, dorso-medial, and posterior nuclei; thalamus: centro-medial nucleus, lateral part of the zona incerta, and lateral geniculate body; hippocampus: dorsal and ventral parts; midbrain: central tegmentum, ventral tegmental area, and substantia nigra. When these results are compared to the distribution of calcitonin binding sites in the brain, two types of discrepancies are found. The first is the absence of effect in areas containing receptors: these areas may be involved in calcitonin-induced behaviors other than food intake. The second is the occurrence of anorexia in areas where no receptors are found: this finding is not easy to explain and raises some speculative hypotheses. In conclusion, calcitonin is active to decrease food intake in several brain areas, the strongest effect occurring in the paraventricular/perifornical area.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Extensive brain mapping of calcitonin-induced anorexia. 771 9

Plasma and cerebrospinal fluid (CSF) concentrations of three well-known satiety neuropeptides, cholecystokinin (CCK), somatostatin and calcitonin gene-related peptide (CGRP), along with two powerful orexigenic neuropeptides, neuropeptide Y (NPY) and beta-endorphin have been measured in elderly persons with idiopathic anorexia and normal weight healthy subjects in a similar age range. Plasma and CSF immunoreactivity levels of the two main fractions of CCK (CCK8s and CCK33) after being separated by HPLC were measured by a radioimmunoassay (RIA) developed in our laboratory, whereas the other neuropeptides were assayed by commercially available RIA kits. Elderly underweight anorectic patients had significantly lower levels of beta-endorphin but increased concentrations of NPY in both plasma and CSF when compared to controls. In addition to significantly higher levels of CCK8s but not CCK33 in plasma, we found a trend to higher CSF concentrations of CCK8s and a positive correlation between the body mass index and either beta-endorphin (r = 0.58, P < 0.05) or CCK8s (r = 0.69, P < 0.01) concentrations in CSF in the anorectic group. CSF somatostatin concentrations were decreased significantly, but plasma somatostatin levels and plasma and CSF concentrations of CGRP were similar in senile anorectics and controls. Treatment of five anorectic patients with megestrol acetate, 480 mg daily for 6 months, reversed only the decrease in CSF beta-endorphin levels but did not normalize the body weight or the fat body mass. On the basis of our findings, we hypothesize that a decrease in CSF beta-endorphin concentration along with a rise in plasma levels of CCK8s might be accounted for the primary anorexia of aging.
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PMID:Alterations in plasma and cerebrospinal fluid levels of neuropeptides in idiopathic senile anorexia. 790 1

This article report a study of 23 cases of hypercalcemia crisis resulting from primary hyperparathyroidism (18 cases), carcinoma (4 cases) and vitamin D intoxication (1 case). In addition to the symptoms of primary diseases, the patients with hypercalcemia crisis often had anorexia, nausea, vomiting, polydipsia, polyuria, psychoneurotic symptoms, arrhthmia. The severity of the symptoms was proportional to the degree of hypercalcimia. Serum calcium concentration of patients in hypercalcemia crisis should be equal or higher than 3.75 mmol/L (15 mg/dl) or serum ionized calcium higher than 1.88 mmol/L. Treatment hypercalcemia crisis consisted of rapidly lowering the serum calcium level by various measures while actively treating the primary diseases. Our experience is to supply normal saline intravenously or orally to increase the extracellular fluid and to enhance excretion of the urine calcium by administrating furosemide. In this paper, serum calcium concentration of 5 patients with hypercalcemia crisis treated with salmen calcitonin was reduced in varying degrees. The above mentioned treatment would be beneficial to the alleviation of the crisis and the preparation for operative treatment.
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PMID:[The preliminary experiences of diagnosis and treatment for hypercalcemia crisis--clinical analysis of 23 cases]. 798 37


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