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)

Nutrition is one of the most important factors affecting wound healing. Patients who have significant protein malnutrition and require emergency surgery are frequently encountered. Conventional nutritional preparation for surgery, with intravenous hyperalimentation, requires 10 to 14 days to demonstrate advantageous reversal of catabolism. Growth hormone is known to have an anabolic effect in malnourished animals. The purpose of this investigation was to study the ability of growth hormone, administered from the time of celiotomy, to improve wound strength in protein-malnourished animals and compare its efficacy with preoperative nutritional repletion. Rats were divided into four groups: Group I--normal control rats, group II--malnourished rats, group III--malnourished rats treated with growth hormone for 5 postoperative days, and group IV--malnourished rats refed normal chow for 3 days before operation. Controlled laparotomy wounds were closed with monofilament nylon which was removed at the time wound bursting strength was tested. Bursting strengths at the sixth day postoperative were as follows (means +/- SD): (table; see text) Wound strength of malnourished animals was significantly less than that of controls, (P less than 0.001). Wound bursting strength of groups III and IV was significantly improved over that of malnourished animals (group II), P less than 0.001. The bursting strength of group IV was significantly higher than that of group III. Growth hormone administration following celiotomy is nearly as effective in improving wound healing as preoperative nutritional repletion. These results suggest that growth hormone may be clinically applicable in preventing wound complications in malnourished patients requiring urgent or emergency laparotomy.
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PMID:Stimulation of wound bursting strength during protein malnutrition. 212 May 15

A case is presented of 14 year old female with hypothalamic obesity due to hydrocephalus caused by aqueductal stenosis. Evidence of hypothalamic obesity included 1) acute hyperphagia and weight gain, 2) neuroradiology showed hydrocephalus with focal enlargement of the third ventricle, 3) endocrinological studies revealed hyperinsulinaemia and impaired growth hormone (GH) response to arginine, but normal GH response to growth hormone-releasing factor (GRF) and 4) Torkildsen's ventriculo-cisternal shunting resulted in improvement in hyperphagia and obesity.
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PMID:Hypothalamic obesity due to hydrocephalus caused by aqueductal stenosis. 229 5

Acromegaly was diagnosed in 14 middle-aged to old cats of mixed breeding. Thirteen (93%) of the cats were male and one was female. The earliest clinical signs in the 14 cats included polyuria, polydipsia, polyphagia, all of which were associated with untreated diabetes mellitus. All developed severe insulin resistance within a few months; peak insulin dosages required to control severe hyperglycemia ranged from 20 to 130 U per day. Other clinical findings weeks to months after diagnosis included enlargement of one or more organs (e.g., liver, heart, kidneys, and tongue) (n = 14), cardiomyopathy (n = 13), increase in body size and weight gain (n = 8), nephropathy associated with azotemia and clinical signs of renal failure (n = 7), degenerative arthropathy (n = 6), and central nervous system signs (i.e., circling and seizures) caused by enlargement of the pituitary tumor (n = 2). The diagnosis of acromegaly was confirmed by demonstration of extremely high basal serum growth hormone concentrations (22 to 131 micrograms/l) in all cats. Computerized tomography disclosed a mass in the region of the pituitary gland and hypothalamus in five of the six cats in which it was performed. Two cats were treated by cobalt radiotherapy followed by administration of a somatostatin analogue (octreotide), whereas two cats were treated with octreotide alone. Treatment had little to no effect in decreasing serum GH concentrations in any of the cats. Eleven of the 14 cats were euthanized or died four to 42 months (median survival time, 20.5 months) after the onset of acromegaly because of renal failure (n = 2), congestive heart failure (n = 1), concomitant renal failure and congestive heart failure (n = 3), progressive neurologic signs (n = 2), persistent anorexia and lethargy of unknown cause (n = 1), the owner's unwillingness to treat the diabetes mellitus (n = 1), or unknown causes (n = 1). Results of necropsy examination in ten cats revealed a large pituitary acidophil adenoma (n = 10), marked left ventricular and septal hypertrophy (n = 7), dilated cardiomyopathy (n = 1), arthropathy affecting the shoulder, elbow, or stifle (n = 5), and glomerulopathy characterized by expansion of the mesangial matrix and variable periglomerular fibrosis (n = 10).
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PMID:Acromegaly in 14 cats. 240 66

Two cases of idiopathic hypothalamic dysfunction (one boy and one girl) are reported. Symptoms of hypothalamic dysfunction were noted by the age of 2 years: initial polyphagia and obesity with subsequent anorexia and emaciation were observed in one patient. Thermoregulation and thirst disorders, recurrent accesses of hypernatremia, acrocyanosis and profuse sweating were present. Impaired growth and delayed puberty in one case, and in the other hypogonadism, absence of growth hormone and gonadotrophins release in response to provocative stimuli were observed as well as abnormal thyroid stimulating hormone response to thyrotropin releasing hormone with hyperprolactinemia. Magnetic resonance imaging showed structural lesion in the lateral part of the lentiform nucleus in one case. Treatment with naltrexone, an opiate antagonist, had little if any effect.
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PMID:[Hypothalamic dysfunction. 2 cases: the contribution of nuclear magnetic resonance, therapeutic trial of naltrexone]. 266 35

Although most children with craniopharyngiomas have multiple hormone deficiencies, some will have normal growth with hyperphagia and obesity postoperatively. Many later fail to maintain this growth. If growth hormone (GH) treatment is not instituted at this time, adult height will be compromised. Normal or accelerated growth following surgery does not indicate the presence of normal GH secretion nor insure continued growth. Children with this syndrome should have careful follow-up with accurate growth measurements so that GH replacement therapy can begin when indicated.
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PMID:Growth in children with a craniopharyngioma. 284 Jun 46

Syrian golden hamsters when allowed free access to food and an exercise wheel will run long distances and develop hyperphagia and accelerated linear body growth with high circulating levels of growth hormone and insulin. Somatostatin, a widely distributed brain-gut neurohormonal peptide, modulates nutrient absorption and may regulate food intake. To examine the role of circulating plasma somatostatin-like immunoreactivity (SRIF-LI; pg/ml) in exercise induced hyperphagia 4 groups of animals were studied; an unrestricted exercise group (279.0 +/- 107.7, n = 10); a sedentary group (121.1 +/- 40.8, n = 8); a restricted exercise group (107.7 +/- 12.4, n = 6); and a restricted no exercise group (115.5 +/- 45.9, n = 9). Thus, the unrestricted exercise group has a significantly elevated SRIF-LI concentration (P less than 0.01) while there was no difference between the other 3 groups. The elevation of plasma SRIF-LI in the unrestricted exercise group may represent a response to modulate increased nutrient entry in this group or may represent an incompletely effective satiety signal.
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PMID:Exercise-induced hyperphagia in the hamster is associated with elevated plasma somatostatin-like immunoreactivity. 288 63

Young and mature, genetically obese and non-obese, spontaneously hypertensive rats (SHR) were injected with saline (controls) or naloxone for 12 weeks. Naloxone stilled the hyperphagia to a normal intake in the obese SHR (Obese/SHR) so that young Obese/SHR did not develop their usual massive obesity and mature Obese/SHR that had become massively obese were reduced to leanness. The naloxone-treated young, obese and non-obese SHR (controls) exhibited marked reduction of the weight of their pituitary and adrenal glands, whereas the pituitary and adrenal glands of naloxone-treated mature, obese and non-obese/SHR were greatly increased in weight. The elevated systolic blood pressure of the obese and non-obese rats was reduced after chronic treatment with naloxone. Naloxone treatment caused reduction of blood ACTH, corticosterone, and beta endorphin levels but elevated growth hormone levels. The characteristic hyperinsulinemia, hyperlipidemia, hyperglycemia, elevated BUN levels, and the Cushingoid spectrum of degenerative changes found in Obese/SHR did not appear in naloxone-treated rats.
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PMID:Anti-opiate (naloxone) suppression of Cushingoid degenerative changes in obese/SHR. 299 79

A 61-year-old male, while recovering from a Whipple's procedure for pancreatic carcinoma, was treated for 13 days with an insulin infusion pump for diabetes exacerbated by enteral hyperalimentation. Treatment with continuous subcutaneous insulin infusion resulted in improved blood glucose control. Associated with this improvement was a reduction in plasma cholesterol, triglyceride and free fatty acid levels. Plasma epinephrine, norepinephrine, glucagon and cortisol concentrations were also lowered although growth hormone levels remained unchanged. It is concluded that enhanced metabolic control during hyperalimentation results in a decrease in counter-regulatory hormone levels and an improvement in the catabolic state in this patient. These preliminary observations provide evidence for maintaining euglycemia in diabetic patients while receiving nutritional support.
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PMID:Continuous subcutaneous insulin infusion (CSII) reduces counter-regulatory hormone concentrations in a patient receiving enteral hyperalimentation. 310 71

Electrolytic lesions of the ventromedial hypothalamus (VMH) result in marked hyperphagia and obesity, but several studies have found the excess food intake and weight gain to be greatly reduced when lesions are produced by electrocauterization with radio-frequency current. Unlike electrolytic lesions, radio-frequency lesions leave few or no deposits of metallic ions that can potentially stimulate adjacent tissue. In the present experiment, weight gain and several endocrine responses previously associated with the VMH syndrome were compared in female rats given either electrolytic, radio-frequency, or sham VMH lesions. Both groups with VMH lesions became obese, but rats with radio-frequency lesions displayed only 63.2% of the weight gain of animals with irritative lesions (120.0 vs. 189.8 g in 20 days). Only rats with electrolytic lesions displayed elevated plasma insulin levels during an initial period of food restriction, but both groups with lesions were hyperinsulinemic when allowed to overeat. Plasma growth hormone levels were decreased by electrolytic lesions but unaffected by radio-frequency lesions. Morning corticosterone levels were elevated in both VMH groups, but only the rats with electrolytic lesions were found to have elevations in plasma adrenocorticotropin. It is concluded that some of the endocrine dysfunctions resulting from electrolytic VMH lesions are due to irritative stimulation rather than to tissue ablation.
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PMID:Radio-frequency vs. electrolytic VMH lesions: differential effects on plasma hormones. 328 3

Hormonal disturbances caused by hypothalamic pathology can be treated effectively by target hormone replacement in the case of failure of glandotropic hormone secretion. Hyposomatotropism in children has to be substituted by parenteral administration of growth hormone. In addition gonadotropins respectively gonadotropin releasing factor have to be given in order to restore fertility in hypothalamic hypogonadism. Posterior pituitary failure can be adequately replaced by administration of analogues of antidiuretic hormone. Hypothalamic pathology causing hypersecretion of anterior pituitary hormones may also be accessable to medical treatment. This pertains particularly to hyperprolactinemia and precocious puberty. However, there is no medical therapy so far for hypothalamic disturbances leading to veterative dysfunction like disturbances of temperature regulation and control of thirst and polyphagia. In this situation symptomatic correction of the abnormality represents the only possibility to keep these patients alive.
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PMID:Medical therapy of hypothalamic diseases. 399 50


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