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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent psychiatric literature is reviewed to demonstrate the general state of clinical psychiatry. The advent of chemical therapies requires that psychiatrists receive comprehensive training in organic and dynamic approaches. Consultative collaboration between psychiatrists and physicians is encouraged though there is also a conspicuous need for physician training in consultative techniques and referrals. Diagnostic classifications by the psychiatrist are discussed. Rehabilitation methods in the community and family require more research and awareness on the part of psychiatrists. The manifold variety of investigations, studies, treatments, and rehabilitation of schizophrenics is discussed at length and the often contradictory conclusions are noted. The scope of analysis and treatment of depression is reviewed and certain etiological hypotheses associated backgrounds and depression are shown to be invalid. Suicide and its prognostication is covered as well as narcotic addiction and other disorders such as hyperphagia, anorexia, and dystonia musculorum deformans. 1 study is cited, based on an investigation of 120 children born as a result of the mothers being refused an abortion, suggesting that early rejection rather than early bereavement contributes to a higher risk of psychiatric difficulties in later life.
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PMID:Clinical psychiatry. 488 Jan 69

Injection of norepinephrine in the lateral ventricles of rats recovering from lateral hypothalamic anorexia caused immediate feeding and, frequently, overeating. Intraventricular administration of the alpha-noradrenergic blocker, phentolamine, suppressed feeding in both normal rats and rats that had recovered from lateral hypothalamic lesions. Feeding is reinforced by ascending medial forebrain bundle fibers that form alpha-noradrenergic synapses in the hypothalamus and forebrain. Damage to these fibers suppresses feeding by reducing noradrenergic transmission and, hence, the rewarding value of food. Recovery of feeding after hypothalamic lesions coincides with the recovery of noradrenergic reward function.
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PMID:Norepinephrine: reversal of anorexia in rats with lateral hypothalamic damage. 554 11

This review summarizes recent work that focuses on the role of endogenous opioids (EOs) and opiate receptors in the control of food intake. Although the anorexic effect of opiate antagonists are now well accepted, the exact EO, site(s), and mechanism(s) of action remain to be established. However, accumulating evidence suggests that dynorphin, an endogenous ligand for kappa-type opiate receptors, is an important regulator (stimulant) of appetite. The roles of other EOs, such as beta-endorphin, are less clear. EOs appear to be involved in maintaining normal feeding behavior and are likely responsible for the overconsumption of fat in genetically obese and stressed subjects. Opiate antagonists block overconsumption of palatable foods, thus offering a promising approach to weight reduction for some overweight individuals. Anorexias may follow from a deficiency of kappa-type opioid activity, and surprisingly, can also result from excess opioid activity. Indeed, opiate antagonists of the mu type (naloxone) can enhance eating and weight gain in certain anorexic conditions. Therefore, it appears that excess opioid agonist activity may result in hyperphagia or anorexia (depending on the opiate receptor type). Finally, opiate antagonists may help normalize both types of pathological feeding states.
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PMID:Opioids, feeding, and anorexias. 614 54

The effects of adrenalectomy on food intake, weight gain, plasma glucose, and corticosterone levels were investigated in normal untreated controls and gold thioglucose-(GTG) treated hyperphagic obese mice. Adrenalectomy of normal untreated mice was followed by a transient reduction in food intake and body weight with a return, after approximately 7 days, to levels which paralleled those of untreated sham-operated mice. Plasma corticosterone levels were significantly depressed in all untreated adrenalectomized mice. Plasma glucose levels were not affected by adrenalectomy. In sharp contrast to the response of untreated adrenalectomized mice, adrenalectomy of GTG-treated hyperphagic obese mice was followed by a sudden and persistent drop in food intake (anorexia) and body weight. These mice were unable to maintain their body weight. Despite this condition, the mice did not appear to be physically debilitated until a short time (6-12 h) before their death which was preceded by a period of severe hypoglycemia. These findings indicate that the hyperphagia and weight gain of GTG-treated obese mice is dependent on adrenal hormones. The anorexia after adrenalectomy of GTG-treated hyperphagic obese mice may be the result of a direct dependence of central or peripheral structures involved in the regulation of food intake on adrenal hormones. Alternatively, these structures may be affected by the action of metabolites or hormones which arise as a consequence of adrenal insufficiency.
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PMID:Anorexia after adrenalectomy in gold thioglucose-treated obese mice. 640 38

A patient with multiple enteric fistulae, after months of parenteral hyperalimentation, developed, severe depression accompanied by delirium, dermatitis, pallor, paresthesia, nausea, vomiting, anorexia, and headaches. His symptoms improved after treatment with parenteral biotin. Biotin-deficiency should be suspected in patients on hyperalimentation (without biotin supplementation) who develop similar symptoms.
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PMID:Biotin-responsive depression during hyperalimentation. 640 8

Two studies were conducted to measure the metabolic influence of tumor growth in rats. Parameters for the metabolic state were wound-healing qualities of colon and skin. Both early and later stages of tumor growth lowered wound healing qualities to a statistically significant degree. No anorexia or weight loss was found in this rat-tumor model during the study period. Intravenous hyperalimentation (IVH; with proteins and carbohydrates) of tumor-bearing rats stimulates tumor growth but at the same time restores wound-healing qualities to control levels, both during early and later stages of tumor growth. It is suggested that tumor growth leads to an as yet not measurable disturbance of the metabolic equilibrium but that IVH can replenish the tumor-bearing host and restore the metabolic equilibrium.
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PMID:The influence of intravenous hyperalimentation (IVH) on wound healing in tumor-bearing rats. 641 78

Rats were made hyperphagic by 6-hydroxydopamine (6-OHDA) injected bilaterally into the ventral midbrain; then they were restricted to a 6 h/day feeding schedule and tested for appetite suppression with amphetamine and fenfluramine in randomized order. Amphetamine anorexia was diminished while fenfluramine anorexia was enhanced (both P less than 0.001). The opposite effect on fenfluramine anorexia shows that the effect of 6-OHDA on amphetamine anorexia was not due to hyperphagia masking the anorexia. Norepinephrine in the forebrain was 90% depleted, but DA and serotonin levels were within 9% of normal. These results demonstrate a new way to dissociate amphetamine and fenfluramine anorexia, as others have done with lateral hypothalamic lesions or DA depletion. The 6-OHDA injections, which were of a type that cause hyperphagia, apparently destroyed a substrate for amphetamine anorexia and also facilitated a substrate for fenfluramine anorexia.
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PMID:Diminished amphetamine anorexia and enhanced fenfluramine anorexia after midbrain 6-hydroxydopamine. 642 Aug 20

A nutritional support team was used in the assessment and management of patients on a general urological service. Indications for nutritional evaluation included history of weight loss, anorexia, significant infection, chronic neoplastic disease, trauma or major surgery. The fat and protein status of the patient was assessed by anthropomorphic and laboratory determinations. The patient then was categorized as having mild, moderate or severe degrees of nutritional depletion. Deficiencies in vitamins, trace elements or essential fatty acids were not noted. Caloric and protein needs were calculated by multiplication of the basal energy expenditure by a metabolic activity factor, which was derived from the degree of illness or stress. Nutritional support was provided by enteral feedings via oral, nasogastric or jejunal feeding tubes and/or intravenous hyperalimentation via peripheral or central venous nutrient lines. During a 6-month interval nutritional consultation was requested for 50 patients, who represented 7 per cent of the urological admissions. Nutritional support was provided for patients who had obstructive uropathy with or without neoplasms, radiation cystitis, sepsis, urinary fistulas, mental depression, end stage renal disease or neurological dysfunction. In patients in whom urological treatment controlled the disease nutritional support maintained the weight, and stabilized serum albumin and lymphocyte counts. We concluded that a nutritional support program has a significant and, often, unappreciated role in the management of urological patients.
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PMID:Nutritional support in a general urological service. 642 56

A variety of recent literature suggests that brain gamma-aminobutyric acid (GABA) plays an important role in the control of feeding. One such line of evidence is that pharmacological inhibition of brain GABA transaminase (GABA-T) produces dose-dependent anorexia in otherwise normal rats. To determine the generality of these findings we tested the ability of the GABA-T inhibitor ethanolamine-O-sulfate (EOS), to produce anorexia in three animal models of obesity: rats with medial hypothalamic lesions, rats exposed to palatable foods or Zucker fatty rats. Following intracisternal injection of 100, 200 or 400 micrograms EOS, all three models of chronic overeating showed dose-dependent anorexia of similar magnitude and duration to that seen in appropriate controls. These observations provide empirical support for previous suggestions that treatments which enhance brain GABA neurotransmission merit investigation for their potential use in treating excess energy consumption.
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PMID:Anorectic potency of inhibiting GABA transaminase in brain: studies of hypothalamic, dietary and genetic obesities. 653 93

Overeating and obesity relative to controls was produced by multiple bilateral injections of 0.5 mg of amphetamine in the lateral ventricles of female rats eating a palatable, high fat diet. This behavioral and physiological rebound following the expected period of anorexia was accompanied by long-term depletion of dopamine in the striatum and of norepinephrine in the hypothalamus. This suggested the next experiment in which 50 micrograms of amphetamine were injected repeatedly in the lateral hypothalamus; again a brief period of anorexia was followed by hyperphagia and chronic obesity. This suggests that amphetamine acts in the lateral hypothalamus not only to suppress feeding, but in high doses it may also have local neurotoxic effects that cause an upward shift in body weight maintained by overeating.
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PMID:Amphetamine-induced hyperphagia and obesity caused by intraventricular or lateral hypothalamic injections in rats. 657 83


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