anorexia/tyrosine

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Tyrosine hydroxylase, tryptophan hydroxylase, biopterin, and neopterin in the brain of anorexia nervosa.

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The activities of tyrosine hydroxylase and tryptophan hydroxylase and contents of biopterin and neopterin were measured for the first time in various regions of human brain from a patient with anorexia nervosa (AN). In AN as compared with controls, tyrosine hydroxylase activity was markedly reduced

A Double Blind, Randomized Cross-Over Trial of Tyrosine Treatment on Cognitive Function and Psychological Parameters in Severe Hospitalized Anorexia Nervosa Patients.

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BACKGROUND Anorexia nervosa (AN) is characterized by self-induced malnutrition, affecting body image, mood, cognition and survival. Tyrosine, an essential amino acid is the precursor of catecholamines. The use of tyrosine to treat AN is based on experiments on diet restricted mice, in which it

Differential expression of monoamine oxidase A, serotonin transporter, tyrosine hydroxylase and norepinephrine transporter mRNA by anorexia mutation and food deprivation.

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The Anorexia (anx) mutation causes reduced food intake in preweanling mice, resulting in death from starvation within 3-4 weeks. We have found serotonin (5HT) hyperinnervation in the anx brain; altered noradrenergic (NE) innervation may also mediate eating disorders. We examined the expression of

Administration of IL-1beta to the 4th ventricle causes anorexia that is blocked by agouti-related peptide and that coincides with activation of tyrosine-hydroxylase neurons in the nucleus of the solitary tract.

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Inflammation-associated cachexia is associated with multiple chronic diseases and involves activation of appetite regulating centers in the arcuate nucleus of the hypothalamus (ARH). The nucleus of the solitary tract (NTS) in the brainstem has also been implicated as an important nucleus involved in

Tyrosine improves appetite, cognition, and exercise tolerance in activity anorexia.

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OBJECTIVE We have modified for mice the activity wheel model of Routtenberg to study the effects of tyrosine on exercise tolerance, behavior, and brain neurochemistry. METHODS Mice were fed for 2 h.d(-1) over a 2-wk period. During the second week, each group was injected daily with either saline or

The tyrosine kinase receptor Tyro3 enhances lifespan and neuropeptide Y (Npy) neuron survival in the mouse anorexia (anx) mutation.

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Severe appetite and weight loss define the eating disorder anorexia nervosa, and can also accompany the progression of some neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS). Although acute loss of hypothalamic neurons that produce appetite-stimulating neuropeptide Y (Npy) and

Involvement of protein kinase C and tyrosine kinase in lipopolysaccharide-induced anorexia.

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Injections of lipopolysaccharide (LPS, 3 microg) into the lateral ventricle elicited anorexia with fever and also decreased body weight in rats. The LPS-induced anorexia was inhibited by intracerebroventicular (i.c.v.) injections of anti-interleukin (IL)-1beta antibody (Ab), chelerythrine, genistein

L-tyrosine potentiates the anorexia induced by mixed-acting sympathomimetic drugs in hyperphagic rats.

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The effects of L-tyrosine (L-TYR) on the anorectic activity of several mixed-acting sympathomimetics were determined during the dark cycle in rats made hyperphagic by food deprivation. L-TYR (200 mg/kg) significantly potentiated the anorectic activity of phenylpropanolamine, (-)-ephedrine and

Studies in mice on the antagonism of (+)-amphetamine anorexia by alpha-methyl-p-tyrosine methyl ester HCl.

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[Imbalances of neutral plasma amino acids as a pathogenetic factor in anorexia].

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Studies in anorectic tumor-bearing rats indicate that anorexia is correlated to imbalances of neutral amino acids in blood and CNS. Consequently plasma amino acids of patients with neoplastic and non-neoplastic internal diseases were studied during phases of anorexia; special regard was given to the

Hyperammonemia and anorexia in Morris hepatoma-bearing rats.

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Inoculation of Buffalo rats with Morris hepatoma produced significant anorexia within four weeks and reduced body weight within two weeks. Blood ammonia concentration was increased by 113% when the rats were euthanized, five days after the development of anorexia. Infusing ammonium salts into normal

Possible role of ammonia in experimental cancer anorexia.

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Plasma concentrations of ammonia were elevated significantly in tumor-bearing rats prior to the onset of anorexia and continued to increase as the tumor grew and anorexia developed. Associated with this hyperammonemia were elevated levels of brain glutamine and large neutral amino acids

Mazindol anorexia is mediated by activation of dopaminergic mechanisms.

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1 Anorexia in rats following injections of mazindol (0.1-8 mg/kg i.p.) could be antagonized by pretreatment with a dopamine receptor blocker (primozide) but not by pretreatment with an alpha-adrenoceptor blocker (phenoxybenzamine), a beta-adrenoceptor blocker ((-)-propranolol), or a

Insulin reverses ammonia-induced anorexia and experimental cancer anorexia.

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Previous experiments suggest that experimental cancer-induced anorexia is associated with hyperammonemia and that daily injections of insulin may attenuate the anorexia for several days. In the present study, we determined whether similar daily insulin treatments would correct anorexia induced by

Amylin increases transport of tyrosine and tryptophan into the brain.

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Injection of amylin (diabetes-associated peptide) into the hypothalamus induces anorexia, increases brain metabolism of dopamine and serotonin and elevates brain level of tryptophan. When male Sprague-Dawley rats were treated with 50 mg/kg L-tryptophan and L-tyrosine ethyl ester 30 min prior to the

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