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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A mentally retarded, 10-year-old female with obesity, hypotonia, clumsiness and mild ocular abnormalities excreted in her urine large amounts of alpha-aminoadipic acid. Amino acid analyser studies and gas-liquid chromatography--mass spectrometry (GC--MS) confirmed the presence of alpha-aminoadipic acid in both urine and plasma but, in contrast to most other patients with this disorder, failed to demonstrate significant levels of alpha-ketoadipic acid in urine. Other known causes of alpha-aminoadipic aciduria were eliminated by showing that levels of lysine, saccharopine and pipecolic acid in plasma and urine were normal and that the activity of glutaryl-CoA dehydrogenase was also normal. Loading with L-lysine and L-tryptophan both increased the concentration of alpha-aminoadipic acid in blood and urine compatible with the primary deficiency of alpha-ketoadipate dehydrogenase, in spite of the absence of alpha-ketoadipic aciduria. Dietary restriction of lysine and administration of vitamins B1 and B6 were unsuccessful in correcting the biochemical abnormality.
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PMID:Biochemical and clinical studies of a new case of alpha-aminoadipic aciduria. 11 47

Treatment of extreme obesity with jejunoileostomy was followed by a decreased level of S-tryptophan; permanently low concentrations were recorded postoperatively in 29 out of 52 patients. Patients in the low tryptophan group had a higher rate of weight loss and a hgiehr incidecnce of electrolyte disturbances and signs of liver injury. Symptoms of depression and anxiety were slightly more common in patients with low S-tryptophan. The influence of a decreased S-albumin and a deranged amino acid pattern on the non-protein-bound fraction of S-tryptophan needs further investigation. Serum levels of tryptophan rose significantly after rwo weeks' oral supplementation with 1.2 g L-tryptophan daily; this dosage was insufficient to normalize a low S-tryptophan level in patients who have undergone jejunoileostomy.
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PMID:S-tryptophan concentrations after intestinal bypass in extreme obesity. 32 48

The possible relationships between altered brain serotonin and calmodulin contents on the development of obesity were studied. Eight groups of mice separated by differences in phenotype, sex and age were used in this study. The brain contents of tryptophan, serotonin, 5-hydroxyindoleacetic acid (5-HIAA) and calmodulin were assayed. The contents of brain tryptophan showed no significant differences in any of the mice. The amount of brain serotonin in obese mice was 82% higher than that in their lean counterparts at four weeks of age, but only 11% higher at eight weeks of age. Regardless of age and sex, brain serotonin was positively correlated to the brain calmodulin in the lean mice (r = 0.559, p < 0.01), yet this was not found in obese mice. There was a strong positive correlation between serotonin and 5-HIAA in all mice (r = 0.679, p < 0.001). The elevated amount of serotonin in the brain of four-week-old obese mice is suggested to have important effects on thermoregulation in young genetically obese mice. The results also suggest that abnormal brain serotonin synthesis in obese mouse regulated by calmodulin might interact with certain factors, such as calcium ions, to complete the activation of serotonin-synthesized enzymes in the development of obesity.
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PMID:Relationship between brain serotonin and calmodulin in young, genetically obese (ob/ob) mice. 136 Feb 91

An association between the ingestion tryptophan and a syndrome characterized by scleroderma-like skin abnormalities, fasciitis, and eosinophilia has recently been recognized in the United States. We report the clinical and histopathological findings in nine patients and the results of biochemical analyses of tryptophan metabolism in seven patients with this syndrome. Edema of the extremities, frequently accompanied by pruritus, paresthesia, and myalgia, developed in the nine patients (six women and three men; age range, 30 to 66 years) 1 to 18 months after the start of therapy with tryptophan (1.5 to 3.0 g daily) for insomnia, depression, or obesity. Five patients were taking drugs (benzodiazepines) known to inhibit hypothalamic-pituitary-adrenal function, and one had adrenal insufficiency. All had blood eosinophilia in the acute phase of their illness (mean eosinophil count [+/- SD], 3.62 +/- 2.87 X 10(9) cells per liter). All had histopathological changes in the dermis and subcutaneous tissue typical of scleroderma, and seven patients had eosinophils. The fascia was inflamed and fibrotic, and adjacent skeletal muscle often showed perifascicular inflammation. Tryptophan was discontinued in all patients, and eight received prednisone. The cutaneous symptoms improved, but only two patients had complete resolution of their illness. The patients had plasma levels of tryptophan before and after an oral dose of tryptophan that were similar to those in normal subjects. Plasma levels of L-kynurenine and quinolinic acid, which are metabolites of tryptophan, were significantly higher in four patients with active disease than in three patients studied after eosinophilia had resolved or in five normal subjects (P less than 0.001)--findings consistent with the activation of the enzyme indoleamine-2,3-dioxygenase. This illness resembles eosinophilic fasciitis and probably represents one aspect of the recently reported eosinophilia-myalgia syndrome. The development of the syndrome may result from a confluence of several factors, including the ingestion of tryptophan, exposure to agents that activate indoleamine-2,3-dioxygenase, and possibly, impaired function of the hypothalamic-pituitary-adrenal axis.
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PMID:Scleroderma, fasciitis, and eosinophilia associated with the ingestion of tryptophan. 231 25

We recruited 10 patients with anorexia nervosa and 6 age- and height-matched control subjects. Basal and postprandial concentrations of glucose, insulin, cholesterol, amino acids, gastrin, and pancreatic polypeptide (PP) were measured in response to a standard mixed meal. The only satiety signal that was significantly different between the anorectic group and the control group was PP (P less than 0.001). Tryptophan-LNAA and tyrosine-LNAA ratios were not significantly different in the two groups; however, there was a trend toward a lower tryptophan-LNAA ratio in the anorectic group. Gastrin concentrations were significantly decreased in the anorectic group (P less than 0.001) as were basal insulin concentrations (P less than 0.05). Decreased gastrin concentrations may play a role in the gastric symptoms associated with anorexia nervosa. Previous findings that PP release is diminished in obesity, together with the present findings of PP increase in anorexia nervosa, suggest that this peptide may play a role in appetite control mechanisms.
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PMID:Potential regulators of feeding behavior in anorexia nervosa. 172 17

This review focuses on neurotransmitter and neuropeptide actions on food ingestion, as well as on some of the mechanisms that may lead to the development and maintenance of obesity. In particular, the role of hypothalamic amines (catecholamines, serotonin) in appetite control is described. Thus, hypothalamic noradrenaline appears to stimulate food intake, while an enhanced brain serotonergic neurotransmission leads to a suppression of food ingestion, preferentially of carbohydrate intake. The involvement of brain serotonin neurons in appetite control is most attractive, since serotonin synthesis and release is readily affected by either precursor loading (i.e., 1-tryptophan) or pharmacological manipulation (e.g., drugs such as fenfluramine or fluoxetine). Recent data now suggest that at least a subgroup of obese patients is characterized by a disturbed serotonergic neurotransmission, thus exhibiting behaviors such as carbohydrate craving. Among neuropeptides involved in appetite control, the most attractive candidate appears to be corticotropin-releasing hormone which is released by neurons of the paraventricular nucleus and produces a stress-like activation of the organism, and has a strong appetite-suppressant effect.
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PMID:[Central nervous appetite regulation: mechanisms and significance for the development of obesity]. 197 Jun 99

Long-term treatment with high doses of corticosteroids leads to the development of truncal obesity and focal fatty deposition. These deposits characteristically are located on the face, the nuchal and truncal areas, and episternally, as well as in the mediastinum and epicardium. We studied a patient with juxta-articular adiposis dolorosa who had L-tryptophan-associated eosinophilia-myalgia syndrome and was treated with high doses of prednisone. This is the first reported case of adiposis dolorosa occurring as a complication of corticosteroid treatment. Alterations of fat metabolism induced by corticosteroid excess may have played a role in the development of this unusual painful syndrome.
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PMID:Corticosteroid-induced juxta-articular adiposis dolorosa. 199 Sep 89

Obesity is a major nutritional disorder that produces many abnormal metabolic responses. The effect of injury-induced stresses acting synergistically with the state of excessive body fat is not well known. Plasma levels of circulating free amino acids reflect the net status of protein breakdown and utilization. Hypoaminoacidemia is a common finding in severe injury and its significance in obese subjects was investigated. We measured in 10 obese (body mass index [BMI] greater than 30) and 10 non-obese (BMI less than 30) traumatized (Injury Severity Score [ISS] 17 to 50) patients, the plasma levels of free amino acids in the early "flow" phase of injury when subjects were receiving maintenance fluids without calories or nitrogen. Postabsorptive control samples were obtained from 10 obese and 10 non-obese volunteers. Obese controls showed an increase in valine, leucine, isoleucine, and glutamic acid levels, and a decrease in glycine, tryptophan, threonine, histidine, taurine, citrulline, and cystine levels compared with lean controls. Hypoaminoacidemia was equally seen in traumatized obese and non-obese patients, and it was mainly due to a 24% decrease in nonessential amino acids. Remarkably, essential amino acid levels were the same in all groups. Arginine and ornithine levels were significantly different in traumatized obese compared with non-obese patients. The hypoglycinemia seen in non-obese trauma patients was absent in obese patients. The changes in levels of sulphur-containing amino acids also suggest that monitoring of these levels should be included in the nutritional management of obese trauma patients.
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PMID:Altered plasma free amino acid levels in obese traumatized man. 201 Oct 79

Age-related cataract is a condition characterized by multiple mechanisms and multiple risk factors. The mechanisms that bring about a loss in transparency include oxidation, osmotic stress, and chemical adduct formation. Risk factors for cataract include diabetes, radiation (ultraviolet B, x-ray), certain pharmaceutical substances, certain nutritional states, and possibly acute episodes of dehydration. Interaction occurs between and among mechanistic factors and risk factors. Thus nutrition must be considered as one part of a tapestry of intertwined events and responses. Certain experimental models for nutritional cataract have been useful for study of the cataractogenic process but are probably not important factors in the human disease. Little current evidence supports significant roles in human senile cataract for imbalances of tryptophan or other amino acids, deficiencies of calcium or selenium, or excessive intake of selenium. Overconsumption of galactose is likely to be hazardous only in subjects with genetic inability to metabolize this sugar. Vitamins with antioxidant potential (riboflavin, vitamin E, vitamin C, carotenoids) deserve further research scrutiny to ascertain their significance in cataract etiology. Excessive caloric intake needs to receive added emphasis as a factor contributing to cataract. Diabetes increases the likelihood of cataract three- to four-fold. Obesity, defined as more than 20% overweight, is considered a major risk factor for non-insulin-dependent, or type II, diabetes (69, 73). Weight control can be recommended as a prudent, safe, economic, and effective means of lowering risk probability for diabetes and the associated complication of cataract.
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PMID:Nutritional factors in cataract. 220 Apr 64

Authentic foods affect brain serotonin synthesis by modifying brain tryptophan levels, carbohydrates increasing and proteins decreasing these levels. The carbohydrate-induced rise in brain serotonin tends to diminish the likelihood that one carbohydrate-rich, protein-poor meal or snack will be followed by another. This mechanism is apparently disturbed in carbohydrate-craving obesity, which may explain why this syndrome responds well to d-fenfluramine, a serotoninergic drug. Pure nutrients like tyrosine or choline can also affect the rates at which their neurotransmitter products, the catecholamines and acetylcholine, are synthesized in and released from nerve terminals, suggesting that these compounds may find uses as drugs.
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PMID:Effects of their nutrient precursors on the synthesis and release of serotonin, the catecholamines, and acetylcholine: implications for behavioral disorders. 305 17


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