Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histochemical investigations on elastic membranes of vessels under normally and diabetic conditions have been accomplished. These studies were made on man (diabetic and non-diabetic subjects) and on rats with streptozotocin-diabetes. The results are comparable among one another. The amino acids histidine, tyrosine and tryptophan were not demonstrable. The detection of primary NH2-groups (ninhydrin-Schiff-method and o-diacetylbenzen-reaction) was positive however. The results of the reactions in healthy men and animals were more distinct than in diabetic human subjects and animals. In healthy children the intensities of the histochemically reactions were higher than in adults.
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PMID:[Histotopochemical investigations on elastic membranes of blood vessels with special regard to diabetes mellitus. I. Proteins (author's transl)]. 12 78

The uptake of the nicotinamide adenine dinucleotide (NAD)-precursors nicotinamide, nicotinic acid and tryptophan in the pancreatic islets of mice was studied by use of autoradiographic methods. The ability of these substances to prevent streptoxotocin diabetes was studied in the same species. It was found that only nicotinamide was strongly accumulated in the pancreatic islets and nicotinamide was also the only NAD-precursor which protected against the streptoxotocin diabetes. Apparently there is a relationship between the ability of the NAD-precursors to be taken up in the pancreatic islets and their ability to prevent streptoxotocin diabetes.
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PMID:The uptake in the pancreatic islets of nicotinamide, nicotinic acid and tryptophan and their ability to prevent streptozotocin diabetes in mice. 13 65

1. Injection of L-tryptophan (750 mg/kg body wt.) led to pronounced hypoglycaemia in fed and 48 h-starved rats. 2. The hypoglycaemic effect is blocked by pretreament with p-chlorophenylalanine, compound MK-486 [Carbidopa: L-alpha-(3,4-dihydroxybenzyl)-alpha-hydrazinopropionic acid monohydrate] or methysergide, and potentiated by pargyline. 3. 5-Hydroxy-L-tryptophan is more potent and induces a more rapid hypoglycaemia than does tryptophan. Other tryptophan metabolites were not associated with hypoglycaemia. 4. Adrenalectomy increases, and acute experimental diabetes strongly decreases, the sensitivity of rats to tryptophan induction of hypoglycaemia. Diabetic animals were also insensitive to 5-hydroxytryptophan. 5. Metabolite concentration changes in the livers from tryptophan-treated 48h-starved and diabetic animals were consistent with a rapid inhibition of gluconeogenesis. This did not correlate with the hypoglycaemic response. 6. Tryptophan treatment was associated with a significant increase in the plasma [beta-hydroxybutyrate]/[acetoacetate] ratio; there were no changes in the plasma concentrations of urea, triacyglycerol, non-esterified fatty acids and glycerol. 7. These observations suggest that the hypoglycaemic action of tryptophan is mediated through formation of intracellular 5-hydroxytryptamine, and is unrelated to the inhibition of gluconeogenesis. It is unlikely that this increased synthesis of 5-hydroxytryptamine involves directly either the adrenal glands or the central nervous system.
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PMID:Tryptophan and the control of plasma glucose concentrations in the rat. 14 76

The effects of streptozotocin-induced diabetes and tryptophan content of the protein fed on protein intake regulation by weanling rats selecting from 10 and 60% casein diets were evaluated. In uncompensated diabetes the ratio of tryptophan to other selected neutral amino acids in plasma and brain tryptophan were reduced, protein intake per unit of body weight was increased, and serotonin, 5-hydroxyindoleacetic acid, and norepinephrine were unaffected. Enrichment of the tryptophan content of the ingested protein caused a decrease in protein, but not energy consumption of both diabetic and nondiabetic rats. The reduction in protein intake correlated inversely with increases in the tryptophan content relative to the neutral amino acids in plasma and with increases in brain tryptophan and serotonin levels in both diabetic and nondiabetic rats. The data suggest that protein-feeding behavior is regulated by a mechanism that includes brain serotonergic activity with insulin, through its influence on circulating amino acids, determining the quantity of protein consumed in relation to body weight.
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PMID:Diabetes, dietary tryptophan, and protein intake regulation in weanling rats. 15 94

Gluconeogenic conditions, such as administration of triamcinolone or alloxan diabetes, cause the following changes in the molecular structure and properties of rabbit liver fructose 1,6-bisphosphatase (D-fructose-1,6-bisphosphate 1-phosphohydrolase, EC 3.1.3.11): (1) the appearance of traces (about 10%) of a lighter subunit; (2) loss of tryptophan from all of the subunits, including those that show no apparent change in molecular weight; (3) increase in requirement for the positive allosteric effector, histidine; (4) increase in amount of enzyme, but not its specific activity. These changes are identical to those induced by cold or fasting, and are related to increased activities of lysosomal proteases. The results suggest that lysosomes may act as mediators of gluconeogenic stimuli.
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PMID:Hormonal effects on structure and catalytic properties of fructose 1,6-bisphosphatase. 17 48

A literature review of the effect of oral contraceptive (o.c.) use on various metabolic processes is presented. Several studies show an adverse effect of o.c. use on subclinical diabetes and on patients with manifest insulin-independent diabetes. Some researchers have found a beneficial effect of o.c. use on older diabetics. It has not been determined whether the estrogen or gestagen component of o.c.s is responsible for this decrease in glucose tolerance, nor has the mechanism for this effect been discovered. Changes in various plasma protein concentrations have been observed during o.c. use, which affect the blood coagulation and the blood pressure regulation systems. The estrogen component appears to be responsible for the increase in the serum triglyceride concentration during o.c. use; the mechanism is still unknown. Some studies indicate that o.c. use causes an increase in serum cholesterol levels, which could promote gall stone formation. An increase in Vitamin A concentration has been observed during o.c. use. Riboflavin, folic acid, vitamin B 12, and ascorbic acid levels have been shown to decrease during o.c. use. A decrease in pyridoxin levels during o.c. use indicates an increased metabolism of tryptophan to nicotinic acid robosyl-5-phosphate. This would cause a decrease in serotonin production, which could be a cause of the depression experienced by some o.c. users. An increase in the plasma copper and caeruloplasmin levels during o.c. use is apparently due to the estrogen component. An increase in transferrin and the serum iron levels have been observed during o.c. use. Contradictory findings are reported concerning the plasma concentration of zinc.
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PMID:[Metabolic studies under administration of oral contraceptives. A review]. 34 1

Ultrastructural characteristics as well as secretory and biosynthetic behavior of monolayer pancreatic cell cultures established from 4-day-old C57BL/KsJ misty diabetic (m db/m db) mice have been studied in comparison to normal littermate controls. Hypersecretion of glucagon by alpha-cells from BL/Ks misty diabetic mice after 2 days in vitro was found to precede any hyperfunction of the insulin-secreting beta-cells. The increased level of glucagon-release in BL/Ks cell cultures from diabetic mice was accompanied by a greatly enhanced level of incorporation of [3H]tryptophan into glucagon-like molecules whose specific radioactivity was up to 15-fold higher than that observed in cultures from genetic controls. The finding of an alpha-cell dysfunction in cultures established from preweaning diabetic BL/Ks mice suggests that glucagon could play an early role in shaping the events that culminate in the expression of frank diabetes in this inbred strain.
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PMID:Endocrine pancreatic cells of postnatal "diabetes" (db) mice in cell culture. 39 18

Thirteen women with chemical diabetes diagnosed in late pregnancy were found to excrete excessive amounts of urinary xanthurenic acid after a tryptophan load, indicative of a relative pyridoxine (vitamin B6) deficiency. Treatment with 100 mg pyridoxine daily for 14 to 23 days restored the urinary xanthurenic acid excretion to normal in all patients. Improvement of glucose tolerance was observed in only two of the patients studied, deterioration in six, and no significant change in the remaining five. The insulin response to glucose was unaltered during pyridoxine therapy.
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PMID:Pyridoxine treatment of chemical diabetes in pregnancy. 44 88

The urinary excretion of metabolites of the tryptophan leads to niacin pathway after an L-tryptophan load in patients with potential and latent diabetes, and in a third of those with chemical diabetes, was normal. In the remaining subjects with chemical diabetes and in those with clinical diabetes it was altered and characterized by an increase of xanthurenic acid and by a reduction of kynurenines and 3-hydroxyanthranilic acid. The thin-layer chromatographic pattern of tryptophan metabolites in the epidermis of patients with potential, latent, chemical, clinical diabetes was characterized by the kynurenine pathway metabolites that were also present in the epidermis of healthy subjects. Morevoer, the above pattern was characterized by the appearance of 5-hydroxytrptamine, and in patients with chemical and clinical diabetes by the appearance of xanthurenic acid.
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PMID:Identification of tryptophan metabolites in the healthy epidermis of diabetics. 59 99

Urine samples from members of 29 families of patients with Indian childhood cirrhosis (ICC) and nine families with related disorders gave positive reactions when tested with ferric chloride. Column chromatography showed that this was due to the presence of abnormally large amounts of tryptophan metabolites, notably 3-hydroxyanthranilic acid. Affected pedigrees had a significantly greater prevalence of peptic ulcer, adult cirrhosis, diabetes mellitus, migraine, and Parkinsonism than a control population. ICC may result from an inborn error of tryptophan metabolism in susceptible ethnic groups.
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PMID:Indian childhood cirrhosis: an inherited disorder of tryptophan metabolism? 69 56


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