Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several assays with young chicks fed crystalline amino acid diets were conducted to investigate the effects of supplemental glycine, serine, threonine, arginine, or adenine on the growth depression resulting from consumption of excess methionine. Glycine was partially effective in alleviating the growth depression caused by excess methionine. The addition of threonine together with glycine improved performance still further. Efficiency of food utilization for weight gain was greater in birds fed the methionine-imbalanced diet supplemented with glycine and threonine than in those fed the control diet. Supplemental glycine, threonine, or adenine, but not arginine, was effective in ameliorating the hypoglycemia resulting from consumption of excess methionine. The rate of oxidation of a tracer dose of threonine was increased markedly by feeding 1.25% excess methionine. This was reflected in a 20% depression in threonine utilization for weight gain as measured by slope ratio. The data suggest that both threonine and glycine are antagonized by consumption of excess methionine.
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PMID:Methionine toxicity in the chick: nutritional and metabolic implications. 115 32

The effect of various doses of serotonin (5-HT) on the basal or insulin-stimulated gastric secretion was studied, for 4 hr after the injection, in unanesthetized rats with chronic gastric fistulas. The blood glucose and serum Na, K and Ca ions concentrations were also determined. Insulin produced hypoglycemia and hypokalemia, most pronounced in the first hr, and increased HCl and pepsin output, with a maximum at 2 hr after the injection. 5-HT significantly inhibited both basal and insulin-stimulated gastric secretion. The amine produced transient hyperglycemia, which was less pronounced in rats simultaneously receiving insulin. The inhibition of insulin-stimulated gastric secretion by 5-HT lasted for a longer period than the prevention of the biochemical changes brought about by insulin. The prevention by 5-HT of insulin hypoglycemia and hypokalemia may be of significant importance in the mechanism of the depression of insulin-stimulated gastric secretion.
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PMID:The influence of serotonin on insulin-stimulated gastric secretion, blood glucose and serum electrolyte levels in the unanesthetized rat. 116 2

Five-hour oral glucose tolerance tests (GTTs) differentiated 30 volunteer patients who considered themselves hypoglycemic into three major groups: those who had reactive hypoglycemia, those who were normal, and those who had diabetes. Clinical psychiatric evaluation and Minnesota Multiphasic Personality Inventory testing revealed that half of the 30 patients were experiencing a current psychiatric disorder, usually depression. Hysterical personality traits were also noted in many of the patients. The idea that reactive hypoglycemic patients have specific personality characteristics was not substantiated by the authors' data. They hypothesize that some patients with psychiatric illness may have their symptoms erroneously attributed to incidental GTT findings.
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PMID:A psychiatric study of patients referred with a diagnosis of hypoglycemia. 125 38

In order to prevent patients from stealing, two categories of delinquents are to be taken into consideration: Those who suffer from somatic diseases and psychoses, e.g. prophyria, hypoglycemia, hebephrenia, schizophrenia, depression, mania or epileptic semiconscious states must be treated according to the basic sickness and by means of a supporting psychotherapy. In court exculpation should be recommended. Other people who fell the urge to steal are psychosocially disturbed. This may begin with lying, bad results at school and during professional or university training, and sometimes with running away from home. As soon as the family doctor observes these or similar phenomena, he should inform the parents, in order to start a preventive therapy of the family together with the prospective thief.
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PMID:[Preventive psychotherapy for prevention of stealing]. 126 57

The covalent modification of receptor proteins via phosphorylation and dephosphorylation is one of the principal mechanisms controlling carbohydrate metabolism and is known to be regulated by various protein kinases. Recent studies indicated that many hormones may exert their effects on cellular metabolism by regulating intracellular c-AMP levels and by activating a c-AMP dependent protein kinase, i.e., protein kinase A. The metabolic disturbances during sepsis are characterized by an initial hyperglycemia followed by a progressive hypoglycemia and a depletion of hepatic glycogen content. The latter is coupled with a slowdown in glycogenesis, an accelerated glycogenolysis, and a depression in gluconeogenesis in the liver. Since the liver is the major organ that regulates the homeostatic level of blood glucose, it is conceivable that the sepsis-induced glucose dyshomeostasis might be mediated by changes in protein kinase activity and the kinetic characteristics of enzymes. The present experiment was designed to study the correlation between protein kinase A and the pathophysiology of hepatic glucose dyshomeostasis during sepsis. Sepsis was induced in rats by cecal ligation and puncture (CLP). Late sepsis occurred 18 hours after CLP. Protein kinase A was extracted from the rat livers by acid precipitation and ammonium sulfate fractionation, and then partially purified by DEAE-cellulose. The results show that in the late sepsis, type-I protein kinase A (eluted at low ionic strength) activity was significantly decreased by 34-52% (P < 0.01). The kinetic parameters such as Vmax's for ATP, histone, and c-AMP were also significantly decreased from the control values of 6.1 +/- 0.9, 5.4 +/- 0.8, and 5.1 +/- 1.9 nmoles/mg.min. to 3.6 +/- 0.5, 2.8 +/- 0.3, and 2.5 +/- 0.5 nmoles/mg.min., respectively. Analysis using Hill's equation indicates that the S0.5 and n (Hill coefficient) values of the various substrates and activators for type-I protein kinase A remained unchanged. In the case of type-II protein kinase A (eluted at high ionic strength), the Vmax, S0.5, and n values for ATP, histone, and c-AMP were unchanged during late sepsis. The results of the present study indicate that the activities and kinetic characteristics of type I protein kinase A in rat liver are modified during late sepsis. Since protein kinase A is known to regulate glucose metabolism through adrenergic receptor mediation, these findings may have a pathophysiological significance in the understanding of hepatic glucose dyshomeostasis during sepsis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Kinetic studies of protein kinase A in rat liver during late sepsis]. 129 61

We electromagnetically measured blood flow to one cerebral hemisphere and determined cerebrovascular reactivity to vasoconstrictor and vasodilator stimuli during normoglycemia and insulin-induced hypoglycemia in unanesthetized goats. Control blood glucose concentration was 84 +/- 4 mg, and insulin, injected intravenously, decreased glycemia with a concomitant increment in cerebral blood flow and reduction in cerebrovascular resistance in all the animals. When glycemia decreased to 60 to 65 mg/dl, the animals began to show signs of increased adrenergic activity, and when it decreased to less than 30 mg/dl, they showed signs of CNS depression. Cerebral blood flow began to rise significantly at a glycemia of 50 to 55 mg/dl, and progressively increased to reach an increment of 36% +/- 4% when glycemia was less than 30 mg/dl. Norepinephrine (0.3 to 9 micrograms), tyramine (50 to 500 micrograms), and 5-hydroxytryptamine (0.1 to 9 micrograms) reduced cerebral blood flow, and this effect was lower during severe hypoglycemia. Acetylcholine (0.01 to 1 microgram), isoproterenol (0.03 to 3 micrograms), diazoxide (0.3 to 9 mg), and inhalation of 10% CO2 in air increased cerebral blood flow, and this effect was also lower during severe hypoglycemia. The results show that insulin-induced hypoglycemia causes cerebral vasodilation and reduction of the capacity of cerebral blood vessels to constrict and dilate. They also show that the glycemic thresholds for increasing cerebral blood flow are near to, or slightly lower than, the thresholds for hypoglycemic symptoms. This experimental model of hypoglycemia closely resembles the conditions in hypoglycemic patients and permits serial evaluation of the cerebrovascular effects of hypoglycemia without using anesthesia.
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PMID:Effects of hypoglycemia on the cerebral circulation in awake goats. 131 45

In this study, 7 hospitalized patients with major depression (MD), 5 hospitalized patients with schizophrenia (S), and 13 control subjects (C) were administered 0.15 units/kg of regular insulin at 1600 h by intravenous bolus infusion. ACTH, cortisol, and glucose levels were measured intermittently for 2h following infusion. Baseline ACTH, cortisol and glucose levels were similar in Cs, MDs, and Ss. The mean glucose nadir was equivalent for Cs, patients with MD, and patients with S. Patients with MD had a blunted ACTH response (F = 3.28; df = 12,126; p = .0004) and cortisol response (F = 4.20; df = 12,132; p = .0001) to hypoglycemia when compared to Cs and patients with S. Carroll Depression Rating Scale scores in patients with S (23 +/- 10) were similar to patients with MD (30 +/- 8) and significantly higher than in controls (1 +/- 2) (F = 55.2; df = 2.22; p = .0001). These findings suggest that patients with MD show different ACTH and cortisol responses to hypoglycemic stress which are not explained by negative feedback of baseline ACTH or cortisol, glucose nadir, or the number of depressive symptoms per se.
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PMID:Blunted ACTH response to hypoglycemic stress in depressed patients but not in patients with schizophrenia. 131 84

In 57 patients with psicovegetative disorders and abnormal MMPI, abnormality in MMPI scales indicating hypochondriasis, hysteria, gender deviant, paranoia, psychastenia, schizophrenia, hypomania or introversion was accompanied by increased plasma catecholamine levels and/or responses to hypoglycemia or by an increased cardiovascular reactivity. A high depression scale was associated with lower plasma catecholamine levels. Blunted plasma growth hormone responses to hypoglycemia were found in abnormal hypomania scale, and augmented responses of plasma cortisol in abnormal hysteria or schizophrenia scales. Paranoia and hypomania traits correlated with absence of morning-evening differences in blood cortisol levels. Electrodermal responses compatible with increased sympathetic activity correlated with high hysteria, gender, paranoia, schizophrenia or hypomania MMPI scales. This study indicates that most psychopathological traits in MMPI are accompanied by humoral and/or electrophysiological signs of abnormality of the autonomic nervous system.
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PMID:Some neurovegetative correlates of Minnesota Multiphasic Personality Inventory (MMPI) 136 36

In this study we have examined the direct glucoregulation of prolactin secretion from normal anterior pituitary cells in vitro and have found that changes in medium glucose concentration regulate the amount of prolactin released. Nature and/or degree of this response to glucose was influenced by some effect, long-lived in vitro, which was correlatable to serum insulin levels. When the cells were derived from animals with mean low-normal serum insulin levels, there was a stimulation of prolactin secretion by hypoglycemia, the response was rapid, transient, dose-dependent, and could be duplicated by 2-deoxyglucose. When the cells were derived from animals with a higher mean serum insulin level, the prolactin secretion from the cells was slowly, adversely affected by hypoglycemia. Conversely, elevated glucose caused a depression in prolactin secretion in the first group and a stimulation of prolactin secretion in the second. We conclude (1) that modulation of glucose levels in vitro regulates prolactin release from pituitary mammotrophs and (2) that this glucose regulation of prolactin release is in turn coregulated with or regulated by insulin.
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PMID:In vitro glucoregulation of prolactin secretion. 136 92

The effects of insulin-induced hypoglycemia on catecholamine secretion were investigated in patients with various neurological disorders affecting the autonomic nervous system. In control subjects, insulin-induced hypoglycemia resulted in marked increases in plasma epinephrine and norepinephrine levels. Heart rates were increased within 15 minutes after the insulin injection which were associated with slight elevation and depression of systolic and diastolic blood pressure, respectively. In patients with upper level spinal cord lesions (C1-T6) of various etiology, Shy-Drager syndrome and familial amyloidosis, insulin-induced hypoglycemia failed to increase plasma epinephrine and norepinephrine levels and resulted in falls in systolic and/or diastolic blood pressure 15 minutes after the injection. Heart rates were increased at 30-45 minutes after the injection. In patients with lower spinal cord lesions (T10-L1), neurosyphilis or brain stem tumor with orthostatic hypotension, the catecholamine responses were normal and blood pressure did not fall during insulin-induced hypoglycemia. In patients with Parkinson's disease and spinocerebellar degeneration with autonomic symptoms catecholamine responses were not impaired. These findings suggest that any lesion involving the sympathetic efferent systems of baroreflex such as the spinal descending pathway, sympathetic preganglionic neuron and peripheral nervous system causes both impairment of catecholamine secretion and a fall in blood pressure during hypoglycemia, and that lesions in sympatho-afferent system may not affect the secretion of catecholamine and neural control of blood pressure.
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PMID:[Effects of insulin-induced hypoglycemia on catecholamine secretion and blood pressure in neurological disorders affecting autonomic nervous system]. 162 51


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