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)

Blood glucose level and forebrain unit activity were simultaneously recorded in rats anesthetized with a ketamine IV infusion. Slight and transient fluctuations in glycemia, occurring either spontaneously or after IV injections of glucose or phlorizin, were observed. The spike frequency of more than 1/3 of the neurons tested in the lateral hypothalamic area was affected by these fluctuations. A majority of the responsive cells displayed either an activation during hypoglycemia or a depression during hyperglycemia. These neurons might mediate the effects of a drop in blood glucose on either meal initiation or neuroendocrine or autonomic events related to nutritional functions.
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PMID:Changes in lateral hypothalamic neuronal activity accompanying hyper- and hypoglycemias. 285 45

Salmon (Oncorhynchus kisutch) somatostatin (sSS; 4 or 8 ng/g body wt) or synthetic Gillichthys urotensin II (UII; 2 or 4 ng/g body wt) were injected intraperitoneally into juvenile freshwater coho salmon. Both sSS and UII caused a dose-dependent increase in plasma free fatty acids (FFA) which diminished with time. sSS induced an initial (1 hr) transient hyperglycemia. By contrast, UII tended to induce hypoglycemia, this effect being significant 5 hr after injection of the higher dose. Both sSS and UII depressed plasma insulin titers 1 hr after injection. By 3 hr, the sSS-associated insulin depression was no longer observed. UII treatment induced a hyperinsulinemia which was present 3 and 5 hr after peptide administration. Although no decreases in liver total lipid concentration or in mesenteric fat total tissue mass were observed, lipolytic enzyme activity within each depot was significantly enhanced by both peptides. Neither sSS nor UII altered 3H2O incorporation into fatty acids or neutral lipids. However, enhanced lipogenesis, particularly by UII, was indicated by increased NADPH production resulting from glucose-6-phosphate dehydrogenase activity. Both sSS and UII enhanced glucose mobilization, as indicated by decreased liver glycogen content and increased liver glucose-6-phosphatase activity. UII, but not sSS, stimulated glycogen synthetase activity. These results suggest that both sSS and UII stimulate hyperlipidemia by enhancing depot lipase activity and that although both factors are potentially gluconeogenetic, sSS seems to be glycogenolytic and hyperglycemic, whereas UII may channel glucose to FFA synthesis.
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PMID:Effects of somatostatin-25 and urotensin II on lipid and carbohydrate metabolism of coho salmon, Oncorhynchus kisutch. 288 97

Adverse effects of beta-adrenergic receptor blocking drugs can be divided into two categories: 1) those that result from known pharmacological consequences of beta-adrenergic receptor blockade; and 2) other reactions that do not appear to result from beta-adrenergic receptor blockade. Adverse effects of the first type include bronchospasm, heart failure, prolonged hypoglycemia, bradycardia, heart block, intermittent claudication, and Raynaud's phenomenon. Neurological reactions include depression, fatigue, and nightmares. It is not yet proven whether the beta 1-selective adrenergic blockers or those with partial agonist activity reduce the overall frequency of adverse reactions seen with propranolol. Patient age does not appear, in itself, to be associated with more beta-blocker side effects. Side effects of the second category are rare. They include an unusual oculomucocutaneous reaction and the possibility of oncogenesis. There are also many drugs that interact with beta-blockers, which may increase toxicity. Finally, there are specific patient characteristics where one beta-blocker may be more effective and safer than another.
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PMID:Beta-adrenergic receptor blockers. Adverse effects and drug interactions. 289 72

The purpose of this study was to determine whether the energy metabolism of an experimental rodent sarcoma was selectively depressed by the combination of inhibition of glycolysis and respiration. In vivo phosphorus-31 nuclear magnetic resonance spectroscopy was used to monitor the response of tumor or brain high-energy phosphate compounds to insulin hypoglycemia, rhodamine 123, or both agents in fasting rats with subcutaneous methylcholanthrene-induced sarcomas. Insulin or rhodamine 123 alone produced a similar 50% to 60% reduction in tumor adenosine triphosphate (ATP) concentration compared with controls injected with saline solution (p less than 0.05, one-way analysis of variance [ANOVA]). The combination of insulin plus rhodamine 123 resulted in a 90% reduction of tumor ATP concentration, which was significantly different from the effect of either agent alone (p less than 0.05, one-way ANOVA). Brain phosphocreatine and ATP concentrations were unchanged by these agents. Administration of dimethyl sulfoxide (DMSO)/glycerol, the vehicle for rhodamine, produced a 35% reduction of tumor ATP, which was similar to the effect of insulin alone but significantly different from rhodamine. The combination of DMSO/glycerol plus insulin hypoglycemia resulted in a 70% reduction in tumor ATP, which was significantly elevated compared with the combination of rhodamine plus insulin. Glucose deprivation induced by insulin, and combined with the inhibition of oxidative phosphorylation, produces an additive depression of tumor energetics. The drug vehicle DMSO/glycerol significantly depresses tumor energy metabolism, presumably because of its DMSO component, which may explain the previously reported antineoplastic efficacy of this solvent. Combinations of inhibitors directed at different points of tumor metabolism produced an enhanced depression of tumor energetics, whereas host tissue was protected.
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PMID:Inhibition of tumor high-energy phosphate metabolism by insulin combined with rhodamine 123. 304 41

A concern for the possible role of the blood-brain barrier (BBB) in the epilepsies was based on ultrastructural studies that demonstrated increased micropinocytosis in cerebral capillaries during seizures. Continued interest in the structure of the BBB has led to the demonstration that, in human psychomotor epilepsy, there is a thickening of the capillary basement membrane. These studies also suggest that an increase in capillary mitochondria and interendothelial tight junctions may characterize seizure-traumatized brain regions. These studies forecast an increased interest and understanding of the ultrastructural events associated with capillaries in seizure states. Additional focus on the BBB comes from the clinical use of anticonvulsant drug levels in the control and treatment of seizures. Debate as to whether free drug levels are appropriate continues. The brain capillary is the interface between blood-borne drug and the target site, and thus an increased understanding of the events associated with brain-plasma exchange has been sought. The concept that only that fraction of drug that is freely dialyzable is available for equilibration across the BBB is not supported by recent studies, which demonstrate that protein-bound ligands are able to dissociate and gain access to the brain in the course of a single capillary transit. It has been established that albumin-bound fatty acids, steroids, and anticonvulsant drugs more readily distribute into tissues than previously believed. Thus, traditional free drug hypotheses need to be expanded to account for the fact that dissociation constants measured in vitro are not the same as those measured in vivo. The BBB also regulates nutrient availability to the brain, and under normal conditions excess substrate is made available to the brain for metabolism. Indirect evidence is available to suggest that during seizures, BBB transport may indeed be the rate-limiting step. Specifically, glucose availability to the seizing brain may be restricted to such a degree that brain glucose utilization rates are no longer independent of plasma glucose levels. If it can be proven that BBB transport is the rate-limiting step during seizures, then it would be possible to augment brain glucose utilization rates by increasing plasma glucose levels. In addition, a depression of brain glucose utilization could be achieved by inducing hypoglycemia. It is not fully understood whether BBB rate limitation would persist postically, nor is it known whether BBB alterations may be global or restricted to the seizure focus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epilepsy and the blood-brain barrier. 308 37

To evaluate the hypothesis that depressed neuromuscular transmission causes dithiobiuret (DTB)-induced muscle weakness in rats, the temporal development of impaired treadmill performance and deficits in the nerve-elicited muscle contractions were compared during daily treatment with the toxicant (DTB, 1 mg/kg/day X 6 days). Diminished treadmill test performance after 4 days of treatment marked the initial detection of impaired motor function. At this time fading (loss of tension during tetanus) of gastrocnemius contractions elicited in response to 100-Hz sciatic nerve stimulation occurred in DTB-treated rats but not in controls. After 5 and 6 days of treatment, treadmill failure became complete, tetanic fade worsened dramatically, and peak contractile tension measured during trains of nerve stimulation (10-250 Hz) decreased progressively. Appearing by Day 6 were marked body weight loss, dehydration, hypothermia, and a depression in serum concentrations of thyroid hormones. Total oxygen content of the blood was not reduced at any time during treatment, and serum concentrations of glucose, sodium, potassium, calcium, chloride, and phosphorus in DTB-treated rats on Day 6 were similar to those of control animals. Therefore, hypoxia, hypoglycemia, or a serum electrolyte imbalance do not initiate or modulate the neuromuscular toxicity. Light microscopic evaluation of liver, kidney, lung, thyroid, and other organs in intoxicated rats was unremarkable and in skeletal muscles and selected sites of brain, spinal cord, and sciatic nerve no morphologically significant lesions were observed. Even when DTB-intoxicated rats were maintained in a state of flaccid muscle weakness for 5 continuous days, peripheral nerve lesions proximal to the intramuscular nerves were not detected. Thus, depressed neuromuscular transmission appears to be the primary cause of the flaccid muscle weakness and no evidence was obtained that nonneural effects of DTB initiate or modulate this effect.
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PMID:Temporal analysis of dithiobiuret neurotoxicity in rats and assessment of potential nonneural causes. 311 11

As part of the Collaborative Study of the Psychobiology of Depression, we have examined the pretreatment growth hormone response (delta GH) to insulin (0.1 U/kg) and the magnitude of the hypoglycaemic response in a large number of well-defined depressed patients (N = 132) and healthy controls (N = 80). After applying rigorous exclusion criteria, data were analysed from 93 patients and 66 controls for blood glucose response and from 56 patients and 52 controls for delta GH. Depressed patients, either unipolar or bipolar, showed less of a fall in glucose than controls. A weak association was found between the magnitude of the fall in glucose and the severity of depression. No significant differences were found in values for delta GH between the unipolar or bipolar depressed patients and controls either for males, pre-menopausal or post-menopausal females, or the total female group. These data do not support previous claims of a lowered delta GH response to insulin in depressed patients. However, the resistance to hypoglycaemia seen in the depressed patients is consistent with previous reports.
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PMID:Insulin-induced hypoglycaemic response and release of growth hormone in depressed patients and healthy controls. 328 9

Twelve trained males, in a fed state, were studied to examine the effect of pre-exercise fructose ingestion on endurance capacity during prolonged cycling exercise. Sixty minutes prior to exercise, subjects ingested either 60 or 85 g fructose or a sweet placebo. Mean exercise intensity initially required 62% of the maximal aerobic power and thereafter increased to elicit 72 and 81% of maximal aerobic power at 90 and 120 min of exercise, respectively. Exercise time (mean +/- SE) to exhaustion was significantly increased after fructose ingestion, as compared to placebo ingestion (145 +/- 4 vs 132 +/- 3 min, P less than 0.01). During the exercise, no differences were observed between both trials for oxygen uptake, heart rate, or perceived exertion. Serum glucose and insulin levels between both trials were not significantly different throughout the experiment. There were also no significant differences in serum-free fatty acids and glycerol levels as well as respiratory exchange ratio between fructose and placebo trials during the exercise. The results suggest that fructose ingestion is of benefit before prolonged exercise, because it provides a carbohydrate source to contracting muscles without transient hypoglycemia and a depression of fat utilization, and thereby delays the fatigue.
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PMID:Effect of pre-exercise fructose ingestion on endurance performance in fed men. 328 17

The multisystem involvement in acute pancreatitis (AP) is a reflection of the pancreatic gland's capacity to produce a number of potent vasoactive peptides, hormones, and enzymes. The various prognostic criteria are early evaluations of these metabolic derangements. The pathogenesis of hypocalcemia, long recognized as an indicator of severity of AP, is multifactorial. Imbalances of parathyroid hormone (PTH)-calcitonin, the interactions of glucagon, gastrin and other pancreatic hormones with PTH-calcitonin, the role of free fatty acids in binding serum calcium with albumin, and the translocation of calcium ion in muscles and liver, have been recently described but remain conflicting theories. Yet, the time-honored theory of calcium-soap formation enjoys wide acceptance. Hyperglycemia, hypoglycemia, and occasional ketoacidosis in acute pancreatitis have been studied thoroughly. The complex cause-and-effect relationship between hyperlipidemia with acute pancreatitis needs further study. The coagulation abnormalities seem to be initiated by activated trypsin, and their role in microvascular coagulation appears to form a unifying hypothesis for major organ dysfunction, but this requires further investigation. Adult respiratory distress syndrome may be the result of active enzymes that digest pulmonary surfactant and/or microvascular thrombosis. The depression of cardiac function and shock are suspected to be secondary to vasoactive peptides such as bradykinin, or myocardial depressant factor, whose structure has yet to be elucidated. The renin-angiotensin alterations and renal complications in acute pancreatitis have received scant attention in the literature. The onset of moderate visual disturbances, or even blindness, in a patient with acute pancreatitis as a result of retinal vessel thrombosis is fortunately uncommon. Rare but interesting are the manifestations such as subcutaneous fat necrosis, arthralgia, and pancreatic encephalopathy. Despite the extensive literature on the complexities of the pathogenesis of complications of acute pancreatitis, there have been very few advances in the prevention and management of specific complications. It is hoped that further work on modification of enzymatic disturbances induced in acute pancreatitis will result in its effective treatment and prevention of serious complications.
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PMID:Systemic complications of acute pancreatitis. 328

Overdose with 300 mg of nifedipine in a 54-year-old woman led to profound hypotension and reflex tachycardia. The patient was treated with intravenous fluids, calcium gluconate, and dopamine. Cardiac rhythm disturbances, hypoglycemia, and myocardial depression were not found. Recovery was rapid and uneventful. The clinical aspects of nifedipine overdose are discussed and possible treatment modalities are given.
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PMID:Nifedipine overdose. 341 17


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