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)

Cerebral glucose utilization is markedly increased in most areas of the cerebral cortex and reduced in many subcortical structures during spreading cortical depression. During recovery, cortical glucose utilization is still elevated, but the increased metabolic activity is distributed in columns running perpendicularly through the cortex.
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PMID:Cerebral glucose utilization: local changes during and after recovery from spreading cortical depression. 75 88

Fenfluramine has been used for a number of years as a short-term adjunct to diet in the management of obesity. Controlled studies and clinical experience have shown that it possesses anorectic activity at least as good as that of other therapeutically useful drugs of its type, but like these drugs it has only a limited role in the overall management of obesity. Tolerance to the anorectic effects of fenfluramine may possibly develop more slowly than to other chemically related drugs in patients with refractory obesity. The mechanism of its anorectic action is probably by an effect on the appetite control centres in the hypothalamus, rather than by an effect on glucose and lipid metabolism. However, its effect in enhancing glucose uptake into skeletal muscle may be of advantage in diabetes mellitus, preliminary studies suggesting that it is of potential use in maturity-onset obese diabetics who cannot be adequately controlled by dietary measures alone. The starting dosage in obesity of 40mg daily should be increased gradually over 2 to 4 weeks to 60 to 120mg. In general, little extra benefit is gained by higher dosage. When a course of therapy is to be discontinued, fenfluramine dosage should be reduced gradually over a period of 2 to 4 weeks in order to avoid mood depression which has occurred in some patients on abrupt withdrawal of the drug. With these recommendations, the majority of patients tolerate fenfluramine satisfactorily, although some patients may have to discontinue the drug because of troublesome gastro-intestinal problems, diarrhoea, drowsiness or dizziness. Unlike other amphetamine-derived anorectics, fenfluramine is not a central stimulant in therapeutic doses, and it probably has little abuse potential.
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PMID:Fenfluramine: a review of its pharmacological properties and therapeutic efficacy in obesity. 76

Propranolol is known to decrease ischaemic damage in developing myocardial infarction. Besides acting on mechanical parameters which help determine the balance of oxygen supply and oxygen demand in the ischaemic tissue, propranolol decreases the myocardial uptake of free fatty acids and increases that of glucose. It is suggested that propranolol may favourably alter developing myocardial infarction in dogs by altering the supply of substrates reaching the ischaemic zone. However, propranolol also decreases enzyme release from isolated rat hearts with coronary ligation at a relative constant arterial free fatty acid concentration. Propranolol causes more marked depression of mechanical function and of heart rate in hearts perfused with free fatty acids than with glucose. It is suggested that the glucose-promoting and anti-lipolytic actions of propranool might be important not only in decreasing infarct size but also in helping to prevent undesirable side effects in hearts with experimental myocardial infarction.
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PMID:Propranolol and experimental myocardial infarction: substrate effects. 78 52

A brief survey of the literature on the side effects of oral contraceptives is given. Of the many influences on laboratory results those related to (reversible) cholestasis or to a change in protein synthesis are the most important ones. A decrease of the tolerance for glucose is sometimes observed. Few of the clinical side effects attributed to oral contraceptives can be directly correlated with the pharmaceutical action of these drugs. Many so-called side effects of the pill are due to other factors such as altered psychosociological or sexual behavior, etc. However, among users of oral contraceptives there is a significant decrease in the number of benign tumors, particularly of the breast, the uterus and the ovaries. It is still an open question if this also signifies protection against cancer. Anemias due to iron deficiency are less frequent among users of the pill. According to recent studies arterial hypertension and cholecystopathies are probably directly related to oral contraceptives, but a causal relation has not been proven for migraine, headaches, depression etc. An elevated risk for vascular complications seems to be well established: there is a 4-6-fold increase of the estimated risk for venous thrombo-embolism and a 4-9-fold increase for cerebrovascular accidents among users of oral contraceptives when compared with nonpregnant women of the same age not using the pill. Oral contraceptives act as a supplementary factor of risk which may cumulate with other similar factors, such as arterial hypertension, hyperlipidemia, overweight, smoking etc. Mortality due to oral contraceptives is very much 10-50 x) inferior to the one caused by delivery and the post partum state. Since the number of failures in prevention of pregnancies is less for oral contraceptives than for any other method of contraception, the overall risk of death under oral contraceptives in this age group of women is least.
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PMID:[Real and seeming side-effects of oral contraceptives with an emphasis on medical and haematological problems. Review of literature (author's transl)]. 79 Mar 74

A double-blind cross-over study was performed on 12 men sith stable angina pectoris in order to determine the effect of antilipolytic treatment on exercise tolerance and exercise-induced electrocardiographic changes. The men were exercised to the onset of anginal pain using a reproducible and standardized ergometric load. A nicotinic acid analogue was used to reduce plasma free fatty acids and free glycerol before and during exercise testing and to eliminate their post-exercise rise. This was associated with significant reduction of exercise-induced ST segment depression (p less than 0-005), though there was no significant difference in the duration of exercise before the oneset of pain. A change in the prportions of lipid and carbohydrate for oxidation by the ischaemic myocardium, making relatively more glucose available, is a likely explanation.
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PMID:Antilipolytic therapy in angina pectoris. Reduction of exercise-induced ST segment depression. 79 43

Coma and other neurologic abnormalities are present in patients with either diabetic ketoacidosis (DKA) or nonketotic coma (NKC), and the cause of such phenomena are not known. Patients with NKC also manifest seizures and focal neurologic changes. Treatment of diabetic coma with insulin may induce cerebral edema by as yet undefined mechanism(s). In patients with DKA, cerebral oxygen utilization is impaired, and there is hyperviscosity of the blood. A substantial part of the brain's energy source is derived from ketones, which in themselves can depress sensorium. Extracellular hyperosomolality is present, which may also contribute to the genesis of coma. In addition, most ketoacidotic patients have associated medical conditions, which may further impair consciousness. Biochemical changes in the brains of animals with DKA include impairment of both phosphofructokinase activity and pyruvate oxidation, and accumulation of citrate. The net effect upon sensorium in ketoacidotic patients probably represents the interaction of most of the above factors and differs markedly among individuals. Patients with NKC manifest not only depression of sensorium, but also focal motor seizures, hemiparesis, and other neurologic changes, such as aphasia, hypereflexia, sensory defects, autonomic changes, and brainstem dysfunction. Most of the aforementioned changes revert to normal after correction of hyperosomolality. Gamma amino butyric acid, which has been shown to elevate the seizure threshold, is normal in brains of ketoacidotic animals, but may be low in nonketotic coma. Also, hyperosomolality per se may produce seizures. Cerebral edema may complicate the treatment of either DKA or NKC. The available experimental evidence suggests that many of the commonly held theories for the production of such brain swelling probably do not occur. There is no breakdown of the sodium pump, sorbitol or fructose do not accumulate in brain, and brain glucose is only about 25 percent of that in plasma; Cerebral edema is probably produced largely by a direct action of insulin on brain at a time when plasma glucose is approaching normal values. Cerebral edema can thus theoretically be avoided by stopping insulin when plasma glucose has been lowered to values approaching normal.
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PMID:Neurologic manifestations of diabetic comas: correlation with biochemical alterations in the brain. 80 37

The three major phases in the secretory process in the exocrine pancreas (synthesis, intracellular transport, zymogen discharge) have been tested in vitro after changing circulating insulin levels in rats in vivo. One group of rats received a continuous infusion of glucose for periods up to 72 hours, which keeps blood glucose levels above 200 mg/100 ml and immunoreactive insulin (IRI) raised to 130 muU/ml. As a result of this treatment, amylase content in the pancreas increases by 25% while chymotrypsinogen and lipase show a comparable decrease. The rate of total protein synthesis increased by 40% after 48 hours of infusion. The basal and carbamylcholine stimulated discharge of newly synthesized proteins are not altered. The baseline discharge of amylase is increased significantly, while the discharge of lipase and chymotrypsinogen decreased below control levels. Similar results are obtained, if circulating insulin levels are raised by the application of glibenblamide (HB419) for a period of 24 hours. Protein synthesis increases by 26.5% and baseline discharge of amylase by 50%. In chronic alloxan diabetic animals the alteration of the exocrine pancreatic function depends on the severity of the diabetes and relates to circulating insulin levels. Animals with highest blood glucose levels and low or undetectable insulin concentrations show a disappearance of amylase from the exocrine pancreas and a depression of the rate of protein synthesis by 30%. The results suggest a direct effect of insulin on protein biosynthesis and zymogen discharge, most pronounced for amylase.
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PMID:Regulation of exocrine pancreatic secretory process by insulin in vivo. 80 10

Ro 2-2985 increased mean arterial blood pressure in both the venous bypass preparation and the intact animal; however, total peripheral resistance increased in the venous bypass preparation with a constant cardiac output but decreased in the intact animal with an increase in cardiac output. These observations indicate a drug-related increase in the distensibility of the aorta at the same arterial pressure. In vivo ventricular function curves were shifted to the left indicating enhanced myocardial performance with the translocation of large volumes of blood to the central circulation since total body venous compliance was significantly decreased. Beta adrenergic blocking doses of propranolol blocked the positive inotropic effect of Ro 2-2985 while myocardial depression produced by toxic doses of propranolol was reversed. This observation suggests several mechanisms for the Ro 2-2985 metabolic mediation of myocardial muscle contraction. The cardiovascular effects produced by Ro 2-2985 were accompanied by a marked polycythemia and a decrease in plasma volume without a change in total circulating blood volume, while blood glucose values showed a nonsignificant increase. Ro 2-2985 produced a marked increase in cardiac output. The increase in myocardial performance appears to be complex since myocardial force of contraction, dT/dt, dP/dt:P40 and Vmax were all increased. RO 2-2985 increased coronary flow without an increase in resistance. There were no significant increases in myocardial arteriovenous glucose, lactate, K+, Ca++, Na+ or Cl.
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PMID:The cardiovascular pharmacology of the antibiotic ionophore Ro 2-2985 (X537A). 83 57

It has previously been shown that nicotinic acid (NA)-induced depression of free fatty acids (FFA) stimulates the secretion of GH and glucagon. To evaluate this hormonal response further, we studied the influence of different doses of glucose administered by continuous iv infusion on the GH and glucagon increase during NA-induced FFA depression. In ten male non-obese volunteers, FFA depression by the infusion of NA (2.3 g over a period of 210 min) resulted in a late rise (from 150 min on) of GH (From 1.1 to 25.9 ng/ml) and an early increase (from 30 min on) of glucagon (from 71.7 to 138.2 pg/ml). When glucose was infused (approximately 60, 120 and 180 g, respectively, over a period of 270 min) during NA-induced FFA depression, the GH rise was reduced and delayed in relation to the amount of glucose infused, but could not be completely abolished (maximal GH concentration during the three NA-plus-glucose infusions: 16.5, 8.0 and 6.1 ng/ml, respectively). The glucagon rise was entirely reversed by the high glucose dose. Insulin did not rise during NA infusion alone. Its secretion in response to glucose infusion was not significantly influenced by FFA depression. Thus, during NA-induced FFA depression the secretion of two lipolytic hormones--GH and glucagon--is stimulated while the secretion of the lipogenetic hormone insulin remains low. Glucose has an inhibitory effect on the GH and glucagon response which, however, is different for each of the hormones.
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PMID:Growth hormone, glucagon, and insulin response to depression of plasma free fatty acids and the effect of glucose infusion. 83 44

The effect of dietary vitamin E on lipid synthesis from U-14 C-D-glucose and 1-14C-acetate was studied in rat lungs in vitro. One-month-old Sprague-Dawley male rats were fed either a basal vitamin E-deficient diet or one supplemented with 45 ppm vitamin E ad libitum for two months. Glucose oxidation to CO2 by lungs was significantly (p less than 0.05) decreased by the exclusion of vitamin E from the diet. Oxidation of acetate to CO2 was not affected by the presence of vitamin E in the diet. The extent of labeled carbons from both glucose and acetate incorporated into total lipids was significantly lower in the lungs of vitamin E-deficient animals than in those of the supplemented group. However, the relative amounts of phospholipids, neutral lipids are free fatty acids in total lipids, and of glyceryl moiety and fatty acids in total lipids and in phospholipid fraction were not significantly altered by the status of dietary vitamin E. The results suggest a general depression of lipid synthesis in the lungs of vitamin E-deficient rats.
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PMID:Effect of dietary vitamin E on lipid synthesis by rat lung in vitro. 84 45


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