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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The understanding of the effects of cannabinoids in human subjects has been obscured by a lack of knowledge about how the various active principles from marijuana act at the cellular level in the brain. For this reason the present study was undertaken to determine the effects of cannabinoids on the enzymes associated with the synaptic membranes. Electron micrographic analysis was performed to determine the purity of synaptic membrane preparations from rat brain, and subsequently such preparations were subjected to additions of ethanol, Tween-80, 80% glycerol, and either delta-tetrahydrocannabinol, 11-hydroxy-delta-tetrahydrocannabinol, or cannabinol. Both sodium and potassium activated ATPase (Na, K-ATPase), and Mg-ATPase were measured as the micrometer orthophosphate (P) released per minute per microgram membrane protein and these specific activities of the enzymes expressed as absolute values and as the percentage depression brought about by the cannabinoids. The ATPase spcific activities are taken from the rate curve over a 30-min incubation time. Additionally, synaptic membrane acetylcholineesterase specific activity was measured by continuous rate enzyme assay. While as low as 10 M delta-tetrahydrocannabinol showed appreciable decrements in both the membrane-bound ATPases, the other cannabinoids did not show such a great depression in enzyme activity. The specific activity of acetylcholinesterase, which is weakly bound to the membrane, showed only slight or no changes in activity with the various cannabinoids. It was additionally shown that the cannabinoids, delta-tetrahydrocannabinol in particular, bound to the synaptic membranes almost irreversibly in the in vitro system, and that the vehicle for dissolving the cannabinoids, while used as background control values when calculating the percentage decrements in enzyme specific activity, did vary the effects on the ATPase enzymes in particular. These data are discussed in relation to psychotomimetic activity of the cannabinoids.
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PMID:Effects of cannabinoids on synaptic membrane enzymes. I. In vitro studies on synaptic membranes isolated from rat brain. 14 40

The present studies were designed to compare physiological and behavioral changes produced by weight loss induced with dieting and the weight loss which follows intestinal bypass. A group of 7 grossly obese individuals were hospitalized in a metabolic unit and studied at their initial weight after 4 weeks on a hypocaloric diet and again following a comparable weight loss after intestinal bypass surgery. The score indicating depression increased after dieting, but returned to initial levels after bypass. A number of other behavioral changes were recorded including a reduction in the time spent thinking about food, the time when the individual felt hungry and a greater percentage of time when they felt "full". After bypass, the patients also selected and ate smaller quantities of food. There were no metabolic differences following the period of dieting. Among the metabolic changes after bypass were an increase in glycerol and a decrease in insulin. The possible relationships between the metabolic and behavioral changes have been reviewed.
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PMID:Metabolic and behavioral differences between dieting and intestinal bypass. 39 58

These investigations were designed to evaluate the effect of excess glucose and sodium chloride on lipolysis in the isolated adipocyte under normal and modelled pathological conditions simulating the hyperglycemic hyperosmolar syndrome. Isolated rat fat cells were incubated in the presence of various combinations of sodium chloride, glucose, epinephrine, and insulin. Lipolysis was measured as glycerol and free fatty acid release, and total medium osmolarity as milliosmoles per liter by freezing point depression. Basal lipolysis was unaffected by changes in osmolarity with sodium chloride, but glucose and glucose plus sodium chloride increased basal glycerol release. Increasing osmolarity with sodium chloride diminished the lipolytic response to epinephrine. Increasing osmolarity with glucose augmented the lipolytic response to epinephrine up to a total medium osmolarity of 550 mosmol. Higher osmolarities produced with glucose suppressed the epinephrine-induced lipolytic response.When the hyperglycemic hyperosmolar syndrome was simulated with 100 mM glucose and 50 mM sodium chloride (total osmolarity = 460 mosmol) the epinephrine-stimulated lipolysis dose-response curve in the isolated fat cell was shifted to the right. Furthermore, in the presence of 100 mM glucose + 50 mM sodium chloride, physiological concentrations of insulin were less effective in opposing epinephrine-stimulated lipolysis. In the presence of 50 mM glucose and 25 mM sodium chloride (total osmolarity = 370 mosmol) epinephrine-stimulated lipolysis measured as free fatty acid release was decreased by 50%. Under conditions simulating the hyperglycemic hyperosmolar syndrome in the isolated rat adipocyte, altered lipolysis reflects impaired effectiveness of both insulin and epinephrine as antilipolytic and lipolytic hormones, respectively. Furthermore, the attenuated response to both hormones appears to be primarily a function of extracellular solute composition. The lack of ketosis is the result of diminished release of free fatty acids from peripheral adipose cells.
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PMID:Simulated hyperglycemic hyperosmolar syndrome. Impaired insulin and epinephrine effects upon lipolysis in the isolated rat fat cell. 42 61

The effect of intravenous somatostatin on blood levels of metabolites and hormones has been examined in normal subjects who performed a 30-minute period of bicycle exercises at 70% maximal exercise capacity. The results have been compared with control studies in the same subjects. Measurements were made of blood levels of lactate, glucose, free fatty acids, glycerol, acetoacetate, 3-hydroxybutyrate, insulin, glucagon, growth hormone (hGH) and prolactin. Growth hormone and glucagon release were suppressed during exercise with somatostatin and there was a subsequent elevation during recovery. There was slight post-exercise depression of insulin, but no alteration of plasma prolactin secretion. Blood glucose was reduced during exercise with somatostatin and increased during recovery. The elevation of ketone bodies after exercise was greater in the investigation with somatostatin, but there were no significant changes in other metabolites. Somatostatin, although causing inhibition of hGH release, appeared to have no significant effect upon fatty acid mobilization during exercise.
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PMID:The effect of somatostatin on metabolic and hormonal changes during and after exercise. 47 77

Rats were kept in barochamber for 2 hours at the pressure of 240 mm Hg after subcutaneous administration of (1)14C-acetate. Hypobaric hypoxia caused depression in the incorporation of labeled acetate similar in both phospholipid (PL) components. But the dependence of depression in the metabolic rate upon hypothermia which accompanied hypoxia was more pronounced for hydrophobic portion of PB (carbon skeleton of fatty acids) than for hydrophilic one. Similarity in the degree of the hypoxia induced depression of incorporation of the precursors containing labeled phosphorus and carbon allows one to suggest that the carbon-containing parts of PL hydrophilic components (glycerol and nitrogen bases) and residues of ortho-phosphoric acid respond to hypoxia as a whole.
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PMID:[Effect of hypobaric hypoxia on the acetate-1-14C incorporation rate in hydrophilic and hydrophobic brain phospholipid components]. 51 97

Clonidine is a hypotensive drug acting as an alpha-mimetic agent in the central nervous system and causing cardiovascular depression. Clonidine administration in animals and man causes slight hyperglycemia and lipid mobilization, as well as an increase in growth hormone levels. We have studied the effect of a 3-day oral treatment (78 microgram three times daily) upon glucose (5 g i.v.)- and tolbutamide (1 g i.v.)-induced insulin release in subjects without metabolic alterations. Acute insulin response (3 min after IVGTT) and insulin release (area between 0 and 10 min) were significantly reduced after clonidine treatment. Blood glucose levels were not affected by clonidine treatment; the insulinogenic index 3 min after the glucose load was significantly reduced by clonidine administration. There was neither an evident effect on tolbutamide-induced insulin release nor a modification of the hypoglycemic effect of tolbutamide. Clonidine did not affect basal lipolysis, evaluated in vitro as glycerol release from human subcutaneous adipose tissue fragments, while norepinephrine-induced lipolysis was slightly reduced. The results presented are compatible with an alpha-mimetic effect of clonidine on pancreatic and adipose tissue.
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PMID:Clonidine effect on insulin secretion and lipolysis in man. 70 1

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

The fever induced by E. coli pyrogen (LPS) is accompanied by a rise of FFA and glycerol level. All tested antipyretics inhibited both thermogenesis of lipolysis produced by LPS. These results suggest that the antipyretic effect of antipyretic drugs is not confined to their action on heat-dissipating mechanisms, but may also be exerted by a depression of lipid metabolism.
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PMID:Studies on antilipolytic activity of antipyretics. Part I. Influence of sodium salicylate, acetylsalicylic acid, phenazone, aminophenazone, and acetophenidin on lipolysis in fever induced by E. coli pyrogen. 79 33

This study describes the effect of hypertonic solutions on isolated muscle fibers of Callinectes danae. Solutions of twice normal tonicity (2.0 T) inhibit both the normal graded membrane responses and the spikes induced by procaine, tetraethylammonium, or barium. The inhibition is maintained throughout exposure to hypertonic solutions prepared by addition of impermeant solutes such as NaCl, sucrose, or Tris-propionate, but is reversible on their withdrawal. In the presence of permeant solutes such as glycerol or acetamide, the inhibition is transient. In both cases the onset of inhibition of the depolarizing Ca electrogenesis is correlated with shrinkage of the fiber. In the case of permeant solutes, the time course of recovery of the graded responses or the spikes follows the recovery of the fiber volume. Changes in the passive electrical characteristics of the fibers due to hypertonic solutions were unrelated to the blockade of membrane Ca activation. The current-voltage relationship in hypertonic sollution revealed no increase in depolarizing K activation. Inhibition of the graded membrane responses and spikes appears to be associated with depression of Ca conductance. Hypertonic solutions might affect the activation of Ca conductance through reduction of the electric field generated by fixed negative surface charges and/or morphological changes in the T tubules. Membrane depolarization elicited little or no tension in 2.0 T solutions while caffeine contracture (10 mM) with an ampliture of 76% of the maximal contractile ability could still be elicited. This indicates that direct effects of hypertonic solutions on the contractile apparatus were not responsible for loss of tension. The latter is attributed to the inhibition of the transmembrane Ca currents.
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PMID:Inhibition by hypertonic solutions of Ca-dependent electrogenesis in single crab muscle fibers. 91 72

Blood lipids and glucose were studied in streptozotocin diabetic rats during hyperthermia. Blood glucose, free fatty acids (F.F.A.) and glycerol of diabetic rats with a rectal temperature of 42 degrees C (hyperthermic) were elevated significantly above those values found in normothermic (TR = 38 degrees C) diabetic or normothermic non-diabetic rats as well as hyperthermic non-diabetic rats. Streptozotocin diabetes caused an elevation in blood triglycerides of normothermic rats, but this hypertriglyceridemia was depressed in diabetic rats during hyperthermia. As in the case of diabetic animals, hyperthermia also caused a depression in the blood triglycerides of non-diabetic rats. However, unlike in the diabetic animals, the blood F.F.A. of non-diabetic rats were depressed during hyperthermia. Although hyperthermia caused a significant increase in the blood glucose of the diabetic animals, no significant change in blood glucose was shown in the hyperthermic non-diabetic rats. Blood cholesterol did not change significantly in the non-diabetic or diabetic animals during hyperthermia. The blood changes of these "energy substrates" are discussed with respect to their possible role in the extreme sensitivity of diabetics to high environmental temperature and "heat stress".
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PMID:Metabolic effect of high environment temperature on non-diabetic and diabetic rats. 92 47


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