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)

Ten hypophysectomized and 10 normal female albino rats, 50-days-old, were kept for 5 days and treated with tritiated thymidine 1 hour before sacrifice of the animals. The animals were weighed and the histomorphology of the palate epithelium was studied including the thickness, cell density, and DNA labeling index. The hypophysectomized rats failed to gain weight after 5 days. The palatal epithelium showed a normal morphology indicating the hypophysectomy allowed for differentiation of squamous epithelium. There was a significant reduction in the thickness of the epithelium and a reduced cell density. This was attributed to a significant decrease in DNA synthesis. The epithelial cells were lost from the surface without adequate replacement due to an expected depression in mitotic activity. DNA synthesis may be depressed due to reduced ATP synthesis resulting from suboptimal glucose metabolism and depression in protein synthesis.
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PMID:The effects of hypophysectomy upon DNA synthesis in rat oral epithelium. 26 47

Dexamethasone acetate (100 microgram IP) protected male Holtzman rats (300-330 gm) against endotoxin shock due to Salmonella enteritidis lipopoly-saccharide B IV. Endotoxin (5.0 mg/rat) produced hypoglycemia within 180 minutes, ie, plasma glucose fell from 87 to 24 mg/dl; dexamethasone prevented the hypoglycemia, ie, plasma glucose levels were 129 mg/dl at 180 minutes after endotoxin. Dexamethasone antagonized both endotoxin-induced depression of hepatic gluconeogenesis and enhanced glucose oxidation as evaluated in vivo. Epididymal fat pads from endotoxic rats (100-110 gm) had increased rates of glucose oxidation as evaluated by the in vitro conversion of 14C-D-glucose to 14CO2. Dexamethasone both in vivo and in vitro antagonized endotoxin glucose hypercatabolism by isolated epididymal fat pads following administrated of endotoxin. Glucocorticoid protection against endotoxin shock is related to antagonism of glucose dyshomeostasis.
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PMID:Dexamethasone antagonism of glucose dyshomeostasis in endotoxin shock. 28 Apr 23

The effects of the ionophores A-23187 and X-537 A on glucose metabolism, ATP content and sucrose permeability in pancreatic islets microdissected from obese-hyperglycemic mice were studied. The formation of 14CO2 from 10 mM D-[U-14C] GLUCOSE WAS INHIBITED BY OMISSION OF Ca2+ from the medium. A-23187 (10 muM) induced a further decrease of 14CO2 formation whereas X-537 A (10 muM) had no effect. At 20 mM glucose both A-23187 (48 muM) and X-537 A (43 muM) decreased the 14CO2 formation in the absence of Ca2+ whereas only X-537 A inhibited in the presence of Ca2+. X-537 A (43 muM) also decreased the formation of 3H2O from 20 mM D-[5-3H] glucose. The islet content of ATP was not changed after incubation in media deficient in either Mg2+ or Ca2+. However, omission of both Mg2+ and Ca2+ resulted in about 50% decrease of the ATP content. A-23187 and X-537 A induced dose-dependent decreases of the islet ATP content. X-537 A was much more potent than A-23187. Both ionophores induced stronger depression of the ATP content when Ca2+ was omitted. X-537 A (43 muM) but not A-23187 (48 muM) increased the beta-cell membrane permeability as indicated by an increased sucrose space in relation to the urea space of islets. Such an effect was not obtained with X-537 A at 1 muM or by omission of Ca2+. It is suggested that the marked metabolic effects of the ionophores reflect an impaired mitochondrial metabolism. These metabolic changes should be considered in interpretations of ionophore action on insulin secretion.
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PMID:Metabolic characteristics of pancreatic beta-cells exposed to calcium-transporting ionophores. 31 39

Intramuscularly administered methylprednisolone sodium phosphate (Medrol Stabisol) in single doses of 40, 80, or 160 mg (methylprednisolone equivalents) had a similar effect as the same doses of methylprednisolone sodium succinate (Solu-Medrol) with regard to eosinophil suppression, elevation of glucose, white blood count differential shifts (lympholytic effect), urinary excretion of sodium and potassium, and localized (pain) and systemic side effects. The average plasma methylprednisolone concentration was approximately 20% higher after the intramuscular administration of methylprednisolone sodium phosphate than after methylprednisolone sodium succinate. The differences in plasma methylprednisolone levels produced by the two esters suggest that either hydrolysis of the succinate ester occurs more slowly or the succinate ester distributes more extensively. This difference in plasma level, however, is not reflected in any other pharmacologic evaluation of the two esters, e.g., both eosinophil depression and hyperglycemic response were identical. No clinically significant changes in the vital signs, standard hematology, and clinical chemistry parameters evaluated were noted after 21 successive doses (q.i.d. for five days with one dose in the morning of day 6) of 80 mg methylprednisolone sodium phosphate. An increase was noted in the systolic blood pressure from a pretreatment mean of 113 mm Hg to a posttreatment mean of 123 mm Hg and an increase in the body weight from a pretreatment mean of 177 pounds to a posttreatment mean of 183 pounds. No signs of adrenal suppression were found as judged by plasma cortisol and ACTH levels. Six (6/12) subjects of the methylprednisolone sodium phosphate group, one (1/12) subject of the vehicle group, and one (1/12) subject of the placebo (sterile saline) group reported the following systemic side effects: gas in stomach, headaches, anorectal itching, and dryness of itching of the skin. No trend was observed for any side effect reported. In these double-blind, randomized studies, single (40, 80, and 160 mg) and multiple (80 mg) intramuscular doses of methylprednisolone sodium phosphate were tolerated in healthy volunteers as well as the same doses of methylprednisolone sodium succinate and similar volumes of vehicle or placebo.
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PMID:The clinical pharmacology of methylprednisolone sodium phosphate. I. Intramuscular route of administration. 32 97

Increasing levels of magnesium were found to cause a marked depression of glucosestimulated insulin secretion at fixed calcium levels, particularly at levels which bracketed the concentration of ultrafiltrable magnesium found in normal rat plasma (1.3 meq/l), i.e., increasing magnesium from 0.6 to 1.2 meq/l depressed secretion, and increasing magnesium from 1.2 to 2.4 meq/l resulted in a further depression. Paradoxically, when magnesium was omitted from the perfusing medium, insulin secretion was also depressed. The data strongly suggest that the calcium/magnesium ratio is a primary regulator of the insulin secretory process, since a relatively slight alteration of the physiologic ratio of calcium to magnesium (approximately 2.5) results in a marked alteration of total insulin secretion. In addition, small amounts of magnesium are necessary for optimum secretion, possibly reflecting the requirement for magnesium in several enzymatic processes. Thus, magnesium may play an important role in the regulation of insulin secretion by altering the sensitivity of the beta cells of the Islets of Langerhans to glucose.
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PMID:Magnesium modulation of glucose-induced insulin secretion by the perfused rat pancreas. 32 55

ATP-Mg++ (10 mumoles/100 g, iv) increased the LD50 for Salmonella enteritidis lipopolysaccharide (endotoxin) in male Holtzman rats (300 +/- 10 g) from 1.3 to 6.0 mg/rat. While endotoxin at 3 mg/rat iv 5 hr previously induced hypoglycemia to 12 +/- 4 mg/dl, ATP cotreatment blunted the hypoglycemia; i.e., plasma glucose values were 78 +/- 6 mg/dl. ATP treatment prevented the depression in gluconeogenesis induced by endotoxin as evaluated in vivo by the conversion of 14C-alanine to 14C-glucose. ATP treatment also reduced the hypercatabolism of U-14 C-glucose to 14CO2 in vivo and by epididymal fat pads in vitro. A role for ATP in preventing disruption of glucose homeostasis and development of endotoxin shock via counteracting insulin is suggested.
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PMID:Protection against endotoxin shock and impaired glucose homeostasis with ATP. 33 38

Recent data reported from this laboratory have documented myocardial functional depression in endotoxin shock. The purpose of the present study was to determine the effects of insulin on the dysfunctioning canine myocardium subjected to lethal endotoxin shock. Experiments were conducted on isolated working left ventricular preparations in which LD90-100 endotoxin was administered prior to, or following, isolation of the heart. Determinations of myocardial performance were conducted under the conditions of controlled mean aortic pressure and cardiac output. Myocardial dysfunction occurred between 2 and 6 h postendotoxin, as evidenced by significantly increased left ventricular end-diastolic pressure, decreased power, and depressed negative dP/dt, although blood glucose concentrations were maintained at control values. Intraatrial infusions of insulin at rates of 6 U/min reversed all signs of myocardial dysfunction. During insulin infusion, heart rates decreased (p less than 0.02) and myocardial lactate uptake increased (p less than 0.02), while oxygen uptake and coronary blood flow were insignificantly altered.
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PMID:Reversal of myocardial dysfunction in endotoxin shock with insulin. 34 82

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

The effect of a new complex oligosaccharide exhibiting potent inhibitory action on alpha-glucoside hydrolases on intestinal absorption of sucrose in man was tested by constant in vivo perfusion of the jejunum. At concentrations of 4.65 or 15.5 X 10(-6)M the alpha-glucosidehydrolase inhibitor (alpha-GHI) markedly inhibited absorption of glucose from sucrose and absorption of sodium and water. Oral administration of the alpha-GHI resulted as well in depression of solute, sodium, and water absorption. This new compound can serve as an interesting tool to induce carbohydrate malabsorption by inhibition of final digestion and may possibly be of beneficial therapeutic effect in dietary control of diabetes or obesity.
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PMID:Effect of alpha-glucosidehydrolase inhibition and intestinal absorption of sucrose, water, and sodium in man. 38 40

Certain physiologic and hematologic data were determined in ponies given Escherichia coli endotoxin by three routes: single IV dose, single intraperitoneal (IP) dose, and multiple IP boluses. In all ponies, the reaction was characterized by weakness, depression, peripheral circulatory abnormalities, and pyrexia. The pyrexia was more severe and was sustained in the ponies given multiple IP bolus endotoxin. Changes in packed cell volume, peripheral blood neutrophil, lymphocyte, and thrombocyte counts, and blood glucose were noticed in the three groups. Blood lactate and beta-glucuronidase values were determined and increases occurred only in the two IP endotoxin administration groups. A fibrinogen increase was observed in only the multiple IP bolus group. Attempts were made to correlate the lactate and beta-glucuronidase values with the severity and prognosis of the endotoxemia response. In general, the single IV bolus and, to a lesser extent, the single IP bolus endotoxin produced abrupt but transient responses. The multiple IP bolus endotoxin administration produced a more gradual and sustained response, which was more closely comparable with a clinical gastrointestinal disease problem than the other routes of administration produced.
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PMID:Equine Escherichia coli endotoxemia: comparison of intravenous and intraperitoneal endotoxin administration. 38 13


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