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)

1. Six weeks after the injection of streptozotocin at 125 mg/kg i.p. in the AV line nondiabetic Chinese hamsters, the animals showed hyperglycemia, increased kidney, pancreas and stomach weights and stomach glucagon contents and depletion of insulin and glucagon in the pancreas. 2. Plasma beta-D-galactosidase and N-acetyl-beta-D-glucosaminidase were elevated; whereas alpha-D-glucosidase was decreased and alpha-D-galactosidase remained unchanged in the plasma. 3. In the kidney, streptozotocin-diabetes led to depression of alpha-D-mannosidase, beta-D-fucosidase and N-acetyl-beta-D-glucosaminidase activities in both 12,000 g supernatant and precipitate fractions, decreases in alpha-D-glucosidase in the supernatant only and no change in alpha-L-fucosidase, alpha-D-galactosidase, beta-D-galactosidase and beta-D-glucuronidase. 4. In the liver, significant increases in N-acetyl-beta-D-glucosaminidase, alpha-D-galactosidase, beta-D-galactosidase, beta-D-fucosidase, beta-D-glucosidase and alpha-D-mannosidase were found in either the supernatant or the precipitate fraction of the diabetic animals. The data indicate diabetes-dependent tissue-specific changes in glycohydrolases in the Chinese hamster.
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PMID:Alterations in glycohydrolase activities in streptozotocin-diabetic Chinese hamsters (Cricetulus griseus). 31 16

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

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

It has recently been suggested from experiments in dogs that somatostatin suppresses insulin release via a stimulation of the inhibitory alpha-adrenoceptors of the pancreatic B-cell. The effect of somatostatin on insulin secretion during alpha-adrenergic blockade with phentolamine was therefore studied in three different species; the rat, the cat and the mouse. It was found that somatostatin significantly depressed insulin release during alpha-adrenoceptor blockade in all three species. In the rat, infusion of somatostatin at a dose of 0.3 microgram/kg/min decreased basal plasma insulin concentration by 92%. In the presence of phentolamine, the same dose of somatostatin lowered plasma insulin by 85%. In the cat, a similar infusion of somatostatin lowered basal plasma insulin concentration by 87%, but its depressive effect during alpha-adrenergic blockade was comparatively less pronounced (68%) than in the rat. In the mouse, a single iv injection of somatostatin induced a short-lasting depression of plasma insulin concentration during alpha-adrenergic blockade. From these results it seems unlikely that somatostatin should inhibit insulin release simply by stimulation of alpha-adrenoceptors on the B-cell. It cannot be ruled out, however, that a more complex interaction exists between somatostatin and the sympatho-adrenal system with regard to the control of insulin secretion.
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PMID:Inhibitory effect of somatostatin on insulin secretion during alpha-adrenergic blockade in three different species. 38 85

The effects of glucose-insulin-potassium (GIK) and placebo normal saline (S) infusion on treadmill-walking time to angina, ST depression, heart rate (HR), systolic blood pressure (SBP), rate pressure product (RPP), blood glucose (G), lactate (L) and free fatty acids (FFA) were studied in 14 non diabetic patients with exertional angina. For the whole group, the post-GIK walking time to angina (393 +/- 33 sec, mean +/- SEM) was greater than the values during control GIK (319 +/- 20 sec, p less than 0.02) and post-S infusion (334 +/- sec, p less than 0.05), but circulatory and ST responses were similar in post-GIK and post-S studies. 7 of the 14 patients experienced significantly greater improvement in exercise tolerance following GIK (467 +/- 39 sec) in comparison to control GIK (313 +/- 29 sec, p less than 0.001) and post-S infusion (334 +/- 32 sec, p less than 0.005) and exercised to a higher HR, SBP and RPP after GIK than after S infusion. At the onset of angina these patients had similar ST-segment depression before and after GIK but when ST segments were assessed after GIK at the same exercise duration when angina had occurred during the control and post-S studies, there was significantly less ST depression (p less than 0.01). Of the remaining 7 patients exercise tolerance following GIK deteriorated in 3, remained unchanged in 2 and increased by 12 and 48 sec in 2 patients in comparison to post-S values. Comparison of post-GUK and post-S values for G, L and FFA for the whole group showed significantly lower resting values of FFA and post-exercise values of G following GIK infusion. The differences in clinical and circulatory responses between patients who improved and those who did not improve following GIK were not related to the angiographically determined severity of coronary artery disease or to GIK-induced metabolic changes. Results suggest that some patients with angina pectoris do benefit from GIK infusion but the response in a given patient to this therapeutic modality is unpredictable.
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PMID:Effects of glucose-insulin-potassium infusion on the angina response during treadmill exercise. 38 19

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

As the prolonged metabolic clearance rate of insulin in chronic uremia cannot be entirely explained by impaired removal and degradation of insulin by the kidney, we set out to determine whether prolonged uremia depresses other major sites of insulin degradation. The study was conducted with livers and skeletal muscle obtained from normal control rats and uremic rats 4 weeks after 80% nephrectomy. Despite a significant difference between renal function in the control and uremic rats (BUN, 18 vs. 46 mg/dl), there was no significant difference in the clearance of insulin by isolated uremic or control livers perfused with a bloodless medium. Similarly, the 125I-insulin degrading activity of liver homogenates was not depressed by uremia. In contrast, binding and degradation by uremic liver cell membranes was significantly reduced to 58% and 85% of the controls, respectively. Degradation by homogenates of skeletal muscle and by intact epitrochlaris muscle was significantly less in uremics than in controls. These results indicate that chronic uremia depresses skeletal muscle insulin degradation but not hepatic insulin removal or degradation despite a decrease in insulin binding and degradation by liver plasma membranes. It thus appears that depression of insulin degradation by muscle may contribute to the prolonged insulin metabolic clearance rate seen in chronic uremia. Furthermore, it is possible that the impaired binding of insulin to liver membranes may play a role in the insulin resistance of uremia.
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PMID:Effect of prolonged uremia on insulin metabolism by isolated liver and muscle. 39 15


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