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)

The activites of alpha-and Beta-galactosidases (alpha-D-galactoside galactohydrolase, EC 3.2.1.22; beta-D-galactoside galactohydrolase, EC 3.2.1.23) were significantly lower in the kidneys of diabetic XA line than those in the nondiabetic M line Chinese hamsters. The depression of these enzymes was found only in the kidney but not in liver, spleen, hind leg muscle, cheek pouch or spinal cord. In young XA animals before onset of glycosuria, renal alpha-galactosidase level was similar to that in age-matched M animals; whereas, their renal beta-galactosidase activity was about 90% of those in the M animals. Partial purification and separation of these enzymes were achieved by chromatography on DEAE-Sepharose CL-6B columns. beta-galactosidase was separated into two isozymes and depression of activity in the XA kidneys was evident in both. alpha-galactosidase was recovered in a single peak. The pH optima of these enzymes from XA and M animals were identical. With p-nitrophenyl glycosides as substrates, the Michaelis constants of these enzymes were also the same of XA and M animals. Molecular weight estimation by gel filtration on Sepharose 6B yielded similar results between M and XA samples: 2.4-10(5) for alpha-galactosidase and 1.6.10(5) and 1.9.10(5) for beta-galactosidase isozymes. The data suggest that the diabetic animals had lower concentrations of alpha-and beta-galactosidase in their kidneys, probably as a consequence of hyperglycemia.
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PMID:Acid glycohydrolase in Chinese hamster with spontaneous diabetes. I. Depressed levels of renal alpha-galactosidase and beta-galactosidase. 2 47

Chlorozotocin was given to 37 patients with advanced malignant tumors in a daily X 5 schedule at 6-week intervals. Total iv doses for each course ranged from 75 to 200 mg/m2. Myelosuppression was dose-limiting, with a platelet count depression regularly observed at doses of greater or equal to 150 mg/m2; leukopenia occurred only at the highest dose level. Nausea and vomiting were mild and uncommon. No hyperglycemia or adverse drug-related effects on renal or hepatic function were observed. No major antitumor activity occurred; however, three patients with renal cell carcinoma and one patient each with lung cancer, ovarian carcinoma, and Hodgkin's disease had minor objective decreases in tumor size. A dose range of 150--200 mg/m2 iv for each 5-day course is recommended for phase II studies.
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PMID:Phase I trial of chlorozotocin. 15 63

Stupor in patients with nonketotic hyperglycemia has been ascribed to hyperosmolarity, but the cause of depressed consciousness in patients with ketoacidosis has been puzzling. In this study, blood pH, serum glucose and sodium concentrations, and serum osmolality were measured in eighty-five consecutive episodes of diabetic ketoacidosis and forty-seven of nonketotic hyperglycemia. In the acidotic patients, as in those with nonketotic hyperglycemia, stupor closely paralleled hyperosmolarity and not the severity of acidemia. Indeed, the mean elevations of serum osmolarity were almost the same in the ketotic and in the nonketotic patients who were deeply obtunded. It seems likely that depression of consciousness in patients with severely uncontrolled diabetes mellitus, if not due to a nonmetabolic disorder, such as acute stroke, is attributable to hyperosmolarity, whether or not ketoacidosis is present.
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PMID:Hyperosmolar nature of diabetic coma. 23 99

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

Bombesin acts within the brain to produce a prompt and sustained hyperglycemia, hyperglucagonemia, and relative or absolute hypoinsulinemia. Bombesin does not decrease plasma glucose turnover. Acute adrenalectomy but not hypophysectomy prevents hyperglycemia and hyperglucagonemia after intracisternal administration of bombesin. Administration of bombesin into the lateral ventricle of awake, unrestrained animals results in elevation of plasma glucose, preceded by a significant increase in plasma epinephrine and no increase in plasma norepinephrine or dopamine. Systemic administration of somatostatin prevents bombesin-induced hyperglycemia and hyperglucagonemia. These data support the conclusion that bombesin acts within the brain to increase sympathetic outflow resulting in increased adrenalmedullary epinephrine secretion, followed by depression of plasma insulin and elevation of plasma glucagon and glucose.
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PMID:Central nervous system action of bombesin: mechanism to induce hyperglycemia. 46 25

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

In this work we have evaluated the effects of blood sugar changes on human pancreatic polypeptide (hPP) secretion in young, healthy subjects. Mean fasting hPP level was 74 +/- 5 (SEM) pg/ml (n = 53). Insulin-induced as well as tolbutamide-induced hypoglycemia clearly provoked hPP secretion (peaks: 1201 +/- 370 pg/ml, P = 0.03, and 520 +/- 112 pg/ml, P = 0.005, respectively). In contrast, the induction of hyperglycemia by intravenous glucose infusion (0.6 g/min) elicited a significant depression of circulating hPP (37-49% of basal values); discontinuing the infusion resulted in an increase of hPP concentrations (peak: 519 +/- 141 pg/ml, P = 0.018), which coincided with the decline of blood sugar to sub-baseline levels. Glucose as an intravenous bolus (0.33 g/kg) also induced a fall in plasma hPP. Glucose ingestion (1.75 g/kg) was followed by a small and short lived elevation of hPP (154 +/- 34 pg/ml at 15 min, P = 0.04) and by a marked rise during the late hypoglycemic phase of the test (538 +/- 168 pg/ml at 120 min, P = 0.028). Finally, after intravenous arginine, a delayed increase of hPP values was observed, occurring subsequently to the plasma glucose drop. The foregoing data indicate that experimental fluctuations in glycemia inversely affect hPP secretion. Nevertheless, this relationship does not necessarily mean that hPP should be directly implicated in glucose homeostasis.
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PMID:Control of pancreatic polypeptide secretion by glucose in man. 75 16

Urethral obstruction induced in adult male cats caused clinical signs identical with those observed in naturally occurring disease. Central nervous system depression, anorexia, dehydration, vomiting, muscle weakness, and hypothermia occurred. Weight loss (due to water loss and catabolism), metabolic acidosis, mild hyponatremia, hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia, hyperglycemia, azotemia, and hyperproteinemia were also observed. Serum amylase, alkaline phosphatase, and alanine aminotransferase activities were normal. Ten of 13 cats (group 1), with 72 hours' induced obstruction but not treated with parenteral fluids, died either before the obstruction was relieved or within 8 days afterward. Eight cats (group 2) with induced obstruction for 49 to 98 hours developed severe clinical and biochemical alterations. Treatment with a multiple-electrolyte solution, in addition to relief of urethral obstruction, resulted in favorable clinical and biochemical responses. These cats survived and were clinically healthy at 9 to 10 days after relief of obstruction. It was concluded that use of a multiple-electrolyte solution to correct acidosis, restore circulatory volume, and enhance renal excretion of potassium was effective supportive therapy after urethral obstruction was removed.
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PMID:Characterization and treatment of water, electrolyte, and acid-base imbalances of induced urethral obstruction in the cat. 87 80

Temporal patterns of plasma GH, immunoreactive insulin (IRI), and glucose were defined by obtaining serial blood samples from freely-moving male rats bearing chronic intracardiac venous cannulae. Blood was withdrawn every 15 min for periods of 6 h. Plasma GH and IRI were determined by radioimmunoassay. The typical ultradian rhythm of GH secretion was evident in each undisturbed animal (peaks greater than 200 ng/ml; troughs less than 1 ng/ml; mean period: 3.40 +/-0.08 h). Basal plasma IRI and glucose levels fluctuated minimally. There was no significant correlation between plasma GH and IRI, GH and glucose, or IRI and glucose levels in unfed rats. The rhythmic GH secretory patterns of feeding animals (mean period: 3.12 +/-0.16 h; peaks greater than 200 ng/ml; troughs less than 1 ng/ml) were similar to those of non-feeding animals (mean period: 3.34 +/-0.15 h; peaks greater than 200 ng/ml; troughs less than 1 ng/ml) despite large fluctuations in plasma IRI levels and a wide variation in the number and size of the meals taken. No consistent relation was observed between the ingestion of meals and the bursts of GH secretion. The mean period of the GH rhythm was not significantly altered by hyperglycemia (mean period; 3.25 +/- 0.08 h), although the amplitude of the pulses of half of the hyperglycemic rats was markedly depressed. Insulin-induced hypoglycemia caused a significant depression in the amplitude of the GH pulses; however, the pattern of this response was not consistent. Despite wide variability in the GH response, the magnitude and time course of recovery of the plasma glucose levels was similar in all animals. These results suggest that GH secretion in the rat is regulated primarily by an endogenous ultradian rhythm which is not dependent on changes in plasma glucose or IRI levels, and continues to function independently of feeding behavior. It is unlikely that GH is an important physiologic regulator of glucose homeostasis in this species.
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PMID:Ultradian growth hormone rhythm in the rat: effects of feeding, hyperglycemia, and insulin-induced hypoglycemia. 95 65

The effect of various doses of serotonin (5-HT) on the basal or insulin-stimulated gastric secretion was studied, for 4 hr after the injection, in unanesthetized rats with chronic gastric fistulas. The blood glucose and serum Na, K and Ca ions concentrations were also determined. Insulin produced hypoglycemia and hypokalemia, most pronounced in the first hr, and increased HCl and pepsin output, with a maximum at 2 hr after the injection. 5-HT significantly inhibited both basal and insulin-stimulated gastric secretion. The amine produced transient hyperglycemia, which was less pronounced in rats simultaneously receiving insulin. The inhibition of insulin-stimulated gastric secretion by 5-HT lasted for a longer period than the prevention of the biochemical changes brought about by insulin. The prevention by 5-HT of insulin hypoglycemia and hypokalemia may be of significant importance in the mechanism of the depression of insulin-stimulated gastric secretion.
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PMID:The influence of serotonin on insulin-stimulated gastric secretion, blood glucose and serum electrolyte levels in the unanesthetized rat. 116 2


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