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

The growth hormone response to insulin induced hypoglycaemia was studied in 7 alcoholic in-patients who had been abstinent for 2-11 days and in 10 normal controls. Blood samples were taken at intervals after the injection of soluble insulin (0-1 U/kg body weight). The growth hormone response was impaired in 4 of the alcoholics and the depression was not related to differences in blood glucose or plasma free fatty acids. The cortisol response was also impaired in the alcoholics. We conclude that alcoholics observed after alcohol withdrawal may have a depression of hypothalamic/pituitary function.
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PMID:The growth hormone response to insulin induced hypoglycaemia in alcoholics. 59 41

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

The present study was designed to develop an animal model applicable to the clinical patient in the investigation of the pathogenesis of septic shock. The model currently described is a lightly anesthetized, unrestrained monkey, carefully monitored during a 24 hour observation period. Varying doses of live Excherichia coli organisms were infused intravenously during a 30 minute period, and a variety of hemodynamic, respiratory and metabolic parameters were monitored. Doses of organisms varied between 7.6X10(9) and 3.0X10(11) organisms per kilogram of body weight, and there was no obvious correlation between size of dose and survival time. Two of nine experimental monkeys survived the Excherichia coli, while times of death of the remaining monkeys varied between three and 27 hours. Two control monkeys, not administered organisms, survived the 24 hour period with minimal changes in all measured parameters. Results reveal two patterns in response to organism administration. These were early acute death, after three to four hours, and prolonged life, death after 20 to 27 hours. The acute response was characterized by marked systemic hypotension, hypoglycemia, hypoinsulinemia, increased lactate level, decreased pH or respiratory depression. The other type of response involved profound sustained hypotension with hypoglycemia and hypoinsulinemia in most monkeys and elevations in lactate, blood urea nitrogen potassium creatinine, serum glutamicoxalacetic, lactic dehydrogenase and fractionatedlactic dehydrogenase levels. Depressions in respiration were not evident in the group which survived a longer period of time. Renal fibrin thrombi, prominent in baboons administered Escherichia coli, were absent in the rhesus monkey regardless of the size of the dose of organisms. The results of this study suggest the operation of a multifactiorial mechanism in septic shock with interactions between hemodynamic and metabolic factors varying within the species.
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PMID:Physiopathologic responses of the rhesus monkey to live Escherichia coli. 82 5

Four cases of suicidal insulin overdose in insulin-requiring diabetics presented to one hospital in three years. In three cases there was a history of depression; but despite huge doses of insulin (3,000 and 1,500 units) in two, no patient died and only one had residual signs of clinical brain damage. The estimated plasma insulin level was not well correlated with the severity of the hypoglycaemia. It is probable that suicidal insulin overdose is more common than reports in the literature suggest, and may often be unrecognized. The dissociation between huge doses of insulin and the severity of the subsequent hypoglycaemia in diabetics is unexplained.
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PMID:Attempted suicide by insulin overdose in insulin-requiring diabetics. 84 89

The administration of 160 mg of propranolol during pregnancy, labor, and delivery was associated with profound hypoglycemia and respiratory depression in a newborn infant. The neonate's plasma propranolol level rose from 40 ng/ml at the time of birth to 90 ng/ml four hours later. This increase in plasma propranolol concentration might be due to redistribution of the drug in the neonate as well as to different elimination mechanisms than in adults. The elevated propranolol level four hours after delivery was not associated with any signs or symptoms of drug toxicity, but drug effect was apparent on the electrocardiogram. The administration of propranolol during pregnancy in doses capable of producing therapeutic maternal blood levels may be dangerous to the neonate.
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PMID:Propranolol therapy during pregnancy, labor, and delivery: evidence for transplacental drug transfer and impaired neonatal drug disposition. 90 24

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

Interest in possible neuroendocrine disturbances in endogenous depression is prompted by two lines of evidence: (1) clinical features of the illness suggest hypothalamic dysfunction; (2) the brain neurotransmitters implicated in depression also regulate neuroendocrine function. Our research reveals a marked, sustained hypersecretion in cortisol in severe depressive illness, which is apparently unrelated to stress and sleep disturbance, and which is associated with a distortion of the 24-hour cortisol secretory pattern. The hypersecretion is manifested primarily in the late afternoon, evening, and early morning hours, when cortisol secretion is normally inhibited. Growth hormone responses to hypoglycemia (but not to L-dopa) are also significantly reduced in endogenous depression, even when factors of age and the menopause are controlled. Postmenopausal depressed women appear to secret significantly less LH than normal postmenopausal women. Since all of these hormonal abnormalities can be reproduced by depletion of brain noradrenalin, the findings provide support for the the hypothesis of reduced functional noradrenergic activity in certain forms of depression.
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PMID:Neuroendocrine studies of depressive illness. 98 19

The effects of carbohydrate (CHO) restriction on the hypoglycemic phase of the glucose tolerance test were studied in ten normal subjects. The mean nadir plasma glucose was 64 +/- 4 mg/dl (x +/- SEM) for the control test, and 48 +/- 4 mg/dl (P less than 0.01) after 3 days of an isocaloric low CHO diet. Following the low CHO diet, six of ten subjects had a nadir plasma glucose less than 50 mg/dl, and five of these six had mild symptoms of hypoglycemia compared to no biochemical or symptomatic hypoglycemia during the control test. Hormone secretory patterns under the two experimental conditions were measured. CHO restriction produced a significant decrease in early insulin release followed by excessive insulin relative to the control test at 3-4 h of the test. Glucose ingestion produced a depression of plasma, glucagon from fasting levels during the control test, which was impaired following CHO restriction. Plasma growth hormone and cortisol responses were not different under the two experimental conditions. These studies demonstrate that CHO restriction followed by concentrated CHO ingestion produces hypoglycemia in normals. They emphasize the need to consider dietary history in evaluation of hypoglycemia. CHO restriction may provide a useful model for further study of the mechanisms of hypoglycemia.
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PMID:Effects of carbohydrate restriction on the hypoglycemic phase of the glucose tolerance test. 99 13

Animal experiments have suggested a FFA control mechanism for glucagon secretion. In man, the potent effect of FFA on HGH secretion and the similarity of the secretory control mechanisms for HGH and IRG also support a role of FFA in IRG secretion. Our studies in man in which plasma FFA were elevated by either an oral lipid emulsion (Lipomul) or an intravenous lipid suspension (Intralipid)suggest only a minor role of lipids in control of IRG secretion. Plasma FFA and triglyceride elevations did not suppress arginine- or hypoglycemia-induced plasma IRG elevations, but an inhibitory effect of Intralipid on basal plasma IRG concentrations was observed. Although nicotinic acid administration, which caused a depression in plasma FFA, did elevate plasma IRG, the IRG elevation was considered more likely a consequence of stress induced by the drug. The failure of lipids to inhibit IRG secretion at FFA concentrations inhibiting HGH secretion indicates a dissociation in the secretory control mechanisms of the two hormones.
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PMID:Effect of lipids on glucagon secretion in man. 111 Jun 25

A patient is described who developed hypoglycemia and generalized neurologic depression after cardiac surgery, while receiving an infusion of glucose, insulin, and potassium (GIK). Hypoglycemia as a complication of the use of GIK solution in patients with hepatic dysfunction, malnutrition and low cardiac output is discussed.
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PMID:Hypoglycemia complicating the use of solution of glucose, insulin and potassium. 111 35


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