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

Based on the glucose infusion test, we find with 17.9 per cent of a group of anamnestically tainted pregnant women gestational diabetes, and with 5.7 per cent of this group a carbohydrate tolerance with disturbed boundaries. With probands having a carbohydrate tolerance with disturbed boundaries we find a significantly more frequent IRI-high-response. This coincidence of a carbohydrate tolerance in the border range and of an IRI-high-response might correspond to the early asymptomatic stage of diabetes. In the following stages, there will take place a depression of the early insulin phase with a pathological carbohydrate tolerance of the pregnant women in the sense of a gestational diabetes. With probands exhibiting a disturbed carbohydrate tolerance, a diminished depression of free fatty acids is found. The total lipid content and cholesterol are not essentially changed. With women suffering from gestational diabetes urinary sugar excretion is significantly higher than with probands showing a normal carbohydrate tolerance.
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PMID:[Incidence of gestational diabetes as well as changes in insulin secretion during pregnancy. 1. Studies on pregnant women suspected of diabetes using the glucose infusion test (GIT)]. 74 51

The role of SRIF in starvation-induced inhibition of GH and insulin secretion was assessed by passive immunization with anti-SRIF serum. Six-hour secretory profiles obtained from chronically cannulated male rats deprived of food for 72 h showed marked suppression of GH secretory bursts and significant depression of plasma insulin levels. Administration of 1 ml SRIF antiserum (SRIF AS) iv to starved rats resulted in rapid (within 15 min) restoration of high amplitude GH pulses (600-800 ng/ml) and sighificant elevation of GH trough values. The mean 6-h GH level of starved SRIF, AS-treated rats (189.2 +/- 23.9 ng/ml) was significantly higher than that of starved, normal sheep serum-treated control animals (62.8 +/- 5.8 ng/ml) (P less than 0.005). In contrast to the effects on GH, plasma insulin levels in starved rats administered SRIF AS remained low. No significant difference was observed in the mean 6-h plasma insulin level of starved-SRIF, AS-treated rats when compared to starved, normal sheep serum-treated controls. These findings suggest that circulating SRIF is a physiological regulator of starvation-induced GH suppression but is not involved in mediating the inhibition of insulin.
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PMID:Antiserum to somatostatin reverses starvation-induced inhibition of growth hormone but not insulin secretion. 74 57

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

Coma and other neurologic abnormalities are present in patients with either diabetic ketoacidosis (DKA) or nonketotic coma (NKC), and the cause of such phenomena are not known. Patients with NKC also manifest seizures and focal neurologic changes. Treatment of diabetic coma with insulin may induce cerebral edema by as yet undefined mechanism(s). In patients with DKA, cerebral oxygen utilization is impaired, and there is hyperviscosity of the blood. A substantial part of the brain's energy source is derived from ketones, which in themselves can depress sensorium. Extracellular hyperosomolality is present, which may also contribute to the genesis of coma. In addition, most ketoacidotic patients have associated medical conditions, which may further impair consciousness. Biochemical changes in the brains of animals with DKA include impairment of both phosphofructokinase activity and pyruvate oxidation, and accumulation of citrate. The net effect upon sensorium in ketoacidotic patients probably represents the interaction of most of the above factors and differs markedly among individuals. Patients with NKC manifest not only depression of sensorium, but also focal motor seizures, hemiparesis, and other neurologic changes, such as aphasia, hypereflexia, sensory defects, autonomic changes, and brainstem dysfunction. Most of the aforementioned changes revert to normal after correction of hyperosomolality. Gamma amino butyric acid, which has been shown to elevate the seizure threshold, is normal in brains of ketoacidotic animals, but may be low in nonketotic coma. Also, hyperosomolality per se may produce seizures. Cerebral edema may complicate the treatment of either DKA or NKC. The available experimental evidence suggests that many of the commonly held theories for the production of such brain swelling probably do not occur. There is no breakdown of the sodium pump, sorbitol or fructose do not accumulate in brain, and brain glucose is only about 25 percent of that in plasma; Cerebral edema is probably produced largely by a direct action of insulin on brain at a time when plasma glucose is approaching normal values. Cerebral edema can thus theoretically be avoided by stopping insulin when plasma glucose has been lowered to values approaching normal.
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PMID:Neurologic manifestations of diabetic comas: correlation with biochemical alterations in the brain. 80 37

Young male rats (100-130 g) were fed diets of equal energy content containing o.5, 1,2,3,5, and 18% lactalbumin consumed either freely or in restricted amounts. The rats receiving low protein diets failed to grow and mature. Those consuming the 0.5 and1% protein diets given freely developed the characteristic features of kwashiorkor including edema, while those receiving the diets in restricted amounts developed the characteristic features of marasmus. The rats fed low protein diets had low plasma levels of essential amino acids; however, the lysine level was well maintained. The plasma levels of nonessential amino acids, especially glycine, alanine, and aspartic and glutamic acids were raised in marasmic rats but were reduced in rats fed low protein diets ad libitum. Young and severly malnourished rats appeared to have limited ability to synthesize urea. Therefore, they excreted more ammonia and other nitrogenous substances such as ethanolamine, and when given an amino acid load, intermediary metabolites of the ingested amino acids. Rats fed low protein diets showed diminution of total liver DNA, RNA, and protein. In addition to the reduction of protein synthesis resulting from decreased cellular RNA, ribosomes from the livers of protein-deficient rats had reduced ability to synthesize proteins. This defect was associated with the detatchment of the ribosomes from endoplasmic reticulum membrane and the elevation of the proportion of monosomes to polyribosomes. Malnutrition did not produce any change in the turnover rate of liver RNA. Protein deficiency caused significant depression of serum insulin, thyroxine, and corticosterone levels. Theoverall conclusion is that mammalian metabolism is well adapted to dietary intake and that this adaptation is achieved through dietary control of synthesis and release of key metabolic hormones.
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PMID:Experimental protein and energy in the rat. 80 70

The three major phases in the secretory process in the exocrine pancreas (synthesis, intracellular transport, zymogen discharge) have been tested in vitro after changing circulating insulin levels in rats in vivo. One group of rats received a continuous infusion of glucose for periods up to 72 hours, which keeps blood glucose levels above 200 mg/100 ml and immunoreactive insulin (IRI) raised to 130 muU/ml. As a result of this treatment, amylase content in the pancreas increases by 25% while chymotrypsinogen and lipase show a comparable decrease. The rate of total protein synthesis increased by 40% after 48 hours of infusion. The basal and carbamylcholine stimulated discharge of newly synthesized proteins are not altered. The baseline discharge of amylase is increased significantly, while the discharge of lipase and chymotrypsinogen decreased below control levels. Similar results are obtained, if circulating insulin levels are raised by the application of glibenblamide (HB419) for a period of 24 hours. Protein synthesis increases by 26.5% and baseline discharge of amylase by 50%. In chronic alloxan diabetic animals the alteration of the exocrine pancreatic function depends on the severity of the diabetes and relates to circulating insulin levels. Animals with highest blood glucose levels and low or undetectable insulin concentrations show a disappearance of amylase from the exocrine pancreas and a depression of the rate of protein synthesis by 30%. The results suggest a direct effect of insulin on protein biosynthesis and zymogen discharge, most pronounced for amylase.
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PMID:Regulation of exocrine pancreatic secretory process by insulin in vivo. 80 10

It has previously been shown that nicotinic acid (NA)-induced depression of free fatty acids (FFA) stimulates the secretion of GH and glucagon. To evaluate this hormonal response further, we studied the influence of different doses of glucose administered by continuous iv infusion on the GH and glucagon increase during NA-induced FFA depression. In ten male non-obese volunteers, FFA depression by the infusion of NA (2.3 g over a period of 210 min) resulted in a late rise (from 150 min on) of GH (From 1.1 to 25.9 ng/ml) and an early increase (from 30 min on) of glucagon (from 71.7 to 138.2 pg/ml). When glucose was infused (approximately 60, 120 and 180 g, respectively, over a period of 270 min) during NA-induced FFA depression, the GH rise was reduced and delayed in relation to the amount of glucose infused, but could not be completely abolished (maximal GH concentration during the three NA-plus-glucose infusions: 16.5, 8.0 and 6.1 ng/ml, respectively). The glucagon rise was entirely reversed by the high glucose dose. Insulin did not rise during NA infusion alone. Its secretion in response to glucose infusion was not significantly influenced by FFA depression. Thus, during NA-induced FFA depression the secretion of two lipolytic hormones--GH and glucagon--is stimulated while the secretion of the lipogenetic hormone insulin remains low. Glucose has an inhibitory effect on the GH and glucagon response which, however, is different for each of the hormones.
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PMID:Growth hormone, glucagon, and insulin response to depression of plasma free fatty acids and the effect of glucose infusion. 83 44

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

Exposure of resting rat diaphragm for one hour in vitro to halothane (1-1.5, 2-2.5 and 4-4.5 per cent in oxygen) produced significant alterations of intracellular glucose disposition. Glycolysis (as measured by lactate production) increased, while glycogen formation was inhibited in a dose-related fashion. Net glucose uptake was unaffected by the anesthetic except during exposure to 4-4.5 per cent halothane, when 14 per cent depression of uptake was found. Total glycogen content decreased, due mainly to the inhibition of glycogen synthesis and to some extent to a stimulation of glycogenolysis. The anesthetic did not interfere with the effect of insulin on glucose uptake or the intracellular disposition of glucose. Creatine phosphate concentrations decreased following exposure of diaphragm to 1-1.5, 2-2.5 and 4-4.5 per cent halothane, while the adenosine triphosphate concentration declined after exposure to 4-4.5 per cent only. Although the mechanism(s) whereby halothane alters glucose and glycogen metabolism are unknown, it is possible that the anesthetic acts primarily by affecting membranes containing enzymes involved in the metabolism of glycogen.
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PMID:Alteration by halothane of glucose and glycogen metabolism in rat skeletal muscle. 85 Dec 40

The endocrinometabolic effects of the aerosol administration of beclomethasone dipropionate (100 microng four times daily) were evaluated in 20 asthmatic patients (11 corticodependent and nine noncorticodependent) during one month. In the noncorticodependent group, aerosol administration of beclomethasone had no statistically significant effect on the results of the glucose tolerance test and the plasma levels of insulin; there was a slight decrease in basal levels of cortisol, but the response of the cortisol level to administration of ACTH remained quite normal. In corticodependent patients, after substitution of aerosol therapy with beclomethasone for the oral therapy with steroids, the depression of adrenal function disappeared, usually quickly (in less than one month), whereas the abnormalities in the results of the glucose tolerance test persisted. Thus, at the dosage used, beclomethasone dipropionate might have minor systemic endocrinometabolic effects.
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PMID:The endocrinometabolic effects of beclomethasone dipropionate in asthmatic patients. 86 40


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