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

This article discusses the results of recent neuroendocrinological research in depressions. The abnormalities found in a given category of vital depressive patients--cortisol hypersecretion, decreased growth hormone response to insulin hypoglycaemia and decreased luteinizing hormone secretion in menopause--are believed to be due to deficient noradrenalin-(NA)-ergic activity in the hypothalmus. Thus explained, they support the so-called MA (monoamine) hypothesis, which postulates that a functional NA deficiency in the brain plays a role in the pathogenesis of certain types of vital depression. Disorders in certain central MA-ergic systems are predictive of disorders in the hormone secretion of the anterior pituitary. Inversely, disorders in the hormone secretion of the anterior pituitary can be indicative of disorders in the MA-ergic transmission in the hypothalamus. Consequently we can expect a convergence of transmitter research and neuroendocrinological research--two lines of research which have so far been largely separated in studies of human individuals.
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PMID:Neuroendocrine disorders in depressions and their significance for the monoamine hypothesis of depression. 2 49

Overnight metabolic studies in 39 poorly controlled insulin-treated diabetic patients aged 9 to 66 years showed hypoglycaemia (blood-glucose less than 2 mmol/1) in 22 patients; it lasted 3 h or more in 17. Hypoglycaemic symptoms were very mild or absent, but 19 patients had other features of overtreatment with insulin. These included lethargy, depression, night sweats, morning headaches, fits (3 patients), glycogen-laden hepatomegaly (3), and acquired tolerance to high doses of insulin (mean 1 u/kg/24 h). The best clinical clue to recurrent nocturnal hypoglycaemia was the intermittent occurrence of symptoms, however "mild" and infrequent these appeared to be. Reduction of insulin by a mean of 25% in these patients (without change of species) did not result in loss of overall control; 1 patient with recurrent ketoacidosis was stablished on 40% of his initial dose. It is difficult, sometimes impossible, to achieve good overnight control with conventional once or twice daily insulin therapy. Since patients readily become tolerant of low blood-glucose levels, reliance on urine tests and symptoms of hypoglycaemia as a guide to dosage easily produces a spiral of overtreatment.
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PMID:Unrecognised nocturnal hypoglycaemia in insulin-treated diabetics. 8 75

The diagnosis of florid Cushing's syndrome is usually made without difficulty but diagnostic problems may arise. Five such cases are described. Difficulties may occur when the features of the syndrome are incomplete. Three such cases were encountered. In each only one clinical feature was present; these respectively were hypertension, osteoporosis and obesity. The diagnosis was confirmed, however, biochemically and eventually histologically and there was a good response to surgery in each case. Another diagnostic problem, both clinically and biochemically is the obese, hirsute, hypertensive female. Two such cases are described, in whom Cushing's syndrome was diagnosed clinically and biochemically but in whom there was no response to adrenalectomy. Retrospectively the validity of the original diagnosis is questioned. It is concluded that Cushing's syndrome may present in a very incomplete form and should be considered in the differential diagnosis, even if only one feature is present. It is stressed that obesity, hirsutism, hypertension and depression are commonly found in association with normal adrenal function. Urinary free cortisol and cortisol response to insulin induced hypoglycaemia may be of value in distinguishing these cases from those with endocrine disease.
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PMID:Problems in the diagnosis of Cushing's syndrome. 19 80

Crude mediators from stimulated rabbit peritoneal leukocytes (LEM) engender numerous physiologic alterations in rats, which are similar to those observed during infection. One hour after the intraperitoneal injection of crude LEM, plasma insulin and glucagon concentrations are elevated; at 2 h the hormonal alterations are manifested by a 30% increase in hepatic cyclic adenosine 3',5'-monophosphate (cAMP), glycogen depression, and uptake of 14C-labeled nonmetabolizable amino acid analogues (AA). Plasma hormone concentrations reach maximum levels by 5 h and decline by 24 h. The hepatic concentrations of AA parallel the insulin and glucagon responses and correlate with the inverse of insulin/glucagon molar ratio. In spite of mobilization of hepatic glycogen evident at 5 h, plasma glucose concentrations were transiently depressed. Plasma insulin, glucagon, and hepatic AA concentrations were dose dependent. Plasma insulin and glucagon responses to crude LEM may explain increases in hepatic cAMP, uptake of AA, and glycogenolysis as well as hypoglycemia. These data partially characterize the role of crude LEM, provide an explanation for the stimuli-inducing hyperglucagonemia and hyperinsulinemia during infection. They implicate the endocrine pancreas as a factor regulating the host's metabolic response to infection.
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PMID:Effect of leukocytic endogenous mediators on endocrine pancreas secretory responses. 19 70

A phytohemagglutinin extract is prepared from raw kidney beans (Phaseolus vulgaris) and incorporated at a level of 1% (dry matter) in the diet of young growing rats. Beside a decrease of feed intakes, the main effects of the experimental diet are the following : growth depression, decrease of dry matter and protein digestibility and hypoglycemia. Biological value, organs weight (liver, kidneys, spleen) did not change significantly. The hemagglutinin extract induces an inhibition of saccharase activity whereas (Na+-K+)-ATPase remains unchanged. Growth depressing effect may be due to an alteration of hydrolysis and absorption mechanisms at the level of brush border of enterocytes.
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PMID:[Effects of a phytohemagglutinin extract on growth, nitrogen digestibility and the activity of invertase and (Na+-K+)-ATPase in the intestinal mucosa of the rat]. 23 10

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

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

Insulin-induced hypoglycemia caused depression of rhythmic monosynaptic EPSP motoneurons of the lumbar cord in acute experiments on narcotized and spinal cats. It was demonstrated that growing depression of monosynaptic transmission was associated with the exhaustion of mediator operative fraction and not with any pre- or postsynaptic delay or inhibition over a period of initial hypoglycemia when the sugar content in the blood fell to the level of 50--60 mg%. The function disturbance of postsynaptic formations of monosynaptic reflex arc of spinal cord occured in more advanced hypoglycemia.
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PMID:[Monosynaptic reflexes of the cat spinal cord during the development of insulin hypoglycemia]. 43 22

The biochemical research of depression did not gain in before the exploration of the nodes of effect of the antidepressants. For the present the point of research was the search for disturbances in metabolism of the biogenic amines in brain. The noradrenalin and serotonin-hypothesis was propounded postulating a disturbance in noradrenalin, or serotonin regulation, respectively at the receptor in depression. Until now experimental results did not support this hypothesis, just as the investigations of electrolytic changes in depression did not lead to homogeneous results. On the contrary the neuroendocrinological research showed important results; In endogenous depressive patients an increased cortisol-secretion was ascertained, and in about 65% of the patients a missing or strongly reduced cortisol-suppression after injection of dexamethason was noted, moreover, the growth-hormone-secretion after insulin-hypoglycemia is reduced in a part of depressive women in the menopause. Finally the thyrotropin-secretion stopped in 20--40% of the endogenous depressive patients after injection of thyrotropin-releasing hormone.
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PMID:[Biochemical research in depression (author's transl)]. 48 Aug 57

The beta-adrenergic blocking agent propranolol had in itself no notable influence on the blood glucose level in rats, but in combination with chlorpropamide it considerably delayed and enhanced the hypoglycaemic and liver glycogenolysis depressing actions of chlorpropamide. This effect was still more pronounced when the rats were treated in addition to propranolol and chlorpropamide with thyroxine or glanduitrine, which in themselves act as stimulators of liver glycogenolysis. The simultaneous administration of propranolol and chlorpropamide depressed considerably the liver glycogenolysis induced by prolonged fasting and inhibited completely the liver glycogenolysis observed after hepatectomy. The reports available in the literature on propranolol-precipitated hypoglycaemia in patients are surveyed and it is supposed that the beta-adrenergic blocking agent produces hypoglycaemia primarily through the depression of liver glycogenolysis. This observation supports the hypothesis that the adrenergic beta-receptors play an important role in the sympathetic control of liver glycogenolysis.
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PMID:Effect of propranolol on drug-induced and physiological glycogenolysis in the liver. 58 7


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