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)

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

The effects of thyrotropin-releasing hormone (TRH) on the release of growth hormone (GH), prolactin (PRL) and thyrotropin (TSH) were investigated in patients with depression. Intravenous injection of synthetic TRH (500 mug) caused a significant increase in plasma GH (peak value: 7.7 minus 35.0 ng/ml) in 8 of 13 patients with mental depression. After clinical recovery these patients had no response of plasma GH to TRH. TRH administration did not raise plasma GH in normal subjects examined. Plasma PRL responses to TRH were significantly enchanced (P smaller than 0.05) in depressed patients compared with control subjects. Plasma TSH responses to TRH were significantly blunted in patients with depression (P smaller than 0.05). These results suggest disorders in the hypothalamo-pituitary function in depression.
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PMID:Growth hormone and prolactin release after injection of thyrotropin-releasing hormone in patients with depression. 80 76

Twenty-five depressed patients were examined as to their growth hormone responses to TRH. An enhanced pituitary growth hormone response to intravenous injection of 500 mug TRH was observed in eight depressed patients, while TRH administration did not raise growth hormone levels in nine of 10 normal subjects examined. Occurrence of enhanced response of growth hormone was not related to the thyrotropin values after TRH administration. Bipolar patients exhibited enhanced growth-hormone response more frequently than unipolar patients. Five patients with involutional depression and neurotic depression who showed the most insufficient thyrotropin release to TRH administration together with lowered thyroid function revealed to be non-responders of growth hormone.
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PMID:Enhanced growth hormone responses to TRH injection in bipolar depressed patients. 81 72

Numerous studies show that most depressed patients show abnormal pituitary responses to challenge by intravenous injection of thyrotropin releasing hormone (TRH). Some patients show after TRH diminished thyroid stimulating hormone (TSH) release, some show unexpected growth hormone release; prolactin release may be increased or decreased. The diminished TSH release is the most widely reported finding. It cannot be accounted for by primary changes in the pituitary or thyroid glands. Interference with TRH-induced TSH release by elevated cortisol may account for some observations, but this possibility has not been studied. The present data provide additional evidence that in depression there is often a disruption of hypothalamic regulatory function.
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PMID:Pituitary responses to thyrotropin releasing hormone in depressed patients: a review. 82 51

The authors studied changes in indices of thyroid function prospectively in a group of 11 patients given amitriptyline to treat depression. The drug caused no significant alteration in these indices, but scores on the Hamilton Depression Rating Scale improved significantly. In another group of subjects with depression, the stimulation of growth hormone secretion by L-dopa was unaffected by amitriptyline therapy.
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PMID:Thyroid function and growth hormone secretion in amitriptyline-treated depression. 91 Sep 82

The study investigated the respective influences of nicotinic acid and somatostatin on plasma concentrations of blood glucose, free fatty acids, glucagon, growth hormone and cortisol in insulin-dependent diabetic subjects. After administration of nicotinic acid alone, marked depression of plasma FFA was accompanied by significant increases of plasma glucagon, growth hormone and cortisol. The glucagon and growth hormone responses to nicotinic acid were significantly reduced when plasma FFA were raised by intravenous administration of heparin and triglycerides. Somatostatin alone induced a significant decrease in blood glucose, plasma glucagon and growth hormone concentrations. Plasma FFA remained unchanged. Somatostatin did not modify the nicotinic acid-induced fall in plasma FFA, but completely blocked the corresponding increments in glucagon and growth hormone. The cortisol rise was not altered by somatostatin. Rebound of glucagon and growth hormone levels were seen upon discontinuation of the somatostatin administration. These results demonstrate that the plasma FFA concentration plays a role in the regulation of glucagon and growth hormone secretion in insulin-dependent diabetics. Furthermore, they indicate that somatostatin, previously shown to be capable of negating the stimulatory effect of various factors on glucagon and growth hormone secretion, also affects the response of these hormones to FFA depression.
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PMID:Effect of somatostatin on metabolic and hormonal changes induced by nicotinic acid in insulin-dependent diabetics. 97 35

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

The effects of bilateral lesions of the ventral noradrenergic bundle (VNA) were studied in male rats. In contrast to data reported by others, hyperphagia and obesity were not observed following VNA lesions. Indeed, except for a depression during the first three postoperative days, food intake (FI) of the VNA lesioned animals (VNAL) was normal. Interestingly, the body weight (BW) of the VNAL was significantly reduced compared to the controls, and a pair feeding study indicated that this depression of BW was not due to their FI. Computation of FI per metabolic size showed that the VNAL actually had a significantly increased FI compared to the controls. After a two day fast the VNAL lost more metabolic size than controls and upon refeeding they defended their pre-fast BW. The VNAL rats showed normal body composition and circulating glucose, insulin and prolactin. They had reduced free fatty acids, triglycerides, growth hormone and body length. The data suggest that the mesencephalon influences BW set point, some metabolites and possibly overall metabolism.
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PMID:Mesencephalic lesions resulting in normophagia, reduced weight and altered metabolism. 99 50

This study was designed to clarify the details of any changes in serum growth hormone levels occurring in surgical patients. Intravenous glucose tolerance tests were performed upon three groups of six patients each, Group I, minor surgery (inguinal herniorrhaphy), Group II, moderate surgery (vagotomy and pyloroplasty), and Group III, major surgery (aortofemoral bypass). Plasma glucose and serum growth hormone levels were measured. Depression of glucose utilization occurred together with elevations of fasting growth hormone levels and increased growth hormone responses to intravenous glucose. It is suggested that the increased serum growth hormone levels are a response to the glucose intolerance caused by operation, modifying the pituitary growth hormone release.
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PMID:The effect of surgical operation on growth hormone levels in plasma. 114 26

The hamster exhibits a biphasic pattern of insulin secretion; however, the dynamic response differs qualitatively from that of the rat in that there is a steady-state second release phase. A marked attenuation of insulin secretion as a result of hypophysectomy was observed after 3 weeks, but not after 2 weeks. This depression of insulin secretion was restored to near or above normal levels by bovine growth hormone, human growth hormone, and prolactin.
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PMID:Dynamics of insulin release by perfused hamster )Mesocricetus auratus) pancreases: effects of hypophysectomy, bovine and human growth hormone, and prolactin. 115 Dec 6


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