Alcoholism Abolishes the Gamma-Aminobutyric Acid (GABA)ergic Control of GH Secretion in Humans

Alcohol ◽  
1998 ◽  
Vol 16 (4) ◽  
pp. 325-328 ◽  
Author(s):  
P.P. Vescovi ◽  
R. Volpi ◽  
V. Coiro
Keyword(s):  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Gh Secretion

scholarly journals Propofol Requirement in Patients with Growth Hormone-Secreting Pituitary Tumors Undergoing Transsphenoidal Surgery

2019 ◽  
Vol 8 (5) ◽  
pp. 571
Author(s):  
Seung Hyun Kim ◽  
Namo Kim ◽  
Eui Hyun Kim ◽  
Sungmin Suh ◽  
Seung Ho Choi
Keyword(s):  
Growth Hormone ◽  
General Anesthesia ◽  
Transsphenoidal Surgery ◽  
Pituitary Tumors ◽  
Aminobutyric Acid ◽  
Loss Of Consciousness ◽  
Gamma Aminobutyric Acid ◽  
Gh Secretion ◽  
Effect Site ◽  
Effect Site Concentration

Growth hormone (GH) secretion is regulated by various hormones or neurotransmitters, including gamma-aminobutyric acid. The aim of this study was to determine the propofol requirement in patients with GH-secreting pituitary tumors undergoing transsphenoidal surgery. General anesthesia was induced in 60 patients with GH-secreting tumors (GH group, n = 30) or nonfunctioning pituitary tumors (NF group, n = 30) using an effect-site target-controlled intravenous propofol infusion. The effect-site concentrations were recorded at both a loss of consciousness and a bispectral index (BIS) of 40, along with the effect-site concentration after extubation, during emergence from the anesthesia. The effect-site concentration of propofol was higher in the GH group than in the NF group at a loss of consciousness and a BIS of 40 (4.09 ± 0.81 vs. 3.58 ± 0.67, p = 0.009 and 6.23 ± 1.29 vs. 5.50 ± 1.13, p = 0.025, respectively) and immediately after extubation (1.60 ± 0.27 vs. 1.40 ± 0.41, p = 0.046). The total doses of propofol and remifentanil during anesthesia were comparable between the groups (127.56 ± 29.25 vs. 108.64 ± 43.16 µg/kg/min, p = 0.052 and 6.67 ± 2.89 vs. 7.05 ± 1.96 µg/kg/h, p = 0.550, respectively). The propofol requirement for the induction of a loss of consciousness and the achievement of a BIS of 40 is increased during the induction of general anesthesia in patients with GH-secreting tumors.

Prolactin and growth hormone secretion in chickens: stimulation by histamine and inhibition by gamma-aminobutyric acid

1984 ◽  
Vol 107 (1) ◽  
pp. 36-41 ◽  
Author(s):  
T. R. Hall ◽  
S. Harvey ◽  
A. Chadwick
Keyword(s):  
Growth Hormone ◽  
Direct Effect ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Gh Secretion ◽  
Pituitary Glands ◽  
Stimulation By Histamine

Abstract. Anterior pituitary glands from chickens (Gallus domesticus) were incubated with or without single, mediobasal chicken hypothalami in medium containing histamine, alone or together with the antagonist diphenhydramine or in medium containing gamma-aminobutyric acid (GABA), alone or together with the antagonists bicuculline or picrotoxin. The release of prolactin (Prl) and growth hormone (GH) was measured by homologous radioimmunoassay. Histamine had no direct effect on the release of either hormone but stimulated Prl (in a dose-related way) and GH release when anterior pituitary glands were co-incubated with hypothalami. Diphenhydramine also had no direct effect on Prl or GH secretion but blocked the stimulatory effect of histamine on hypothalamusinduced Prl and GH release. When anterior pituitary glands were incubated without hypothalami, GABA, bicuculline and picrotoxin had no effect on the release of Prl or GH. However, GABA inhibited the release of both hormones in a concentration-related manner, when anterior pituitary glands were co-incubated with hypothalami. This inhibition was blocked by both bicuculline and picrotoxin. These results suggest that histamine and GABA may be involved in controlling the secretion of Prl and GH from the avian pituitary gland, possibly by modifying the secretion of hypothalamic releasing and/or release-inhibiting hormones.

Evidence for a sex difference in the basal growth hormone response to GABAergic stimulation in humans

1988 ◽  
Vol 119 (3) ◽  
pp. 353-357 ◽  
Author(s):  
Palmiero Monteleone ◽  
Mario Maj ◽  
Michele Iovino ◽  
Luca Steardo
Keyword(s):  
Growth Hormone ◽  
Sex Difference ◽  
Healthy Subjects ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Hormone Response ◽  
Blood Samples ◽  
Gh Secretion ◽  
Plasma Gh ◽  
Healthy Males

Abstract. Evidence has been provided supporting the existence of a sex-related difference in the GH secretion following different GH-releasing stimuli. Since pharmacological activation of the endogenous gamma-aminobutyric acid (GABA) system results in increased basal GH release in humans, the present study was undertaken to investigate whether a sex difference is present in the GH response to GABAergic stimulation. Sixteen healthy subjects (8 women and 8 men) received orally 10 mg of baclofen, the direct GABAB agonist which freely crosses the blood-brain barrier. Blood samples were collected before (T = −30 and 0) and 30, 60, 90, 120 and 180 min after the drug administration for plasma GH measurements. Following baclofen administration, plasma GH rose in healthy males (F = 19.417, P < 0.0001), but not in females (F = 1.67, NS). These results suggest that GABA modulation of human GH release is sex-dependent.

Neuroendocrine effects of chronic administration of sodium valproate in epileptic patients

1988 ◽  
Vol 118 (3) ◽  
pp. 381-388 ◽  
Author(s):  
C. Invitti ◽  
L. Danesi ◽  
A. Dubini ◽  
F. Cavagnini
Keyword(s):  
Body Weight ◽  
Sodium Valproate ◽  
Chronic Administration ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Gh Secretion ◽  
Epileptic Patients ◽  
Significant Attenuation ◽  
Hypothalamic Pituitary Axis ◽  
Normal Controls

Abstract. In 10 untreated epileptic patients, we evaluated the functional integrity of the hypothalamic-pituitary axis before and during chronic treatment with sodium valproate, a gamma-aminobutyric acid-mimetic compound. The GH response to L-dopa (250–500 mg po) was absent in 3 and severely impaired in 2 of the 10 patients though being, on the average, only slightly lower in the epileptic subjects than in normal controls. Conversely, the GH rise following GHRH (0.5 μg/kg body weight, iv) was normal in 9 of the patients. A significant blunting of the GH response to L-dopa occurred in the 7 patients initially responsive after 6 month of sodium valproate (P < 0.05). The GH response to GHRH also underwent an evident though not significant attenuation. The ACTH and the ACTH/cortisol elevations elicited by metyrapone (35 mg/kg body weight infused over 4 h), and by CRH (1 μg/kg body weight, iv), respectively, normal before treatment, were significantly impaired (P <0.05, <0.01) during antiepileptic therapy. Prolactin and TSH dynamics following metoclopramide (0.1 mg/kg body weight, iv) and TRH (200 μg iv) remained normal over the whole study period. Growth arrest ensued in 1 patient after 6 months of sodium valproate and disappeared after drug withdrawl. These observations point to a defective hypothalamic control of GH secretion in some epileptic patients. They also indicate that chronic administration of sodium valproate, hence activation of central gamma-aminobutyric acid system, results in a blunting of the stimulated GH and ACTH secretion. Occasionally, a reversible arrest of skeletal growth may also ensue.

Purification of Antihemophilic Factor (Factor VIII) by Amino Acid Precipitation*

1964 ◽  
Vol 11 (01) ◽  
pp. 064-074 ◽  
Author(s):  
Robert H Wagner ◽  
William D McLester ◽  
Marion Smith ◽  
K. M Brinkhous
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Factor Viii ◽  
Plasma Protein ◽  
Acid Precipitation ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Specific Procedure ◽  
Beta Alanine ◽  
Antihemophilic Factor

Summary1. The use of several amino acids, glycine, alpha-aminobutyric acid, alanine, beta-alanine, and gamma-aminobutyric acid, as plasma protein precipitants is described.2. A specific procedure is detailed for the preparation of canine antihemophilic factor (AHF, Factor VIII) in which glycine, beta-alanine, and gammaaminobutyric acid serve as the protein precipitants.3. Preliminary results are reported for the precipitation of bovine and human AHF with amino acids.

A Simple Method for Preparing Fibrinogen

1966 ◽  
Vol 16 (01/02) ◽  
pp. 198-206 ◽  
Author(s):  
W Straughn ◽  
R. H Wagner
Keyword(s):  
Barium Sulfate ◽  
Caproic Acid ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Human Fibrinogen ◽  
Simple Method ◽  
High Yields ◽  
Marked Stability

SummaryA simple new procedure is reported for the isolation of canine, bovine, porcine, and human fibrinogen. Two molar β-alanine is used to precipitate fibrinogen from barium sulfate adsorbed plasma. The procedure is characterized by dependability and high yields. The material is 95% to 98% clottable protein but still contains impurities such as plasminogen and fibrin-stabilizing factor. Plasminogen may be removed by adsorption with charcoal. The fibrinogen preparations exhibit marked stability to freezing, lyophilization, and dialysis. Epsilon-amino-n-caproic acid and gamma-aminobutyric acid which were also studied have the property of precipitating proteins from plasma but lack the specificity for fibrinogen found with β-alanine.

Understanding Schizophrenia: Genetic Causes and Treatment

2019 ◽  
Vol 1 (1) ◽  
pp. 6-12
Author(s):  
Fatima Javeria ◽  
Shazma Altaf ◽  
Alishah Zair ◽  
Rana Khalid Iqbal
Keyword(s):  
Copy Number ◽  
Drug Targets ◽  
Disease Risk ◽  
Mental Disease ◽  
Copy Number Variants ◽  
Aminobutyric Acid ◽  
Epigenetic Mechanisms ◽  
Gamma Aminobutyric Acid ◽  
Wide Range ◽  
Severe Mental Disease

Schizophrenia is a severe mental disease. The word schizophrenia literally means split mind. There are three major categories of symptoms which include positive, negative and cognitive symptoms. The disease is characterized by symptoms of hallucination, delusions, disorganized thinking and speech. Schizophrenia is related to many other mental and psychological problems like suicide, depression, hallucinations. Including these, it is also a problem for the patient’s family and the caregiver. There is no clear reason for the disease, but with the advances in molecular genetics; certain epigenetic mechanisms are involved in the pathophysiology of the disease. Epigenetic mechanisms that are mainly involved are the DNA methylation, copy number variants. With the advent of GWAS, a wide range of SNPs is found linked with the etiology of schizophrenia. These SNPs serve as ‘hubs’; because these all are integrating with each other in causing of schizophrenia risk. Until recently, there is no treatment available to cure the disease; but anti-psychotics can reduce the disease risk by minimizing its symptoms. Dopamine, serotonin, gamma-aminobutyric acid, are the neurotransmitters which serve as drug targets in the treatment of schizophrenia. Due to the involvement of genetic and epigenetic mechanisms, drugs available are already targeting certain genes involved in the etiology of the disease.

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