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[About the human health safety estimation of ractopamine intake together with the food].

https://arctichealth.org/en/permalink/ahliterature105651
Source
Vestn Ross Akad Med Nauk. 2013;(6):4-8
Publication Type
Article
Date
2013
Author
G G Onishchenko
A Iu Popova
V A Tutel'ian
N V Zaitseva
S A Khotimchenko
I V Gmoshinskii
S A Sheveleva
V N Rakitskii
P Z Shur
A B Lisitsyn
D A Kir'ianov
Source
Vestn Ross Akad Med Nauk. 2013;(6):4-8
Date
2013
Language
Russian
Publication Type
Article
Keywords
Adrenergic beta-Agonists - pharmacology
Animals
Growth Substances
Health status
Humans
Meat - analysis - utilization
Phenethylamines - chemistry - pharmacology
Russia - epidemiology
Abstract
The analysis of scientific data including American and European scientific communities concerning use of ractopamine as a growth factor in food animal production and the argumentation of the maximum permitted levels of ractopamine and levels of ractopamine in meat and byproducts (offal) is carried out. The position of the Russian side stated at the Codex Alimentarius commission 35th session that acceptable ractopamine daily intake is insufficiently validated and cannot be used for the determination of maximum permitted levels of ractopamine in meat and byproducts (offal) is confirmed. It is represented that residual ractopamine intake together with food on the levels which are recommended by the Codex Alimentarius commission and by taking into account the levels of animal products consumption in Russian Federation will lead to unacceptable human health risk level that will promote increasing heart diseases and life expectancy reduction. In this connection Russia states against of acceptance of maximum permitted levels of ractopamine in food.
PubMed ID
24340628 View in PubMed
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The arrestin domain-containing 3 protein regulates body mass and energy expenditure.

https://arctichealth.org/en/permalink/ahliterature130643
Source
Cell Metab. 2011 Nov 2;14(5):671-83
Publication Type
Article
Date
Nov-2-2011
Author
Parth Patwari
Valur Emilsson
Eric E Schadt
William A Chutkow
Samuel Lee
Alessandro Marsili
Yongzhao Zhang
Radu Dobrin
David E Cohen
P Reed Larsen
Ann Marie Zavacki
Loren G Fong
Stephen G Young
Richard T Lee
Author Affiliation
Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. parth@alum.mit.edu
Source
Cell Metab. 2011 Nov 2;14(5):671-83
Date
Nov-2-2011
Language
English
Publication Type
Article
Keywords
Adipose Tissue, Brown - metabolism
Adipose Tissue, White - metabolism
Adrenergic beta-Agonists - pharmacology
Animals
Arrestins - genetics - metabolism
Body mass index
Chromosomes, Human, Pair 5
Cohort Studies
Energy Metabolism - genetics
Female
Genetic Loci
Humans
Iceland - epidemiology
Linkage Disequilibrium
Male
Mice
Mice, Knockout
Obesity - epidemiology - genetics - metabolism
Receptors, Adrenergic, beta - metabolism
Sequence Homology, Amino Acid
Sex Factors
Signal Transduction
Thermogenesis - genetics
Abstract
A human genome-wide linkage scan for obesity identified a linkage peak on chromosome 5q13-15. Positional cloning revealed an association of a rare haplotype to high body-mass index (BMI) in males but not females. The risk locus contains a single gene, "arrestin domain-containing 3" (ARRDC3), an uncharacterized a-arrestin. Inactivating Arrdc3 in mice led to a striking resistance to obesity, with greater impact on male mice. Mice with decreased ARRDC3 levels were protected from obesity due to increased energy expenditure through increased activity levels and increased thermogenesis of both brown and white adipose tissues. ARRDC3 interacted directly with ß-adrenergic receptors, and loss of ARRDC3 increased the response to ß-adrenergic stimulation in isolated adipose tissue. These results demonstrate that ARRDC3 is a gender-sensitive regulator of obesity and energy expenditure and reveal a surprising diversity for arrestin family protein functions.
Notes
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PubMed ID
21982743 View in PubMed
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Beta-receptor agonists in obstetrics. Based on the symposium arranged by AB Draco in Malmö, Sweden on March 6,1981.

https://arctichealth.org/en/permalink/ahliterature65785
Source
Acta Obstet Gynecol Scand Suppl. 1982;108:1-72
Publication Type
Article
Date
1982
Source
Acta Obstet Gynecol Scand Suppl. 1982;108:1-72
Date
1982
Language
English
Publication Type
Article
Keywords
Adrenergic beta-Agonists - pharmacology
Female
Humans
Labor, Obstetric - drug effects
Pregnancy - drug effects
Uterus - drug effects
PubMed ID
6126984 View in PubMed
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cAMP- and cGMP-independent stretch-induced changes in the contraction of rat atrium.

https://arctichealth.org/en/permalink/ahliterature10288
Source
Pflugers Arch. 2000 Nov;441(1):65-8
Publication Type
Article
Date
Nov-2000
Author
P. Tavi
M. Weckström
H. Ruskoaho
Author Affiliation
Department of Physiology, University of Oulu, Finland. pasi.tavi@oulu.fi
Source
Pflugers Arch. 2000 Nov;441(1):65-8
Date
Nov-2000
Language
English
Publication Type
Article
Keywords
Adrenergic beta-Agonists - pharmacology
Animals
Atrial Function
Biomechanics
Calcium - metabolism
Cyclic AMP - metabolism
Cyclic GMP - metabolism
Isoproterenol - pharmacology
Male
Mechanoreceptors - physiology
Myocardial Contraction - drug effects - physiology
Rats
Rats, Sprague-Dawley
Abstract
The stretch-induced changes in contraction force, cAMP and cGMP in isolated rat left atrium were studied. Increasing the diastolic intra-atrial pressure from 1 cmH2O to 8 cmH2O caused an immediate (
PubMed ID
11205063 View in PubMed
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Cardiovascular responses to beta-stimulation with isoproterenol in deep hypothermia.

https://arctichealth.org/en/permalink/ahliterature11195
Source
J Appl Physiol. 1996 Aug;81(2):573-7
Publication Type
Article
Date
Aug-1996
Author
T. Lauri
Author Affiliation
Department of Physiology, University of Oulu, Finland.
Source
J Appl Physiol. 1996 Aug;81(2):573-7
Date
Aug-1996
Language
English
Publication Type
Article
Keywords
Adrenergic beta-Agonists - pharmacology
Algorithms
Animals
Blood Gas Analysis
Blood Pressure - drug effects - physiology
Body Temperature - drug effects - physiology
Calibration
Dogs
Electrocardiography
Heart Rate - drug effects - physiology
Hemodynamic Processes - drug effects
Hypothermia, Induced
Isoproterenol - pharmacology
Stroke Volume - drug effects - physiology
Abstract
The aim of this study was to investigate the effects of beta-stimulation in deep (25 degrees C) hypothermia. Cardiac catheterization was performed on seven anesthetized beagle dogs. They were cooled between ice bags down to 25 degrees C and received isoproterenol administered intravenously three times: at the normal body temperature (37 degrees C) before cooling, after cooling at 25 degrees C, and after rewarming at 37 degrees C. Circulatory function was measured for every 1 degree C of temperature change. Isoproterenol infusion at 37 degrees C induced cardiac acceleration, including the increases of heart rate, cardiac output, and peak first derivative of the left ventricular pressure curve. Systemic vascular and mean outflow resistances and mean aortic pressure decreased. During cooling, shivering thermogenesis continued, even down to 25 degrees C. At 25 degrees C, cardiac acceleration after isoproterenol infusion did not exist but relaxation rate increased slightly. Systemic vascular and mean outflow resistances decreased, but left ventricular end-diastolic and filling pressures increased. beta-Stimulation at normal body temperature increases shivering thermogenesis during cooling. The venous return to the left ventricle at 25 degrees C increased after isoproterenol infusion while systemic vascular resistance decreased, indicating systemic vasodilatation. This increase in preload is probably due to vasoconstriction in pulmonary vessels, which may be mediated by prejunctional beta-adrenoceptors. For cardiac inotrophy, the isoproterenol had no physiologically significant effects at 25 degrees C. After rewarming at 37 degrees C, the effects of isoproterenol were physiologically similar to the effects at the same temperature before cooling.
PubMed ID
8872620 View in PubMed
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Clenbuterol in the prevention of muscle atrophy: a study of hindlimb-unweighted rats.

https://arctichealth.org/en/permalink/ahliterature10190
Source
Arch Phys Med Rehabil. 2001 Jul;82(7):930-4
Publication Type
Article
Date
Jul-2001
Author
N M Herrera
A N Zimmerman
D D Dykstra
L V Thompson
Author Affiliation
Department of Physical Medicine and Rehabilitation, Medical School, University of Minnesota, Minneapolis, MN 55455, USA.
Source
Arch Phys Med Rehabil. 2001 Jul;82(7):930-4
Date
Jul-2001
Language
English
Publication Type
Article
Keywords
Adrenergic beta-Agonists - pharmacology
Analysis of Variance
Animals
Clenbuterol - pharmacology
Hindlimb Suspension
Muscular Atrophy - prevention & control
Rats
Rats, Inbred BN
Rats, Inbred F344
Research Support, Non-U.S. Gov't
Abstract
OBJECTIVE: To determine whether the administration of clenbuterol, a beta2-adrenergic agonist, prevents loss of muscle mass during a period of imposed inactivity. DESIGN: Randomized trial. SETTING: Basic laboratory research. ANIMALS: Thirty Fischer 344 Brown Norway F1 Hybrid rats, 12 and 30 months of age. INTERVENTIONS: The rats were randomly assigned to a control group, or to 1 of 2 experimental groups: hindlimb unweighted for 2 weeks (HU-2), or hindlimb unweighted with daily injections of clenbuterol for 2 weeks (HU-2Cl). MAIN OUTCOME MEASURES: Muscle mass weighed in milligrams and single fiber cross-sectional area histochemically evaluated. RESULTS: In both age groups, the HU-2 animals had greater muscle atrophy (decrease in muscle mass) in the soleus muscle than the extensor digitorum longus (EDL) muscle. In the HU-2Cl groups, the decline in muscle mass of both the soleus and EDL muscles was attenuated by about 4% to 20%. In the HU-2 group, single fiber cross-sectional area decreased for both fiber types (type I, 20%-40%; type II, 37%-50%) in both age groups. Clenbuterol retarded the inactivity-induced decline in single fiber cross-sectional area by 12% to 50%. In the EDL muscles of the HU-2Cl group, we found hypertrophy in both fiber types in the 30-month-old animals and in type I fibers in the 12-month-old animals. CONCLUSIONS: Clenbuterol attenuated the decrease in muscle mass and single fiber cross-sectional area in both age groups. By preventing the loss of muscle mass, clenbuterol administered early in rehabilitation may benefit severely debilitated patients imposed by inactivity. The attenuated muscle atrophy found with clenbuterol in the present study provides cellular evidence for the reported change in muscle strength after its administration after knee surgery. Thus, the administration of clenbuterol may lead to a more rapid rate of rehabilitation.
PubMed ID
11441380 View in PubMed
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Control of beta 3-adrenergic receptor gene expression in brown adipocytes in culture.

https://arctichealth.org/en/permalink/ahliterature11423
Source
Mol Cell Endocrinol. 1995 Apr 1;109(2):189-95
Publication Type
Article
Date
Apr-1-1995
Author
S. Klaus
P. Muzzin
J P Revelli
M A Cawthorne
J P Giacobino
D. Ricquier
Author Affiliation
Fachbereich Biologie/Zoologie, Philipps Universität, Marburg, Germany.
Source
Mol Cell Endocrinol. 1995 Apr 1;109(2):189-95
Date
Apr-1-1995
Language
English
Publication Type
Article
Keywords
Adrenergic beta-Agonists - pharmacology
Animals
Base Sequence
Brown Fat - cytology - drug effects - metabolism
Cell Differentiation
Cells, Cultured
Cricetinae
Ethanolamines - pharmacology
Gene Expression Regulation - drug effects
Half-Life
Isoproterenol - pharmacology
Molecular Sequence Data
Phodopus
Receptors, Adrenergic, beta - biosynthesis - genetics
Receptors, Adrenergic, beta-3
Research Support, Non-U.S. Gov't
Abstract
Brown adipose tissue is a mammalian thermogenic tissue. Its ability to dissipate energy as heat is due to a unique mitochondrial protein, uncoupling protein (UCP). Activation and expression of UCP is under control of the sympathetic nervous system acting through beta -adrenergic receptors (AR). In this study we used Siberian hamster brown adipocytes differentiated in vitro to investigate the expression of the fat specific beta 3-AR. Binding studies using the new labelled beta 3 adrenergic ligand [3H]SB 206606 showed a density of beta 3-AR in brown adipocyte plasma membranes comparable to that measured in vivo. beta 3-AR mRNA expression was very high in mature brown adipocytes and was started to be expressed during differentiation before UCP mRNA. Its half-life was approximately 50 min. Treatment of cells with non-specific beta adrenergic agonists, specific beta 3-adrenergic agonists, and dibutyryl cyclic AMP resulted in a marked down regulation of beta 3-AR mRNA level within several hours.
PubMed ID
7664982 View in PubMed
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Divergent effects of weight reduction and oral anticonception treatment on adrenergic lipolysis regulation in obese women with the polycystic ovary syndrome.

https://arctichealth.org/en/permalink/ahliterature20977
Source
J Clin Endocrinol Metab. 1999 Jun;84(6):2182-7
Publication Type
Article
Date
Jun-1999
Author
H. Wahrenberg
I. Ek
S. Reynisdottir
K. Carlström
A. Bergqvist
P. Arner
Author Affiliation
Department of Medicine, Research Center, Huddinge University Hospital, Karolinska Institute, Sweden.
Source
J Clin Endocrinol Metab. 1999 Jun;84(6):2182-7
Date
Jun-1999
Language
English
Publication Type
Article
Keywords
Adipocytes - drug effects - metabolism
Adipose Tissue - drug effects - pathology
Adrenergic alpha-Agonists - pharmacology
Adrenergic beta-Agonists - pharmacology
Adult
Contraceptives, Oral, Combined - pharmacology
Contraceptives, Oral, Sequential - pharmacology
Diet, Reducing
Estradiol Congeners - pharmacology
Estrogens - pharmacology
Ethinyl Estradiol - pharmacology
Female
Humans
Lipolysis - drug effects
Norethindrone - pharmacology
Obesity - diet therapy - metabolism
Polycystic Ovary Syndrome - metabolism - physiopathology
Radioligand Assay
Research Support, Non-U.S. Gov't
Sympathetic Nervous System - drug effects - physiology
Weight Loss
Abstract
The influence of weight reduction and female sex hormones on the regulation of lipolysis was investigated in isolated abdominal sc adipocytes from 20 obese hyperandrogenic women with polycystic ovary syndrome (PCOS). Nine PCOS women were reinvestigated after 8-12 weeks of weight reduction therapy (WR) with a very low calorie diet, inducing a mean loss of 8 +/- 3 kg, and 8 PCOS women were reinvestigated after 12 weeks of treatment with combined oral contraceptives (OC), containing ethinyl estradiol and norethisterone; the remaining 3 subjects were drop-outs. Both WR and OC normalized hyperandrogenicity. WR caused a 50% reduction of basal lipolysis rate and a 5- to 7-fold increased noradrenaline and terbutaline sensitivity (P
PubMed ID
10372729 View in PubMed
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[Effect of ultra-low dose of ionizing radiation on the surface potential of erythrocytes]

https://arctichealth.org/en/permalink/ahliterature9672
Source
Ukr Biokhim Zh. 2002 Sep-Oct;74(5):117-9
Publication Type
Article
Author
V V Zhirnov
L E Kalashnikova
V N Gavii
Author Affiliation
Institute of Bioorganic Chemistry and Petrochemistry, NAS of Ukraine, Kyiv.
Source
Ukr Biokhim Zh. 2002 Sep-Oct;74(5):117-9
Language
Russian
Publication Type
Article
Keywords
Action Potentials
Adrenergic beta-Agonists - pharmacology
Adrenergic beta-Antagonists - pharmacology
Dose-Response Relationship, Drug
Dose-Response Relationship, Radiation
English Abstract
Epinephrine - pharmacology
Erythrocyte Membrane - physiology - radiation effects
Humans
Isoproterenol - pharmacology
Propranolol - pharmacology
Radiation, Ionizing
Receptors, Adrenergic - physiology
Abstract
Effect of ionizing radiation in ultralow dose (5 microGy) on responses of erythrocyte electrophoretic motility (EPM) as a result of adrenoreceptor ligands binding (0.01-100 microM) has been investigated. The opposite directional EPM responses to agonists (adrenaline, isoprenaline) and antagonist (propranolol) of beta-adrenoreceptors was shown. At that, EPM response to the radiation coincides both with the direction and value of acting the beta-adrenoreceptor agonists depressing EPM. The EPM response to a combined action of beta-adrenoreceptors antagonist, propranolol (10 microM), and ionizing radiation is additive. The above listed is capable to evidence about the essential role of adrenoreceptors at formation of erythrocyte membrane surface charge under action of ionizing radiation in ultralow doses.
PubMed ID
12916167 View in PubMed
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Effects of ageing and adrenergic stimulation on alpha 1- and beta-adrenoceptors and phospholipid fatty acids in rat heart.

https://arctichealth.org/en/permalink/ahliterature11398
Source
Eur J Pharmacol. 1995 May 26;289(3):419-27
Publication Type
Article
Date
May-26-1995
Author
V E Benediktsdóttir
G V Skúladóttir
S. Gudbjarnason
Author Affiliation
Science Institute, University of Iceland, Reykjavík.
Source
Eur J Pharmacol. 1995 May 26;289(3):419-27
Date
May-26-1995
Language
English
Publication Type
Article
Keywords
Adrenergic beta-Agonists - pharmacology
Aging - metabolism
Animals
Catecholamines - metabolism
Dihydroalprenolol - diagnostic use
Epinephrine - pharmacology
Fatty Acids - metabolism
Heart - drug effects
In Vitro
Kinetics
Male
Membranes - drug effects - metabolism
Myocardium - metabolism
Phosphatidylethanolamines - metabolism
Phospholipids - metabolism
Rats
Rats, Wistar
Receptors, Adrenergic, alpha-1 - agonists
Abstract
The purpose of this study was to examine the influence of ageing on the alterations in binding characteristics of adrenoceptors and membrane phospholipid fatty acids in rat heart following repeated administration of epinephrine. The maximal number of binding sites (Bmax) and dissociation constant (Kd) of [3H]prazosin and [3H]dihydroalprenolol binding to alpha 1- and beta-adrenoceptors, respectively, changed significantly during ageing. The downregulation of alpha 1- and beta-adrenoceptors after repeated epinephrine administration for one week, did not differ with age, but the response of the affinity (1/Kd) of both alpha 1- and beta-adrenoceptors to epinephrine treatment was age dependent. In 3-month-old rats the affinity of alpha 1-adrenoceptors was decreased after epinephrine treatment but the affinity of beta-adrenoceptors was unchanged. In 10- and 23-month-old rats the affinity of beta-adrenoceptors decreased after epinephrine treatment but the affinity of alpha 1-adrenoceptors did not change. During ageing the linoleic acid (18:2(n-6)) level decreased in phosphatidylcholine and the arachidonic acid (20:4(n-6)) level increased in phosphatidylcholine and phosphatidylethanolamine. After epinephrine administration the 18:2(n-6) level decreased and the docosahexaenoic acid (22:6(n-3)) level increased in phosphatidylcholine and phosphatidylethanolamine and those changes were not age dependent. The 20:4(n-6) level increased in phosphatidylcholine after epinephrine administration, but that increase was smaller in old than in young rats. The results show that both ageing and epinephrine administration simultaneously modify the fatty acid composition of membrane phospholipids and the binding properties of alpha 1- and beta-adrenoceptors in rat heart.
PubMed ID
7556410 View in PubMed
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30 records – page 1 of 3.