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Article ; Online: Quercetin's Effects on Glutamate Cytotoxicity.

Riche, Kade / Lenard, Natalie R

2022 Volume 27, Issue 21

Abstract: The potentially therapeutic effects of the naturally abundant plant flavonoid quercetin have been extensively studied. An extensive body of literature suggests that quercetin's powerful antioxidant effects may relate to its ability to treat disease. ... ...

Abstract	The potentially therapeutic effects of the naturally abundant plant flavonoid quercetin have been extensively studied. An extensive body of literature suggests that quercetin's powerful antioxidant effects may relate to its ability to treat disease. Glutamate excitotoxicity occurs when a neuron is overstimulated by the neurotransmitter glutamate and causes dysregulation of intracellular calcium concentrations. Quercetin has been shown to be preventative against many forms of neuronal cell death resulting from glutamate excitotoxicity, such as oncosis, intrinsic apoptosis, mitochondrial permeability transition, ferroptosis, phagoptosis, lysosomal cell death, parthanatos, and death by reactive oxygen species (ROS)/reactive nitrogen species (RNS) generation. The clinical importance for the attenuation of glutamate excitotoxicity arises from the need to deter the continuous formation of tissue infarction caused by various neurological diseases, such as ischemic stroke, seizures, neurodegenerative diseases, and trauma. This review aims to summarize what is known concerning glutamate physiology and glutamate excitotoxic pathophysiology and provide further insight into quercetin's potential to hinder neuronal death caused by cell death pathways activated by glutamate excitotoxicity. Quercetin's bioavailability may limit its use clinically, however. Thus, future research into ways to increase its bioavailability are warranted.
MeSH term(s)	Humans ; Glutamic Acid/metabolism ; Quercetin/pharmacology ; Antioxidants/pharmacology ; Reactive Oxygen Species/metabolism ; Neurodegenerative Diseases
Chemical Substances	Glutamic Acid (3KX376GY7L) ; Quercetin (9IKM0I5T1E) ; Antioxidants ; Reactive Oxygen Species
Language	English
Publishing date	2022-11-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules27217620
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Article ; Online: Quercetin’s Effects on Glutamate Cytotoxicity

Kade Riche / Natalie R. Lenard

Molecules, Vol 27, Iss 7620, p

2022 Volume 7620

Abstract: The potentially therapeutic effects of the naturally abundant plant flavonoid quercetin have been extensively studied. An extensive body of literature suggests that quercetin’s powerful antioxidant effects may relate to its ability to treat disease. ... ...

Abstract	The potentially therapeutic effects of the naturally abundant plant flavonoid quercetin have been extensively studied. An extensive body of literature suggests that quercetin’s powerful antioxidant effects may relate to its ability to treat disease. Glutamate excitotoxicity occurs when a neuron is overstimulated by the neurotransmitter glutamate and causes dysregulation of intracellular calcium concentrations. Quercetin has been shown to be preventative against many forms of neuronal cell death resulting from glutamate excitotoxicity, such as oncosis, intrinsic apoptosis, mitochondrial permeability transition, ferroptosis, phagoptosis, lysosomal cell death, parthanatos, and death by reactive oxygen species (ROS)/reactive nitrogen species (RNS) generation. The clinical importance for the attenuation of glutamate excitotoxicity arises from the need to deter the continuous formation of tissue infarction caused by various neurological diseases, such as ischemic stroke, seizures, neurodegenerative diseases, and trauma. This review aims to summarize what is known concerning glutamate physiology and glutamate excitotoxic pathophysiology and provide further insight into quercetin’s potential to hinder neuronal death caused by cell death pathways activated by glutamate excitotoxicity. Quercetin’s bioavailability may limit its use clinically, however. Thus, future research into ways to increase its bioavailability are warranted.
Keywords	glutamate ; excitotoxicity ; reactive oxygen species ; reactive nitrogen species ; Organic chemistry ; QD241-441
Subject code	610
Language	English
Publishing date	2022-11-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Dietary Quercetin Attenuates Adipose Tissue Expansion and Inflammation and Alters Adipocyte Morphology in a Tissue-Specific Manner.

Forney, Laura A / Lenard, Natalie R / Stewart, Laura K / Henagan, Tara M

International journal of molecular sciences

2018 Volume 19, Issue 3

Abstract: Chronic inflammation in adipose tissue may contribute to depot-specific adipose tissue expansion, leading to obesity and insulin resistance. Dietary supplementation with quercetin or botanical extracts containing quercetin attenuates high fat diet (HFD)- ... ...

Abstract	Chronic inflammation in adipose tissue may contribute to depot-specific adipose tissue expansion, leading to obesity and insulin resistance. Dietary supplementation with quercetin or botanical extracts containing quercetin attenuates high fat diet (HFD)-induced obesity and insulin resistance and decreases inflammation. Here, we determined the effects of quercetin and red onion extract (ROE) containing quercetin on subcutaneous (inguinal, IWAT) vs. visceral (epididymal, EWAT) white adipose tissue morphology and inflammation in mice fed low fat, high fat, high fat plus 50 μg/day quercetin or high fat plus ROE containing 50 μg/day quercetin equivalents for 9 weeks. Quercetin and ROE similarly ameliorated HFD-induced increases in adipocyte size and decreases in adipocyte number in IWAT and EWAT. Furthermore, quercetin and ROE induced alterations in adipocyte morphology in IWAT. Quercetin and ROE similarly decreased HFD-induced IWAT inflammation. However, quercetin and red onion differentially affected HFD-induced EWAT inflammation, with quercetin decreasing and REO increasing inflammatory marker gene expression. Quercetin and REO also differentially regulated circulating adipokine levels. These results show that quercetin or botanical extracts containing quercetin induce white adipose tissue remodeling which may occur through inflammatory-related mechanisms.
MeSH term(s)	Adipocytes/drug effects ; Adipocytes/pathology ; Adipokines/blood ; Animals ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Diet, High-Fat/adverse effects ; Dietary Supplements ; Inflammation/drug therapy ; Inflammation/pathology ; Insulin Resistance ; Intra-Abdominal Fat/drug effects ; Intra-Abdominal Fat/pathology ; Mice ; Mice, Inbred C57BL ; Obesity/drug therapy ; Obesity/pathology ; Onions/chemistry ; Plant Extracts/pharmacology ; Plant Extracts/therapeutic use ; Quercetin/pharmacology ; Quercetin/therapeutic use ; Subcutaneous Fat/drug effects ; Subcutaneous Fat/pathology
Chemical Substances	Adipokines ; Antioxidants ; Plant Extracts ; Quercetin (9IKM0I5T1E)
Language	English
Publishing date	2018-03-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms19030895
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Article ; Online: Dietary Quercetin Attenuates Adipose Tissue Expansion and Inflammation and Alters Adipocyte Morphology in a Tissue-Specific Manner

Laura A. Forney / Natalie R. Lenard / Laura K. Stewart / Tara M. Henagan

International Journal of Molecular Sciences, Vol 19, Iss 3, p

2018 Volume 895

Abstract	Chronic inflammation in adipose tissue may contribute to depot-specific adipose tissue expansion, leading to obesity and insulin resistance. Dietary supplementation with quercetin or botanical extracts containing quercetin attenuates high fat diet (HFD)-induced obesity and insulin resistance and decreases inflammation. Here, we determined the effects of quercetin and red onion extract (ROE) containing quercetin on subcutaneous (inguinal, IWAT) vs. visceral (epididymal, EWAT) white adipose tissue morphology and inflammation in mice fed low fat, high fat, high fat plus 50 μg/day quercetin or high fat plus ROE containing 50 μg/day quercetin equivalents for 9 weeks. Quercetin and ROE similarly ameliorated HFD-induced increases in adipocyte size and decreases in adipocyte number in IWAT and EWAT. Furthermore, quercetin and ROE induced alterations in adipocyte morphology in IWAT. Quercetin and ROE similarly decreased HFD-induced IWAT inflammation. However, quercetin and red onion differentially affected HFD-induced EWAT inflammation, with quercetin decreasing and REO increasing inflammatory marker gene expression. Quercetin and REO also differentially regulated circulating adipokine levels. These results show that quercetin or botanical extracts containing quercetin induce white adipose tissue remodeling which may occur through inflammatory-related mechanisms.
Keywords	quercetin ; inflammation ; browning ; mulilocular adipocyte ; red onion extract ; botanical extract ; adipose tissue ; adipocyte ; adipokine ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2018-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article: Central and peripheral regulation of food intake and physical activity: pathways and genes.

Lenard, Natalie R / Berthoud, Hans-Rudolf

Obesity (Silver Spring, Md.)

2009 Volume 16 Suppl 3, Page(s) S11–22

Abstract: A changing environment and lifestyle on the background of evolutionary engraved and perinatally imprinted physiological response patterns is the foremost explanation for the current obesity epidemic. However, it is not clear what the mechanisms are by ... ...

Abstract	A changing environment and lifestyle on the background of evolutionary engraved and perinatally imprinted physiological response patterns is the foremost explanation for the current obesity epidemic. However, it is not clear what the mechanisms are by which the modern environment overrides the physiological controls of appetite and homeostatic body-weight regulation. Food intake and energy expenditure are controlled by complex, redundant, and distributed neural systems involving thousands of genes and reflecting the fundamental biological importance of adequate nutrient supply and energy balance. There has been much progress in identifying the important role of hypothalamus and caudal brainstem in the various hormonal and neural mechanisms by which the brain informs itself about availability of ingested and stored nutrients and, in turn, generates behavioral, autonomic, and endocrine output. Some of the genes involved in this "homeostatic" regulator are crucial for energy balance as manifested in the well-known monogenic obesity models. However, it can be clearly demonstrated that much larger portions of the nervous system of animals and humans, including the cortex, basal ganglia, and the limbic system, are concerned with the procurement of food as a basic and evolutionarily conserved survival mechanism to defend the lower limits of adiposity. By forming representations and reward expectancies through processes of learning and memory, these systems evolved to engage powerful emotions for guaranteed supply with, and ingestion of, beneficial foods from a sparse and often hostile environment. They are now simply overwhelmed with an abundance of food and food cues no longer contested by predators and interrupted by famines. The anatomy, chemistry, and functions of these elaborate neural systems and their interactions with the "homeostatic" regulator in the hypothalamus are poorly understood, and many of the genes involved are either unknown or not well characterized. This is regrettable because these systems are directly and primarily involved in the interactions of the modern environment and lifestyle with the human body. They are no less "physiological" than metabolic-regulatory mechanisms that have attracted most of the research during the past 15 years.
MeSH term(s)	Animals ; Appetite Regulation/genetics ; Appetite Regulation/physiology ; Energy Intake/genetics ; Energy Intake/physiology ; Energy Metabolism/genetics ; Energy Metabolism/physiology ; Humans ; Neural Pathways/metabolism ; Obesity/genetics ; Obesity/metabolism
Language	English
Publishing date	2009-02-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2230457-5
ISSN	1930-739X ; 1930-7381 ; 1071-7323
ISSN (online)	1930-739X
ISSN	1930-7381 ; 1071-7323
DOI	10.1038/oby.2008.511
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Zs.A 4061: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Dietary quercetin supplementation in mice increases skeletal muscle PGC1α expression, improves mitochondrial function and attenuates insulin resistance in a time-specific manner.

Henagan, Tara M / Lenard, Natalie R / Gettys, Thomas W / Stewart, Laura K

PloS one

2014 Volume 9, Issue 2, Page(s) e89365

Abstract: Aims/hypothesis: High fat diet (HFD)-induced insulin resistance (IR) is partially characterized by reduced skeletal muscle mitochondrial function and peroxisome proliferator activated receptor gamma coactivator 1 alpha (PGC1α) expression. Our previous ... ...

Abstract	Aims/hypothesis: High fat diet (HFD)-induced insulin resistance (IR) is partially characterized by reduced skeletal muscle mitochondrial function and peroxisome proliferator activated receptor gamma coactivator 1 alpha (PGC1α) expression. Our previous study showed that a high dose of the bioflavonoid quercetin exacerbated HFD-induced IR; yet, others have demonstrated that quercetin improves insulin sensitivity. The aim of this study was to investigate whether differing doses of quercetin act in a time-dependent manner to attenuate HFD-induced IR in association with improved skeletal muscle mitochondrial function and PGC1α expression. Methods: C57BL/6J mice were fed HFD for 3 or 8 wks, with or without a low (50 ug/day; HF+50Q) or high (600 ug/day, HF+600Q) dose of quercetin. Whole body and metabolic phenotypes and insulin sensitivity were assessed. Skeletal muscle metabolomic analysis of acylcarnitines and PGC1α mRNA expression via qRT-PCR were measured. Results: Quercetin at 50 ug/day for 8 wk attenuated HFD-induced increases in fat mass, body weight and IR and increased PGC1α expression, whereas 600 ug/day of quercetin exacerbated fat mass accumulation without altering body weight, IR or PGC1α. PGC1α expression correlated with acylcarnitine levels similarly in HF and HF+600Q; these correlations were not present in HF+50Q. At both time points, energy expenditure increased in HF+50Q and decreased in HF+600Q, independent of PGC1α and IR. Conclusions/interpretation: Chronic dietary quercetin supplementation at low but not higher dose ameliorates the development of diet-induced IR while increasing PGC1α expression in muscle, suggesting that skeletal muscle may be an important target for the insulin-sensitizing effects of a low dose of quercetin.
MeSH term(s)	Animals ; Diet, High-Fat ; Dietary Supplements ; Insulin/metabolism ; Insulin Resistance/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria, Muscle/drug effects ; Mitochondria, Muscle/metabolism ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Quercetin/administration & dosage ; Time Factors ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Insulin ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Ppargc1a protein, mouse ; Transcription Factors ; Quercetin (9IKM0I5T1E)
Language	English
Publishing date	2014-02-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0089365
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Article ; Online: Food reward, hyperphagia, and obesity.

Berthoud, Hans-Rudolf / Lenard, Natalie R / Shin, Andrew C

American journal of physiology. Regulatory, integrative and comparative physiology

2011 Volume 300, Issue 6, Page(s) R1266–77

Abstract: Given the unabated obesity problem, there is increasing appreciation of expressions like "my eyes are bigger than my stomach," and recent studies in rodents and humans suggest that dysregulated brain reward pathways may be contributing not only to drug ... ...

Abstract	Given the unabated obesity problem, there is increasing appreciation of expressions like "my eyes are bigger than my stomach," and recent studies in rodents and humans suggest that dysregulated brain reward pathways may be contributing not only to drug addiction but also to increased intake of palatable foods and ultimately obesity. After describing recent progress in revealing the neural pathways and mechanisms underlying food reward and the attribution of incentive salience by internal state signals, we analyze the potentially circular relationship between palatable food intake, hyperphagia, and obesity. Are there preexisting individual differences in reward functions at an early age, and could they be responsible for development of obesity later in life? Does repeated exposure to palatable foods set off a cascade of sensitization as in drug and alcohol addiction? Are reward functions altered by secondary effects of the obese state, such as increased signaling through inflammatory, oxidative, and mitochondrial stress pathways? Answering these questions will significantly impact prevention and treatment of obesity and its ensuing comorbidities as well as eating disorders and drug and alcohol addiction.
MeSH term(s)	Animals ; Behavior, Addictive/physiopathology ; Behavior, Addictive/psychology ; Humans ; Hyperphagia/physiopathology ; Hyperphagia/psychology ; Models, Animal ; Neural Pathways/physiopathology ; Obesity/physiopathology ; Obesity/psychology ; Reward ; Signal Transduction/physiology
Language	English
Publishing date	2011-03-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00028.2011
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Article: Mechanisms and significance of the increased brain uptake of tryptophan.

Lenard, Natalie R / Dunn, Adrian J

Neurochemical research

2005 Volume 30, Issue 12, Page(s) 1543–1548

Abstract: Changes in brain tryptophan concentrations may affect the synthesis of brain serotonin (5-hydroxytryptamine, 5-HT). Concentrations of tryptophan are regulated more than those of any other amino acid. Such stimuli as acute stress, carbohydrate ingestion, ... ...

Abstract	Changes in brain tryptophan concentrations may affect the synthesis of brain serotonin (5-hydroxytryptamine, 5-HT). Concentrations of tryptophan are regulated more than those of any other amino acid. Such stimuli as acute stress, carbohydrate ingestion, and treatment with various drugs increase the brain content of tryptophan. Treatment of rats and mice with interleukin-1 (IL-1), interleukin-6 (IL-6), lipopolysaccharide (LPS), and beta-adrenoceptor agonists, as well as a variety of stressors, such as footshock and restraint, all increase brain concentrations of tryptophan. The peak effect following both acute stress and beta-adrenoceptor agonist administration occurs within 30-60 min, whereas the peak effect following LPS and the cytokines occurs much later at around 4-8 h. Experiments using the ganglionic blocker chlorisondamine, and beta-adrenoceptor antagonists suggest that the sympathetic nervous system plays an important role in the modulation of brain tryptophan concentrations. The mechanisms involved in the increases observed in brain tryptophan are discussed, as well as their possible biological significance.
MeSH term(s)	Animals ; Brain/metabolism ; Receptors, Adrenergic, beta/metabolism ; Stress, Physiological/metabolism ; Tryptophan/metabolism
Chemical Substances	Receptors, Adrenergic, beta ; Tryptophan (8DUH1N11BX)
Language	English
Publishing date	2005-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	199335-5
ISSN	1573-6903 ; 0364-3190
ISSN (online)	1573-6903
ISSN	0364-3190
DOI	10.1007/s11064-005-8832-x
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Zs.A 1368: Show issues

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Article: Development of antinociceptive tolerance and physical dependence following morphine i.c.v. infusion in mice.

Lenard, Natalie R / Roerig, Sandra C

European journal of pharmacology

2005 Volume 527, Issue 1-3, Page(s) 71–76

Abstract: The chronic i.c.v. infusion of morphine has been reported for rats but not for mice. In the current report, the antinociceptive tolerance to both i.c.v. morphine infusion and s.c. implantation of morphine pellets in mice was compared. Physical dependence ...

Abstract	The chronic i.c.v. infusion of morphine has been reported for rats but not for mice. In the current report, the antinociceptive tolerance to both i.c.v. morphine infusion and s.c. implantation of morphine pellets in mice was compared. Physical dependence after i.c.v. morphine infusion was also evaluated. Osmotic minipumps were filled with morphine (50 mM), connected to i.c.v. cannulae, and implanted s.c. to deliver 50 nmol/h for 3 days (i.e., 3.6 micromol total). Robust jumping precipitated by naloxone (1 mg/kg, s.c.) indicated the development of physical dependence. Tolerance to i.c.v., i.t., and i.v. morphine (6.3-, 2.0-, and 4.4-fold, respectively) was observed using the tail flick test. Mice implanted with pellets containing 75 mg morphine for 3 days (i.e., approximately 260 micromol total) were also tolerant to morphine (6.5-, 7.5- and 18-fold, respectively). Thus, the tolerance developed using the two methods was not identical. These results allow comparison of morphine tested by 3 different routes (i.c.v., i.t., and i.v.) after chronic morphine treatment by two routes (i.c.v. and s.c.) in a single study.
MeSH term(s)	Adaptation, Physiological/drug effects ; Adaptation, Physiological/physiology ; Animals ; Dose-Response Relationship, Drug ; Drug Administration Schedule ; Drug Implants ; Infusion Pumps ; Injections, Intraventricular ; Male ; Mice ; Mice, Inbred ICR ; Morphine/administration & dosage ; Morphine/pharmacokinetics ; Morphine Dependence/physiopathology ; Naloxone/administration & dosage ; Naloxone/pharmacokinetics ; Pain Measurement/methods ; Pain Threshold/drug effects ; Stereotyped Behavior/drug effects ; Stereotyped Behavior/physiology ; Time Factors
Chemical Substances	Drug Implants ; Naloxone (36B82AMQ7N) ; Morphine (76I7G6D29C)
Language	English
Publishing date	2005-12-19
Publishing country	Netherlands
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2005.10.031
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Article: Potential role for nonesterified fatty acids in beta-adrenoceptor-induced increases in brain tryptophan.

Lenard, Natalie R / Dunn, Adrian J

Neurochemistry international

2005 Volume 46, Issue 2, Page(s) 179–187

Abstract: We tested the hypothesis that beta2- and beta3-adrenergic receptor-mediated increases in brain tryptophan are due to the liberation of fatty acids, which in turn displace tryptophan from its albumin-binding site and thus facilitate its entry into the ... ...

Abstract	We tested the hypothesis that beta2- and beta3-adrenergic receptor-mediated increases in brain tryptophan are due to the liberation of fatty acids, which in turn displace tryptophan from its albumin-binding site and thus facilitate its entry into the brain. Male CD-1 mice were injected with subtype-selective beta-adrenergic agonists 1h before brain samples were collected for analysis of tryptophan content by HPLC with electrochemical detection, and blood samples were collected for analysis of total and free tryptophan and nonesterified fatty acid (NEFA) concentrations. The beta2-selective agonist, clenbuterol (0.1 mg/kg), increased concentrations of tryptophan in all brain regions studied and decreased plasma total tryptophan, but had no effect on plasma free tryptophan or NEFAs. The beta3-selective agonists, BRL 37344 (0.2 mg/kg) or CL 316243 (0.01 mg/kg), increased brain tryptophan, plasma NEFAs and free tryptophan. Pretreatment with nicotinic acid (500 mg/kg), an inhibitor of lipolysis, almost completely prevented the increase in plasma free tryptophan and NEFAs, and attenuated the increase in brain tryptophan induced by CL 316243. These results suggest that beta2- and beta3-adrenergic agonists increase brain tryptophan by a mechanism other than the liberation of NEFAs. Nonetheless, beta3-adrenergic agonists appear to increase brain tryptophan by a mechanism that may depend partially on elevations of plasma NEFAs.
MeSH term(s)	Adrenergic beta-2 Receptor Agonists ; Adrenergic beta-Agonists/pharmacology ; Animals ; Binding, Competitive/drug effects ; Brain Chemistry/drug effects ; Brain Chemistry/physiology ; Clenbuterol/pharmacology ; Dioxoles/pharmacology ; Ethanolamines/pharmacology ; Fatty Acids, Nonesterified/metabolism ; Hypolipidemic Agents/pharmacology ; Male ; Mice ; Niacin/pharmacology ; Oleic Acid/pharmacology ; Receptors, Adrenergic, beta/physiology ; Serum Albumin/drug effects ; Serum Albumin/metabolism ; Tryptophan/blood ; Tryptophan/metabolism
Chemical Substances	Adrenergic beta-2 Receptor Agonists ; Adrenergic beta-Agonists ; Dioxoles ; Ethanolamines ; Fatty Acids, Nonesterified ; Hypolipidemic Agents ; Receptors, Adrenergic, beta ; Serum Albumin ; disodium (R,R)-5-(2-((2-(3-chlorophenyl)-2-hydroxyethyl)-amino)propyl)-1,3-benzodioxole-2,3-dicarboxylate (138908-40-4) ; Niacin (2679MF687A) ; Oleic Acid (2UMI9U37CP) ; BRL 37344 (5DZZ1926YW) ; Tryptophan (8DUH1N11BX) ; Clenbuterol (XTZ6AXU7KN)
Language	English
Publishing date	2005-01
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	283190-9
ISSN	1872-9754 ; 0197-0186
ISSN (online)	1872-9754
ISSN	0197-0186
DOI	10.1016/j.neuint.2004.07.010
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