| Records |
| Author |
Touma, C.; Sachser, N.; Mostl, E.; Palme, R. |
Title  |
Effects of sex and time of day on metabolism and excretion of corticosterone in urine and feces of mice |
Type |
Journal Article |
| Year |
2003 |
Publication |
General and Comparative Endocrinology |
Abbreviated Journal |
Gen Comp Endocrinol |
| Volume |
130 |
Issue |
3 |
Pages |
267-278 |
| Keywords |
Animals; Chromatography, High Pressure Liquid; Circadian Rhythm/*physiology; Corticosterone/*metabolism/urine; Feces/*chemistry; Female; Immunoenzyme Techniques; Kinetics; Male; Mice; Mice, Inbred C57BL; Reference Values; Sex Factors; Stress/metabolism; Time Factors; Tritium |
| Abstract |
Non-invasive techniques to monitor stress hormones in small animals like mice offer several advantages and are highly demanded in laboratory as well as in field research. Since knowledge about the species-specific metabolism and excretion of glucocorticoids is essential to develop such a technique, we conducted radiometabolism studies in mice (Mus musculus f. domesticus, strain C57BL/6J). Each mouse was injected intraperitoneally with 740 kBq of 3H-labelled corticosterone and all voided urine and fecal samples were collected for five days. In a first experiment 16 animals (eight of each sex) received the injection at 9 a.m., while eight mice (four of each sex) were injected at 9 p.m. in a second experiment. In both experiments radioactive metabolites were recovered predominantly in the feces, although males excreted significantly higher proportions via the feces (about 73%) than females (about 53%). Peak radioactivity in the urine was detected within about 2h after injection, while in the feces peak concentrations were observed later (depending on the time of injection: about 10h postinjection in experiment 1 and about 4h postinjection in experiment 2, thus proving an effect of the time of day). The number and relative abundance of fecal [3H]corticosterone metabolites was determined by high performance liquid chromatography (HPLC). The HPLC separations revealed that corticosterone was extensively metabolized mainly to more polar substances. Regarding the types of metabolites formed, significant differences were found between males and females, but not between the experiments. Additionally, the immunoreactivity of these metabolites was assessed by screening the HPLC fractions with four enzyme immunoassays (EIA). However, only a newly established EIA for 5alpha-pregnane-3beta,11beta,21-triol-20-one (measuring corticosterone metabolites with a 5alpha-3beta,11beta-diol structure) detected several peaks of radioactive metabolites with high intensity in both sexes, while the other EIAs showed only minor immunoreactivity. Thus, our study for the first time provides substantial information about metabolism and excretion of corticosterone in urine and feces of mice and is the first demonstrating a significant impact of the animals' sex and the time of day. Based on these data it should be possible to monitor adrenocortical activity non-invasively in this species by measuring fecal corticosterone metabolites with the newly developed EIA. Since mice are extensively used in research world-wide, this could open new perspectives in various fields from ecology to behavioral endocrinology. |
| Address |
Department of Behavioral Biology, Institute of Neuro and Behavioral Biology, University of Muenster, Badestrasse 9, D-48149 Muenster, Germany. touma@uni-muenster.de |
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English |
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Abbreviated Series Title |
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Edition |
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| ISSN |
0016-6480 |
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| Notes |
PMID:12606269 |
Approved |
no |
| Call Number |
Equine Behaviour @ team @ |
Serial |
4086 |
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| Author |
Guo, G.L.; Moffit, J.S.; Nicol, C.J.; Ward, J.M.; Aleksunes, L.A.; Slitt, A.L.; Kliewer, S.A.; Manautou, J.E.; Gonzalez, F.J. |
| Title |
Enhanced acetaminophen toxicity by activation of the pregnane X receptor |
Type |
Journal Article |
| Year |
2004 |
Publication |
Toxicological sciences : an official journal of the Society of Toxicology |
Abbreviated Journal |
Toxicol Sci |
| Volume |
82 |
Issue |
2 |
Pages |
374-380 |
| Keywords |
Acetaminophen/pharmacokinetics/*toxicity; Analgesics, Non-Narcotic/pharmacokinetics/*toxicity; Animals; Aryl Hydrocarbon Hydroxylases/biosynthesis; Biotransformation; Blotting, Northern; Chromatography, High Pressure Liquid; Cytochrome P-450 CYP3A; Membrane Proteins; Mice; Mice, Knockout; Oxidoreductases, N-Demethylating/biosynthesis; Pregnenolone Carbonitrile/pharmacology; Receptors, Cytoplasmic and Nuclear/*drug effects; Receptors, Steroid/*drug effects; Sulfhydryl Compounds/metabolism |
| Abstract |
The pregnane X receptor (PXR) is a ligand-activated transcription factor and member of the nuclear receptor superfamily. Activation of PXR represents an important mechanism for the induction of cytochrome P450 3A (CYP3A) enzymes that can convert acetaminophen (APAP) to its toxic intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Therefore, it was hypothesized that activation of PXR plays a major role in APAP-induced hepatotoxicity. Pretreatment with the PXR activator, pregnenolone 16alpha-carbonitrile (PCN), markedly enhanced APAP-induced hepatic injury, as revealed by increased serum ALT levels and hepatic centrilobular necrosis, in wild-type but not in PXR-null mice. Further analysis showed that following PCN treatment, PXR-null mice had lower CYP3A11 expression, decreased NAPQI formation, and increased maintenance of hepatic glutathione content compared to wild-type mice. Thus, these results suggest that PXR plays a critical role in APAP-induced hepatic toxicity, probably by inducing CYP3A11 expression and hence increasing bioactivation. |
| Address |
Laboratory of Metabolism, CCR, NCI, NIH, Bethesda, Maryland 20892, USA |
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English |
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Series Issue |
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Edition |
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| ISSN |
1096-6080 |
ISBN |
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Medium |
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Expedition |
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Conference |
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| Notes |
PMID:15456926 |
Approved |
no |
| Call Number |
refbase @ user @ |
Serial |
71 |
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| Author |
Boray, J.C. |
| Title |
Experimental fascioliasis in Australia |
Type |
Journal Article |
| Year |
1969 |
Publication |
Advances in Parasitology |
Abbreviated Journal |
Adv Parasitol |
| Volume |
7 |
Issue |
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Pages |
95-210 |
| Keywords |
Adaptation, Biological; Adaptation, Physiological; Animal Nutrition Physiology; Animals; Animals, Laboratory; Australia; Cattle; *Cattle Diseases/pathology; Climate; *Disease Vectors; Ecology; Electron Transport; Estivation; Fasciola hepatica/enzymology/*growth & development/metabolism/physiology; Fascioliasis/epidemiology/immunology/*prevention & control/veterinary; Glycolysis; Guinea Pigs; Horses; Humans; Larva/growth & development/physiology; Marsupialia; Metamorphosis, Biological; Mice; New Guinea; New Zealand; Parasite Egg Count; Rats; Seasons; Sheep; *Sheep Diseases/pathology |
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English |
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Series Title |
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Abbreviated Series Title |
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Series Issue |
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Edition |
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| ISSN |
0065-308X |
ISBN |
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Medium |
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Expedition |
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Conference |
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| Notes |
PMID:4935272 |
Approved |
no |
| Call Number |
Equine Behaviour @ team @ |
Serial |
2744 |
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| Author |
Hoogstraal, H.; Mitchell, R.M. |
| Title |
Haemaphysalis (Alloceraea) aponommoides Warburton (Ixodoidea: Ixodidae), description of immature stages, hosts, distribution, and ecology in India, Nepal, Sikkim, and China |
Type |
Journal Article |
| Year |
1971 |
Publication |
The Journal of Parasitology |
Abbreviated Journal |
J Parasitol |
| Volume |
57 |
Issue |
3 |
Pages |
635-645 |
| Keywords |
Altitude; Animals; Artiodactyla; Birds; Buffaloes; Carnivora; Cattle; China; Deer; Dogs; Ecology; Female; Goats; Horses; Humans; India; Insectivora; Larva/anatomy & histology; Male; Mice; Nepal; Rats; Rodentia; Sciuridae; Seasons; Sheep; Tick Infestations/*epidemiology; Ticks/*anatomy & histology/growth & development |
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English |
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Series Issue |
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Edition |
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0022-3395 |
ISBN |
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Conference |
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| Notes |
PMID:5090972 |
Approved |
no |
| Call Number |
Equine Behaviour @ team @ |
Serial |
2730 |
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| Author |
Nelson, W.A.; Keirans, J.E.; Bell, J.F.; Clifford, C.M. |
| Title |
Host-ectoparasite relationships |
Type |
Journal Article |
| Year |
1975 |
Publication |
Journal of Medical Entomology |
Abbreviated Journal |
J Med Entomol |
| Volume |
12 |
Issue |
2 |
Pages |
143-166 |
| Keywords |
Animal Nutrition Physiology; Animals; Anoplura/physiology; *Arthropods; Birds/parasitology; Chickens/parasitology; Dermacentor/parasitology; Diptera; Ecology; Feeding Behavior; Female; Horses/parasitology; Humans; Male; Mallophaga/physiology; Mice/parasitology; Mites/physiology; Reproduction; Sarcoptes scabiei/physiology; Sheep/parasitology; Skin/parasitology; Ticks/physiology; Toxins, Biological/toxicity; Trombiculidae/physiology |
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Thesis |
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Place of Publication |
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Editor |
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English |
Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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Series Issue |
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Edition |
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| ISSN |
0022-2585 |
ISBN |
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Medium |
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Conference |
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| Notes |
PMID:808617 |
Approved |
no |
| Call Number |
Equine Behaviour @ team @ |
Serial |
2704 |
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| Author |
Crosby, M.B.; Zhang, J.; Nowling, T.M.; Svenson, J.L.; Nicol, C.J.; Gonzalez, F.J.; Gilkeson, G.S. |
| Title |
Inflammatory modulation of PPAR gamma expression and activity |
Type |
Journal Article |
| Year |
2006 |
Publication |
Clinical immunology |
Abbreviated Journal |
Clin Immunol |
| Volume |
118 |
Issue |
2-3 |
Pages |
276-283 |
| Keywords |
Age Factors; Animals; Cell Line, Transformed; Cells, Cultured; Female; Inflammation Mediators/*physiology; Kidney/metabolism; Mesangial Cells/metabolism; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Inbred MRL lpr; Mice, Knockout; Nitric Oxide/biosynthesis; Nitric Oxide Synthase Type II/biosynthesis/genetics; PPAR gamma/*biosynthesis/*genetics/metabolism; Up-Regulation/immunology |
| Abstract |
Nitric oxide (NO) production increases with age in the lupus-prone MRL/lpr mouse, paralleling disease activity. One mechanism for excess NO production in MRL/lpr mice may be a defect in down-regulatory mechanisms of the iNOS pathway. A potential modulator of NO is the nuclear hormone receptor peroxisome proliferation activated receptor gamma (PPARgamma). We demonstrate that renal PPARgamma protein expression was altered as disease progressed in MRL/lpr mice, which paralleled increased iNOS protein expression. Additionally, MRL/lpr-derived primary mesangial cells expressed less PPARgamma than BALB/c mesangial cells and produced more NO in response to LPS and IFNgamma. Furthermore, PPARgamma activity was reduced in mesangial cells following exposure to inflammatory mediators. This activity was restored with the addition of a NOS enzyme inhibitor. These results indicate that the activation of inflammatory pathways may lead to reduced activity and expression of PPARgamma, further exacerbating the disease state. |
| Address |
Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA |
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Place of Publication |
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Editor |
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English |
Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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Series Issue |
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Edition |
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| ISSN |
1521-6616 |
ISBN |
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Medium |
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Expedition |
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Conference |
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| Notes |
PMID:16303334 |
Approved |
no |
| Call Number |
refbase @ user @ |
Serial |
67 |
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| Author |
Gavrilova, O.; Haluzik, M.; Matsusue, K.; Cutson, J.J.; Johnson, L.; Dietz, K.R.; Nicol, C.J.; Vinson, C.; Gonzalez, F.J.; Reitman, M.L. |
| Title |
Liver peroxisome proliferator-activated receptor gamma contributes to hepatic steatosis, triglyceride clearance, and regulation of body fat mass |
Type |
Journal Article |
| Year |
2003 |
Publication |
The Journal of biological chemistry |
Abbreviated Journal |
J Biol Chem |
| Volume |
278 |
Issue |
36 |
Pages |
34268-34276 |
| Keywords |
Adipose Tissue/*metabolism; Animals; Blotting, Southern; Blotting, Western; Female; Hypoglycemia/genetics; Insulin Resistance/genetics; Lipid Metabolism; Liver/*metabolism; Liver Diseases/genetics/*metabolism; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; RNA/metabolism; Receptors, Cytoplasmic and Nuclear/*genetics/*physiology; Recombination, Genetic; Thiazoles/pharmacology; *Thiazolidinediones; Time Factors; Transcription Factors/*genetics/*physiology; Triglycerides/*metabolism |
| Abstract |
Peroxisome proliferator-activated receptor gamma (PPAR gamma) is a nuclear receptor that mediates the antidiabetic effects of thiazolidinediones. PPAR gamma is present in adipose tissue and becomes elevated in fatty livers, but the roles of specific tissues in thiazolidinedione actions are unclear. We studied the function of liver PPAR gamma in both lipoatrophic A-ZIP/F-1 (AZIP) and wild type mice. In AZIP mice, ablation of liver PPAR gamma reduced the hepatic steatosis but worsened the hyperlipidemia, triglyceride clearance, and muscle insulin resistance. Inactivation of AZIP liver PPAR gamma also abolished the hypoglycemic and hypolipidemic effects of rosiglitazone, demonstrating that, in the absence of adipose tissue, the liver is a primary and major site of thiazolidinedione action. In contrast, rosiglitazone remained effective in non-lipoatrophic mice lacking liver PPAR gamma, suggesting that adipose tissue is the major site of thiazolidinedione action in typical mice with adipose tissue. Interestingly, mice without liver PPAR gamma, but with adipose tissue, developed relative fat intolerance, increased adiposity, hyperlipidemia, and insulin resistance. Thus, liver PPAR gamma regulates triglyceride homeostasis, contributing to hepatic steatosis, but protecting other tissues from triglyceride accumulation and insulin resistance. |
| Address |
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. oksanag@bdg10.niddk.nih.gov |
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Place of Publication |
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Editor |
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English |
Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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Edition |
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0021-9258 |
ISBN |
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Medium |
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Expedition |
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Conference |
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| Notes |
PMID:12805374 |
Approved |
no |
| Call Number |
refbase @ user @ |
Serial |
81 |
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| Author |
Etienne, A.S.; Maurer, R.; Seguinot, V. |
| Title |
Path integration in mammals and its interaction with visual landmarks |
Type |
Journal Article |
| Year |
1996 |
Publication |
The Journal of Experimental Biology |
Abbreviated Journal |
J Exp Biol |
| Volume |
199 |
Issue |
Pt 1 |
Pages |
201-209 |
| Keywords |
Animals; Cognition/physiology; Cricetinae; Gerbillinae; Humans; Locomotion/*physiology; Mammals/*physiology; Mesocricetus; Mice; Proprioception/physiology; Rats; Visual Pathways/*physiology; Visual Perception/*physiology |
| Abstract |
During locomotion, mammals update their position with respect to a fixed point of reference, such as their point of departure, by processing inertial cues, proprioceptive feedback and stored motor commands generated during locomotion. This so-called path integration system (dead reckoning) allows the animal to return to its home, or to a familiar feeding place, even when external cues are absent or novel. However, without the use of external cues, the path integration process leads to rapid accumulation of errors involving both the direction and distance of the goal. Therefore, even nocturnal species such as hamsters and mice rely more on previously learned visual references than on the path integration system when the two types of information are in conflict. Recent studies investigate the extent to which path integration and familiar visual cues cooperate to optimize the navigational performance. |
| Address |
Laboratoire d'Ethologie, FPSE, Universite de Geneve, Carouge, Switzerland |
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Thesis |
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Place of Publication |
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Editor |
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English |
Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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Series Issue |
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Edition |
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| ISSN |
0022-0949 |
ISBN |
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Medium |
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Expedition |
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Conference |
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| Notes |
PMID:8576691 |
Approved |
no |
| Call Number |
Equine Behaviour @ team @ |
Serial |
2758 |
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| Author |
Crosby, M.B.; Svenson, J.L.; Zhang, J.; Nicol, C.J.; Gonzalez, F.J.; Gilkeson, G.S. |
| Title |
Peroxisome proliferation-activated receptor (PPAR)gamma is not necessary for synthetic PPARgamma agonist inhibition of inducible nitric-oxide synthase and nitric oxide |
Type |
Journal Article |
| Year |
2005 |
Publication |
The Journal of pharmacology and experimental therapeutics |
Abbreviated Journal |
J Pharmacol Exp Ther |
| Volume |
312 |
Issue |
1 |
Pages |
69-76 |
| Keywords |
Animals; Cell Line; Gene Expression/drug effects; Macrophages/drug effects/metabolism; Mice; Mice, Inbred C57BL; Nitric Oxide/*metabolism; Nitric Oxide Synthase/*metabolism; Nitric Oxide Synthase Type II; PPAR delta/metabolism; PPAR gamma/*agonists/deficiency; Thiazolidinediones/pharmacology |
| Abstract |
Peroxisome proliferation-activated receptor (PPAR)gamma agonists inhibit inducible nitric-oxide synthase (iNOS), tumor necrosis factor-alpha, and interleukin-6. Because of these effects, synthetic PPARgamma agonists, including thiazolidinediones, are being studied for their impact on inflammatory disease. The anti-inflammatory concentrations of synthetic PPARgamma agonists range from 10 to 50 microM, whereas their binding affinity for PPARgamma is in the nanomolar range. The specificity of synthetic PPARgamma agonists for PPARgamma at the concentrations necessary for anti-inflammatory effects is thus in question. We report that PPARgamma is not necessary for the inhibition of iNOS by synthetic PPARgamma agonists. RAW 264.7 macrophages possess little PPARgamma, yet lipopolysaccharide (LPS)/interferon (IFN)gamma-induced iNOS was inhibited by synthetic PPARgamma agonists at 20 microM. Endogenous PPARgamma was inhibited by the transfection of a dominant-negative PPARgamma construct into murine mesangial cells. In the transfected cells, synthetic PPARgamma agonists inhibited iNOS production at 10 microM, similar to nontransfected cells. Using cells from PPARgamma Cre/lox conditional knockout mice, baseline and LPS/IFNgamma-induced nitric oxide levels were higher in macrophages lacking PPARgamma versus controls. However, synthetic PPARgamma agonists inhibited iNOS at 10 microM in the PPARgamma-deficient cells, similar to macrophages from wild-type mice. These results indicate that PPARgamma is not necessary for inhibition of iNOS expression by synthetic PPARgamma agonists at concentrations over 10 microM. Intrinsic PPARgamma function, in the absence of synthetic agonists, however, may play a role in inflammatory modulation. |
| Address |
Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA |
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Place of Publication |
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English |
Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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Series Issue |
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Edition |
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0022-3565 |
ISBN |
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Expedition |
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Conference |
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| Notes |
PMID:15356214 |
Approved |
no |
| Call Number |
refbase @ user @ |
Serial |
73 |
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| Author |
Harman, F.S.; Nicol, C.J.; Marin, H.E.; Ward, J.M.; Gonzalez, F.J.; Peters, J.M. |
| Title |
Peroxisome proliferator-activated receptor-delta attenuates colon carcinogenesis |
Type |
Journal Article |
| Year |
2004 |
Publication |
Nature medicine |
Abbreviated Journal |
Nat Med |
| Volume |
10 |
Issue |
5 |
Pages |
481-483 |
| Keywords |
Animals; Azoxymethane/toxicity; Colonic Neoplasms/etiology/genetics/*prevention & control; Colonic Polyps/etiology/genetics/pathology/prevention & control; Disease Models, Animal; Mice; Mice, Knockout; Mice, Mutant Strains; Phenotype; Receptors, Cytoplasmic and Nuclear/deficiency/genetics/*physiology; Transcription Factors/deficiency/genetics/*physiology |
| Abstract |
Peroxisome proliferator-activated receptor-delta (PPAR-delta; also known as PPAR-beta) is expressed at high levels in colon tumors, but its contribution to colon cancer is unclear. We examined the role of PPAR-delta in colon carcinogenesis using PPAR-delta-deficient (Ppard(-/-)) mice. In both the Min mutant and chemically induced mouse models, colon polyp formation was significantly greater in mice nullizygous for PPAR-delta. In contrast to previous reports suggesting that activation of PPAR-delta potentiates colon polyp formation, here we show that PPAR-delta attenuates colon carcinogenesis. |
| Address |
Department of Veterinary Science and The Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. jmp21@psu.edu |
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English |
Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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Series Issue |
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Edition |
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| ISSN |
1078-8956 |
ISBN |
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Medium |
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Expedition |
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Conference |
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| Notes |
PMID:15048110 |
Approved |
no |
| Call Number |
refbase @ user @ |
Serial |
77 |
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