Records |
Author |
Jeong, S.; Han, M.; Lee, H.; Kim, M.; Kim, J.; Nicol, C.J.; Kim, B.H.; Choi, J.H.; Nam, K.-H.; Oh, G.T.; Yoon, M. |
Title |
Effects of fenofibrate on high-fat diet-induced body weight gain and adiposity in female C57BL/6J mice |
Type |
Journal Article |
Year |
2004 |
Publication |
Metabolism: clinical and experimental |
Abbreviated Journal |
Metabolism |
Volume |
53 |
Issue |
10 |
Pages |
1284-1289 |
Keywords |
Adipose Tissue/*anatomy & histology/drug effects; Animals; Antilipemic Agents/*pharmacology; Body Composition/*drug effects; Body Weight/drug effects; Dietary Fats/*pharmacology; Eating/drug effects; Fatty Acids/metabolism; Female; Gene Expression Regulation/drug effects; Leptin/metabolism; Liver/metabolism; Mice; Mice, Inbred C57BL; Ovariectomy; Procetofen/*pharmacology; RNA, Messenger/biosynthesis/genetics; Receptors, Cytoplasmic and Nuclear/biosynthesis/genetics/metabolism; Transcription Factors/biosynthesis/genetics/metabolism; Weight Gain/*drug effects |
Abstract |
Our previous study suggested that fenofibrate affects obesity and lipid metabolism in a sexually dimorphic manner in part through the differential activation of hepatic peroxisome proliferator-activated receptor alpha (PPARalpha) in male and female C57BL/6J mice. To determine whether fenofibrate reduces body weight gain and adiposity in female sham-operated (Sham) and ovariectomized (OVX) C57BL/6J mice, the effects of fenofibrate on not only body weight, white adipose tissue (WAT) mass, and food intake, but also the expression of both leptin and PPARalpha target genes were measured. Compared to their respective low-fat diet-fed controls, both Sham and OVX mice exhibited increases in body weight and WAT mass when fed a high-fat diet. Fenofibrate treatment decreased body weight gain and WAT mass in OVX, but not in Sham mice. Furthermore, fenofibrate increased the mRNA levels of PPARalpha target genes encoding peroxisomal enzymes involved in fatty acid beta-oxidation, and reduced apolipoprotein C-III (apo C-III) mRNA, all of which were expressed at higher levels in OVX compared to Sham mice. However, leptin mRNA levels were found to positively correlate with WAT mass, and food intake was not changed in either OVX or Sham mice following fenofibrate treatment. These results suggest that fenofibrate differentially regulates body weight and adiposity due in part to differences in PPARalpha activation, but not to differences in leptin production, between female OVX and Sham mice. |
Address |
Department of Life Sciences, Mokwon University, Taejon, Korea |
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English |
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ISSN |
0026-0495 |
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PMID:15375783 |
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no |
Call Number |
refbase @ user @ |
Serial |
72 |
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Author |
Jordan, J. |
Title |
[Modern views on the structure and function of the vomeronasal (Jacobson's) organ in mammals] |
Type |
Journal Article |
Year |
1970 |
Publication |
Otolaryngologia Polska. The Polish Otolaryngology |
Abbreviated Journal |
Otolaryngol Pol |
Volume |
24 |
Issue |
4 |
Pages |
457-462 |
Keywords |
Animals; Cats; Dogs; Guinea Pigs; Horses; Humans; Mice; Nasal Septum/anatomy & histology/blood supply/cytology/innervation/physiology; Nose/*anatomy & histology/blood supply/innervation/*physiology; Rabbits; Rats; Sheep; Smell |
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Language |
Polish |
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Original Title |
Obecne poglady na budowe i czynnosc narzadu lemieszowo-nosowego (Jacobsona) u ssakow |
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ISSN |
0030-6657 |
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Notes |
PMID:4918960 |
Approved |
no |
Call Number |
Equine Behaviour @ team @ |
Serial |
4315 |
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Author |
Rumiantsev, S.N. |
Title |
[Biological function of Clostridium tetani toxin (ecological and evolutionary aspects)] |
Type |
Journal Article |
Year |
1973 |
Publication |
Zhurnal Evoliutsionnoi Biokhimii i Fiziologii |
Abbreviated Journal |
Zh Evol Biokhim Fiziol |
Volume |
9 |
Issue |
5 |
Pages |
474-480 |
Keywords |
Animals; Cats; Chickens; Dogs; Ecology; Evolution; Goats; Guinea Pigs; Haplorhini; Horses; Insectivora; Mice; Perissodactyla; Rabbits; Rats; Sheep; *Tetanus Toxin |
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Language |
Russian |
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Original Title |
K voprosu biologicheskoi funktsii toksina Clostridium tetani (ekologicheskie i evolutsionnye aspekty |
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Series Volume |
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Edition |
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ISSN |
0044-4529 |
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Conference |
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Notes |
PMID:4203684 |
Approved |
no |
Call Number |
Equine Behaviour @ team @ |
Serial |
2713 |
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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 |
|
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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Language |
English |
Summary Language |
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Series Editor |
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Series Title |
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Abbreviated Series Title |
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Series Volume |
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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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Area |
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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 |
Nicol, C.J.; Yoon, M.; Ward, J.M.; Yamashita, M.; Fukamachi, K.; Peters, J.M.; Gonzalez, F.J. |
Title |
PPARgamma influences susceptibility to DMBA-induced mammary, ovarian and skin carcinogenesis |
Type |
Journal Article |
Year |
2004 |
Publication |
Carcinogenesis |
Abbreviated Journal |
Carcinogenesis |
Volume |
25 |
Issue |
9 |
Pages |
1747-1755 |
Keywords |
9,10-Dimethyl-1,2-benzanthracene/*toxicity; Animals; DNA Primers/chemistry; Disease Susceptibility; Female; Heterozygote; Humans; Mammary Neoplasms, Experimental/chemically induced/*pathology; Mice; Ovarian Neoplasms/chemically induced/*pathology; RNA, Messenger/genetics/metabolism; Receptors, Cytoplasmic and Nuclear/genetics/*physiology; Reverse Transcriptase Polymerase Chain Reaction; Skin Neoplasms/chemically induced/*pathology; Survival Rate; Transcription Factors/genetics/*physiology; Zinc Fingers |
Abstract |
Peroxisome proliferator-activated receptor gamma (PPARgamma), a member of the nuclear receptor superfamily, plays a role in adipocyte differentiation, type II diabetes, macrophage response to inflammation and is suggested to influence carcinogen-induced colon cancer. Studies done in vitro and in vivo also revealed that PPARgamma ligands might promote differentiation and/or regression of mammary tumors. To directly evaluate the role of PPARgamma in mammary carcinogenesis, PPARgamma wild-type (+/+) or heterozygous (+/-) mice were administered 1 mg 7,12-dimethylbenz[a]anthracene (DMBA) by gavage once a week for 6 weeks and followed for a total of 25 weeks. Compared with congenic PPARgamma(+/+) littermate controls, PPARgamma(+/-) mice had early evidence for increased susceptibility to DMBA-mediated carcinogenesis based on a 1.6-fold increase in the percentage of mice with skin papillomas, as well as a 1.7-fold increase in the numbers of skin papillomas per mouse (P < 0.05). Similarly, PPARgamma(+/-) mice also had a 1.5-fold decreased survival rate (P = 0.059), and a 1.7-fold increased incidence of total tumors per mouse (P < 0.01). Moreover, PPARgamma(+/-) mice had an almost 3-fold increase in mammary adenocarcinomas (P < 0.05), an over 3-fold increase in ovarian granulosa cell carcinomas (P < 0.05), an over 3-fold increase in malignant tumors (P < 0.02) and a 4.6-fold increase in metastatic incidence. These results are the first to demonstrate an increased susceptibility in vivo of PPARgamma haploinsufficiency to DMBA-mediated carcinogenesis and suggest that PPARgamma may act as a tumor modifier of skin, ovarian and breast cancers. The data also support evidence suggesting a beneficial role for PPARgamma-specific ligands in the chemoprevention of mammary, ovarian and skin carcinogenesis. |
Address |
Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA |
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English |
Summary Language |
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Abbreviated Series Title |
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Series Volume |
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Series Issue |
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Edition |
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ISSN |
0143-3334 |
ISBN |
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Medium |
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Area |
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Expedition |
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Conference |
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Notes |
PMID:15073042 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
76 |
Permanent link to this record |
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Author |
Valova, G.P.; Mefod'ev, V.V. |
Title |
[Specific features of an epidemic process in leptospiroses in northern conditions in Western Siberia] |
Type |
Journal Article |
Year |
1972 |
Publication |
Zhurnal Mikrobiologii, Epidemiologii, i Immunobiologii |
Abbreviated Journal |
Zh Mikrobiol Epidemiol Immunobiol |
Volume |
49 |
Issue |
11 |
Pages |
138-145 |
Keywords |
Animals; Bird Diseases/epidemiology; Birds; Carnivora; Cattle; Cattle Diseases/epidemiology; Dog Diseases/epidemiology; Dogs; Ecology; Foxes; Horse Diseases/epidemiology; Horses; Humans; Insectivora; Leptospirosis/*epidemiology/veterinary; Mice; Rats; Reindeer; Rodent Diseases/epidemiology; Rodentia; Sheep; Sheep Diseases/epidemiology; Siberia |
Abstract |
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Address |
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Place of Publication |
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Language |
Russian |
Summary Language |
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Original Title |
Nekotorye spetsificheskie cherty epidemicheskogo protsessa pri leptospirozakh v usloviiakh Severa v Zapadnoi Sibiri |
Series Editor |
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Series Title |
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Abbreviated Series Title |
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Series Volume |
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Series Issue |
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Edition |
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ISSN |
0372-9311 |
ISBN |
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Medium |
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Area |
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Expedition |
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Conference |
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Notes |
PMID:4645851 |
Approved |
no |
Call Number |
Equine Behaviour @ team @ |
Serial |
2718 |
Permanent link to this record |
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Author |
Nicol, C.J.; Adachi, M.; Akiyama, T.E.; Gonzalez, F.J. |
Title |
PPARgamma in endothelial cells influences high fat diet-induced hypertension |
Type |
Journal Article |
Year |
2005 |
Publication |
American journal of hypertension : journal of the American Society of Hypertension |
Abbreviated Journal |
Am J Hypertens |
Volume |
18 |
Issue |
4 Pt 1 |
Pages |
549-556 |
Keywords |
Administration, Oral; Animals; Antihypertensive Agents/pharmacology; Blood Pressure/drug effects; Diabetes Mellitus, Type 2/physiopathology; Dietary Fats/*administration & dosage/pharmacology; Dose-Response Relationship, Drug; Endothelial Cells/*metabolism; Female; Heart Rate/drug effects; Hypertension/*etiology; Ligands; Male; Mice; Mice, Knockout; PPAR gamma/*metabolism; Sodium Chloride/administration & dosage/pharmacology; Thiazolidinediones/pharmacology |
Abstract |
BACKGROUND: Peroxisome proliferator-activated receptor gamma (PPARgamma) ligands improve human hypertension. However, the mechanism and site of this effect remains unknown, confounded by PPARgamma expression in many cell types, including endothelial cells (ECs). METHODS: To evaluate the vascular role of PPARgamma we used a conditional null mouse model. Specific disruption of PPARgamma in ECs was created by crossing Tie2-Cre+ transgenic (T2T+) and PPARgamma-floxed (fl/fl) mice to generate PPARgamma (fl/fl)T2T+ (PPARgamma E-null) mice. Conscious 8- to 12-week-old congenic PPARgamma (fl/fl)Cre- (wild type) and PPARgamma E-null mice were examined for changes in systolic blood pressure (BP) and heart rate (HR), untreated, after 2 months of salt-loading (drinking water), and after treatment for 3 months with high fat (HF) diet alone or supplemented during the last 2 weeks with rosiglitazone (3 mg/kg/d). RESULTS: Untreated PPARgamma E-nulls were phenotypically indistinguishable from wild-type littermates. However, compared to similarly treated wild types, HF-treated PPARgamma E-nulls had significantly elevated systolic BP not seen after normal diet or salt-loading. Despite sex-dependent baseline differences, salt-loaded and HF-treated PPARgamma E-nulls of either sex had significantly elevated HR versus wild types. Interestingly, rosiglitazone improved serum insulin levels, but not HF diet-induced hypertension, in PPARgamma E-null mice. CONCLUSIONS: These results suggest that PPARgamma in ECs not only is an important regulator of hypertension and HR under stressed conditions mimicking those arising in type 2 diabetics, but also mediates the antihypertensive effects of rosiglitazone. These data add evidence supporting a beneficial role for PPARgamma-specific ligands in the treatment of hypertension, and suggest therapeutic strategies targeting ECs may prove useful. |
Address |
Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA |
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English |
Summary Language |
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Series Editor |
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Abbreviated Series Title |
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Series Volume |
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Series Issue |
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Edition |
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ISSN |
0895-7061 |
ISBN |
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Area |
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Conference |
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Notes |
PMID:15831367 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
69 |
Permanent link to this record |
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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 |
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Series Volume |
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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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Area |
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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 |
Permanent link to this record |
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Author |
Miller, G. |
Title |
Animal behavior. Signs of empathy seen in mice |
Type |
Journal Article |
Year |
2006 |
Publication |
Science (New York, N.Y.) |
Abbreviated Journal |
Science |
Volume |
312 |
Issue |
5782 |
Pages |
1860-1861 |
Keywords |
Altruism; Animals; Behavior, Animal; *Empathy; Formaldehyde/administration & dosage; Mice/*psychology; Motivation; Pain/*psychology; *Social Behavior |
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English |
Summary Language |
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Original Title |
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Series Editor |
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Series Title |
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Abbreviated Series Title |
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Series Volume |
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Series Issue |
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Edition |
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ISSN |
1095-9203 |
ISBN |
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Conference |
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Notes |
PMID:16809499 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
461 |
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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 Editor |
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Series Volume |
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Series Issue |
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Edition |
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ISSN |
1096-6080 |
ISBN |
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Notes |
PMID:15456926 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
71 |
Permanent link to this record |