Effect of leptin administration versus re-feeding on hypothalamic neuropeptide gene expression in fasted male rats
Adipocytes are the primary source of circulating leptin. Leptin inhibits eating, increases metabolism, and stimulates the reproductive axis. Numerous hypothalamic neuropeptides have been implicated in leptin's behavioral and neuroendocrine effects, including neuropeptide Y (NPY) and cocaine- an...
Saved in:
Published in | Canadian journal of physiology and pharmacology Vol. 82; no. 12; pp. 1128 - 1134 |
---|---|
Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Ottawa, Canada
NRC Research Press
01.12.2004
National Research Council of Canada Canadian Science Publishing NRC Research Press |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | Adipocytes are the primary source of circulating leptin. Leptin inhibits eating, increases metabolism, and stimulates the reproductive axis. Numerous hypothalamic neuropeptides have been implicated in leptin's behavioral and neuroendocrine effects, including neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART). The aim of this study was to investigate the physiological relevance of leptin's signaling of nutritional status by comparing the effects of leptin with the effects of re-feeding on fasting-induced changes in the expression of the long form of the leptin receptor (Ob-Rb), NPY, and CART. Adult male rats were fasted for 48 h and treated with either intra cere broventricular (i.c.v.) or subcutaneous (s.c.) leptin throughout the fast, or fed ad libitum for 24 h after terminating the fast. Expression of NPY, Ob-Rb, and CART mRNA in the arcuate nucleus (ARC) was determined by in situ hybridization histochemistry and compared with vehicle-treated fed or fasted controls. Fasting increased NPY and Ob-Rb expression and decreased CART expression in the ARC. Leptin (regardless of route) and re-feeding were equally effective in normalizing CART mRNA expression. A similar trend was observed with Ob-Rb expression. In contrast, neither re-feeding nor s.c. leptin reversed the increased expression of NPY that was induced by fasting. Only i.c.v. leptin was effective in this regard. Our results indicate leptin and re-feeding are equally effective in normalizing fasting-induced changes in CART and Ob-Rb expression, but less effective in normalizing NPY expression. These results suggest that leptin is the primary nutritional signal regulating CART and Ob-Rb expression in the ARC, and highlight potential differences between CART and NPY neuron sensitivity to leptin signaling.Key words: CART, leptin receptor, NPY, neuropeptide gene expression, fasting, refeeding, hypothalamus. |
---|---|
AbstractList | Adipocytes are the primary source of circulating leptin. Leptin inhibits eating, increases metabolism, and stimulates the reproductive axis. Numerous hypothalamic neuropeptides have been implicated in leptin's behavioral and neuroendocrine effects, including neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART). The aim of this study was to investigate the physiological relevance of leptin's signaling of nutritional status by comparing the effects of leptin with the effects of re-feeding on fasting-induced changes in the expression of the long form of the leptin receptor (Ob-Rb), NPY, and CART. Adult male rats were fasted for 48 h and treated with either intra cere broventricular (i.c.v.) or subcutaneous (s.c.) leptin throughout the fast, or fed ad libitum for 24 h after terminating the fast. Expression of NPY, Ob-Rb, and CART mRNA in the arcuate nucleus (ARC) was determined by in situ hybridization histochemistry and compared with vehicle-treated fed or fasted controls. Fasting increased NPY and Ob-Rb expression and decreased CART expression in the ARC. Leptin (regardless of route) and re-feeding were equally effective in normalizing CART mRNA expression. A similar trend was observed with Ob-Rb expression. In contrast, neither re-feeding nor s.c. leptin reversed the increased expression of NPY that was induced by fasting. Only i.c.v. leptin was effective in this regard. Our results indicate leptin and re-feeding are equally effective in normalizing fasting-induced changes in CART and Ob-Rb expression, but less effective in normalizing NPY expression. These results suggest that leptin is the primary nutritional signal regulating CART and Ob-Rb expression in the ARC, and highlight potential differences between CART and NPY neuron sensitivity to leptin signaling.Original Abstract: Les adipocytes constituent une source essentielle de leptine circulante. La leptine inhibe la prise alimentaire, augmente le metabolisme et stimule l'axe reproducteur. De nombreux neuropeptides hypothalamiques ont ete mis en cause dans les effets neuroendocriniens et comportementaux de la leptine, dont le neuropeptide Y (NPY) et le transcrit regule par la cocaiene et l'amphetamine (CART). La presente etude a eu pour but d'examiner la pertinence physiologique de la signalisation de l'etat nutritionnel par la leptine, en comparant les effets de la leptine avec a ceux de la reprise alimentaire sur les variations induites par le jeune dans l'expression de la forme longue du recepteur de la leptine (Ob-Rb), de NPY et de CART. Des rats males adultes ont ete soumis a un jeune de 48 heures et ont recu de la leptine par voie intracerebroventriculaire (i.c.v.) ou sous-cutanee (s.c.) pendant la duree du jeune, ou ont ete nourris ad libitum pendant 24 heures apres la levee du jeune. L'expression des ARNm de NPY, Ob-Rb et CART dans le noyau arque (ARQ) a ete determinee par histochimie et hybridation in situ et comparee a celle de temoins nourris avec un vehicule ou a jeun. Le jeune a augmente l'expression de NPY et Ob-Rb et diminue celle de CART dans le noyau ARQ. La leptine (peu importe la voie d'administration) et la reprise alimentaire ont normalise aussi efficacement l'expression de l'ARNm de CART. Une tendance similaire a ete observee pour l'expression de Ob-Rb. En revanche, ni la reprise alimentaire ni la leptine s.c. n'ont renverse l'augmentation de l'expression de NPY induite par le jeune. Seule la leptine i.c.v. a ete efficace a cet egard. Nos resultats indiquent que la leptine et la reprise alimentaire sont aussi efficaces pour normaliser les variations de l'expression de CART et Ob-Rb induites par le jeune, mais qu'elles le sont moins pour normaliser l'expression de NPY. Ces resultats donnent a penser que la leptine est le signal nutritionnel regulant l'ex pression de CART et Ob-Rb dans le noyau ARQ et ils mettent en lumiere les differences potentielles entre la sensibilite des neurones CART et NPY a la signalisation par la leptine. Adipocytes are the primary source of circulating leptin. Leptin inhibits eating, increases metabolism, and stimulates the reproductive axis. Numerous hypothalamic neuropeptides have been implicated in leptin's behavioral and neuroendocrine effects, including neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART). The aim of this study was to investigate the physiological relevance of leptin's signaling of nutritional status by comparing the effects of leptin with the effects of re-feeding on fasting-induced changes in the expression of the long form of the leptin receptor (Ob-Rb), NPY, and CART. Adult male rats were fasted for 48 h and treated with either intracerebroventricular (i.c.v.) or subcutaneous (s.c.) leptin throughout the fast, or fed ad libitum for 24 h after terminating the fast. Expression of NPY, Ob-Rb, and CART mRNA in the arcuate nucleus (ARC) was determined by in situ hybridization histochemistry and compared with vehicle-treated fed or fasted controls. Fasting increased NPY and Ob-Rb expression and decreased CART expression in the ARC. Leptin (regardless of route) and re-feeding were equally effective in normalizing CART mRNA expression. A similar trend was observed with Ob-Rb expression. In contrast, neither re-feeding nor s.c. leptin reversed the increased expression of NPY that was induced by fasting. Only i.c.v. leptin was effective in this regard. Our results indicate leptin and re-feeding are equally effective in normalizing fasting-induced changes in CART and Ob-Rb expression, but less effective in normalizing NPY expression. These results suggest that leptin is the primary nutritional signal regulating CART and Ob-Rb expression in the ARC, and highlight potential differences between CART and NPY neuron sensitivity to leptin signaling. Adipocytes are the primary source of circulating leptin. Leptin inhibits eating, increases metabolism, and stimulates the reproductive axis. Numerous hypothalamic neuropeptides have been implicated in leptin's behavioral and neuroendocrine effects, including neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART). The aim of this study was to investigate the physiological relevance of leptin's signaling of nutritional status by comparing the effects of leptin with the effects of re-feeding on fasting-induced changes in the expression of the long form of the leptin receptor (Ob-Rb), NPY, and CART. Adult male rats were fasted for 48 h and treated with either intra cere broventricular (i.c.v.) or subcutaneous (s.c.) leptin throughout the fast, or fed ad libitum for 24 h after terminating the fast. Expression of NPY, Ob-Rb, and CART mRNA in the arcuate nucleus (ARC) was determined by in situ hybridization histochemistry and compared with vehicle-treated fed or fasted controls. Fasting increased NPY and Ob-Rb expression and decreased CART expression in the ARC. Leptin (regardless of route) and re-feeding were equally effective in normalizing CART mRNA expression. A similar trend was observed with Ob-Rb expression. In contrast, neither re-feeding nor s.c. leptin reversed the increased expression of NPY that was induced by fasting. Only i.c.v. leptin was effective in this regard. Our results indicate leptin and re-feeding are equally effective in normalizing fasting-induced changes in CART and Ob-Rb expression, but less effective in normalizing NPY expression. These results suggest that leptin is the primary nutritional signal regulating CART and Ob-Rb expression in the ARC, and highlight potential differences between CART and NPY neuron sensitivity to leptin signaling.Key words: CART, leptin receptor, NPY, neuropeptide gene expression, fasting, refeeding, hypothalamus. |
Abstract_FL | Les adipocytes constituent une source essentielle de leptine circulante. La leptine inhibe la prise alimentaire, augmente le métabolisme et stimule l'axe reproducteur. De nombreux neuropeptides hypothalamiques ont été mis en cause dans les effets neuroendocriniens et comportementaux de la leptine, dont le neuropeptide Y (NPY) et le transcrit régulé par la cocaïne et l'amphétamine (CART). La présente étude a eu pour but d'examiner la pertinence physiologique de la signalisation de l'état nutritionnel par la leptine, en comparant les effets de la leptine avec à ceux de la reprise alimentaire sur les variations induites par le jeûne dans l'expression de la forme longue du récepteur de la leptine (Ob-Rb), de NPY et de CART. Des rats mâles adultes ont été soumis à un jeûne de 48 heures et ont reçu de la leptine par voie intracérébroventriculaire (i.c.v.) ou sous-cutanée (s.c.) pendant la durée du jeûne, ou ont été nourris ad libitum pendant 24 heures après la levée du jeûne. L'expression des ARNm de NPY, Ob-Rb et CART dans le noyau arqué (ARQ) a été déterminée par histochimie et hybridation in situ et comparée à celle de témoins nourris avec un véhicule ou à jeun. Le jeûne a augmenté l'expression de NPY et Ob-Rb et diminué celle de CART dans le noyau ARQ. La leptine (peu importe la voie d'administration) et la reprise alimentaire ont normalisé aussi efficacement l'expression de l'ARNm de CART. Une tendance similaire a été observée pour l'expression de Ob-Rb. En revanche, ni la reprise alimentaire ni la leptine s.c. n'ont renversé l'augmentation de l'expression de NPY induite par le jeûne. Seule la leptine i.c.v. a été efficace à cet égard. Nos résultats indiquent que la leptine et la reprise alimentaire sont aussi efficaces pour normaliser les variations de l'expression de CART et Ob-Rb induites par le jeûne, mais qu'elles le sont moins pour normaliser l'expression de NPY. Ces résultats donnent à penser que la leptine est le signal nutritionnel régulant l'ex pression de CART et Ob-Rb dans le noyau ARQ et ils mettent en lumière les différences potentielles entre la sensibilité des neurones CART et NPY à la signalisation par la leptine.Mots clés : CART, récepteur de la leptine, NPY, expression génique du neuropeptide, jeûne, reprise alimentaire, hypothalamus.[Traduit par la Rédaction] |
Author | Van Vugt, Dean A McAlister, Edward D |
Author_xml | – sequence: 1 givenname: Edward D surname: McAlister fullname: McAlister, Edward D – sequence: 2 givenname: Dean A surname: Van Vugt fullname: Van Vugt, Dean A |
BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16548822$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/15644956$$D View this record in MEDLINE/PubMed |
BookMark | eNqF0duK1TAUBuAgI85B8Q0kCCoI1aycml7KMB5gwBu9LmmyMrtDm9akHdxvb_ZY3DCgXoWEL39W-M_JSZwiEvIc2DsA0bzfM1kB54_IGXCmqlpJOCFnjDFTSQ78lJznfFu22gjzhJyC0lI2Sp-RdBUCuoVOgQ44L32k1o997POS7NJPkd5hymumCauA6Pt4Q8vhbj9Py84OduwdjbimaT5c9khvMCLFn3PCnA_XS2CweUFPRzsgLaH5KXkc7JDx2bZekO8fr75dfq6uv376cvnhunJKwFJZ2SHzUAevnew6rFnHGPfCCKsBoFEWPXPOKWWFVkY4xmQnDAaJ2DSKiwvy5nfunKYfK-alHfvscBhsxGnNbaOkqk2BRb7-p9Q1B8W4_i-ERgKDe_jyAbyd1hTLd1vOQTdG1Oo4oEtTzglDO6d-tGnfAmsPtbal1rbUWuSLLW7tRvRHt_VYwKsN2OzsEJKNrs9Hp5U05j5o-0BMrlSENrndH7W91s4-FPj27_DheL8AUhTHxA |
CODEN | CJPPA3 |
CitedBy_id | crossref_primary_10_1016_j_peptides_2005_12_009 crossref_primary_10_1097_01_mco_0000172580_02138_20 crossref_primary_10_1111_bph_12949 crossref_primary_10_1016_j_brainres_2007_05_077 crossref_primary_10_1007_s00335_010_9307_1 crossref_primary_10_1002_cne_20971 crossref_primary_10_1007_s12031_007_0064_x crossref_primary_10_1210_me_2011_1180 crossref_primary_10_1016_j_brainres_2006_10_030 crossref_primary_10_1002_cne_22569 crossref_primary_10_1590_S0100_879X2006001200014 |
Cites_doi | 10.1073/pnas.82.11.3940 10.1038/29993 10.1152/ajpregu.00501.2001 10.1097/00001756-200011270-00031 10.1126/science.7624778 10.1210/endo.140.11.7105 10.1016/0006-8993(85)90730-9 10.1210/endo.139.11.6297 10.1038/sj.ijo.0801863 10.1177/34.10.3745909 10.2337/diab.46.3.335 10.1301/002966402320634878 10.1038/296659a0 10.2337/diab.46.11.1782 10.1159/000054716 10.1126/science.7624777 10.1016/0196-9781(88)90112-X 10.1038/377530a0 10.1038/oby.2000.76 10.2337/diabetes.47.4.538 10.1161/01.HYP.37.2.663 10.1152/ajpendo.00292.2001 10.1159/000125209 10.1038/372425a0 10.2337/diab.45.4.531 10.1046/j.1365-2826.2002.00830.x 10.1002/(SICI)1096-9861(19980615)395:4<535::AID-CNE9>3.0.CO;2-2 10.1016/S0006-8993(99)01252-4 10.2337/diabetes.48.4.828 10.1016/S0031-9384(98)00243-1 10.1210/endo.137.7.8770941 10.1179/014788889794651870 10.1210/mend.11.4.9907 10.1016/0196-9781(86)90149-X 10.1073/pnas.88.23.10931 10.1016/S0006-8993(00)02570-1 10.1002/cne.1085 10.1016/0306-4522(85)90260-X |
ContentType | Journal Article |
Copyright | 2005 INIST-CNRS Copyright National Research Council of Canada Dec 2004 |
Copyright_xml | – notice: 2005 INIST-CNRS – notice: Copyright National Research Council of Canada Dec 2004 |
DBID | IQODW CGR CUY CVF ECM EIF NPM AAYXX CITATION 3V. 7QP 7QR 7RV 7TK 7X7 7XB 88A 88E 88I 8AF 8AO 8FD 8FE 8FH 8FI 8FJ 8FK 8FQ 8FV ABUWG AFKRA AZQEC BBNVY BENPR BHPHI CCPQU DWQXO FR3 FYUFA GHDGH GNUQQ HCIFZ K9. KB0 LK8 M0S M1P M2P M3G M7P NAPCQ P64 PQEST PQQKQ PQUKI PRINS Q9U RC3 7X8 |
DOI | 10.1139/y04-122 |
DatabaseName | Pascal-Francis Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed CrossRef ProQuest Central (Corporate) Calcium & Calcified Tissue Abstracts Chemoreception Abstracts Nursing & Allied Health Database Neurosciences Abstracts Health & Medical Collection ProQuest Central (purchase pre-March 2016) Biology Database (Alumni Edition) Medical Database (Alumni Edition) Science Database (Alumni Edition) STEM Database ProQuest Pharma Collection Technology Research Database ProQuest SciTech Collection ProQuest Natural Science Collection Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) Canadian Business & Current Affairs Database Canadian Business & Current Affairs Database (Alumni Edition) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials Biological Science Collection ProQuest Central Natural Science Collection ProQuest One Community College ProQuest Central Korea Engineering Research Database Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student SciTech Premium Collection ProQuest Health & Medical Complete (Alumni) Nursing & Allied Health Database (Alumni Edition) ProQuest Biological Science Collection Health & Medical Collection (Alumni Edition) Medical Database Science Database CBCA Reference & Current Events Biological Science Database Nursing & Allied Health Premium Biotechnology and BioEngineering Abstracts ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central China ProQuest Central Basic Genetics Abstracts MEDLINE - Academic |
DatabaseTitle | MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) CrossRef ProQuest Central Student Technology Research Database ProQuest Central Essentials ProQuest Health & Medical Complete (Alumni) ProQuest AP Science ProQuest Central (Alumni Edition) SciTech Premium Collection ProQuest One Community College ProQuest Natural Science Collection ProQuest Pharma Collection ProQuest Central China ProQuest Biology Journals (Alumni Edition) ProQuest Central CBCA Complete (Alumni Edition) Health Research Premium Collection Health and Medicine Complete (Alumni Edition) Natural Science Collection ProQuest Central Korea Biological Science Collection CBCA Complete Chemoreception Abstracts ProQuest Medical Library (Alumni) ProQuest Science Journals (Alumni Edition) ProQuest Biological Science Collection ProQuest Central Basic ProQuest Science Journals ProQuest One Academic Eastern Edition CBCA Reference & Current Events ProQuest Nursing & Allied Health Source ProQuest Hospital Collection Health Research Premium Collection (Alumni) Biological Science Database ProQuest SciTech Collection Neurosciences Abstracts ProQuest Hospital Collection (Alumni) Biotechnology and BioEngineering Abstracts Nursing & Allied Health Premium ProQuest Health & Medical Complete ProQuest Medical Library ProQuest One Academic UKI Edition ProQuest Nursing & Allied Health Source (Alumni) Engineering Research Database ProQuest One Academic Calcium & Calcified Tissue Abstracts ProQuest Central (Alumni) Genetics Abstracts MEDLINE - Academic |
DatabaseTitleList | Genetics Abstracts MEDLINE MEDLINE - Academic ProQuest Central Student Genetics Abstracts CrossRef |
Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database – sequence: 3 dbid: BENPR name: ProQuest Central url: https://www.proquest.com/central sourceTypes: Aggregation Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Anatomy & Physiology Pharmacy, Therapeutics, & Pharmacology |
EISSN | 1205-7541 |
EndPage | 1134 |
ExternalDocumentID | 800879421 10_1139_y04_122 15644956 16548822 |
Genre | Article Research Support, Non-U.S. Gov't Journal Article |
GroupedDBID | - 0R 1AW 29B 2QV 3V. 4.4 53G 55 5GY 5RE 5RP 7RV 7X7 88A 88E 88I 8AF 8AO 8FE 8FH 8FI 8FJ 8FQ AALRV ABDBF ABFLS ABPTK ABUWG ACGFS ACGOD ACIWK ACPRK ADBBV ADBIT AENEX AFFNX AFKRA AFRAH AHMBA ALMA_UNASSIGNED_HOLDINGS AZQEC BBAFP BBNVY BCR BENPR BES BHPHI BKEYQ BLC BPHCQ BVXVI CAG COF CS3 D8U DU5 DWQXO DXH EAD EAP EAS EBD EBS ECC EDH EJD EMB EMK EPL ESX EX3 F5P FYUFA GNUQQ HCIFZ HZ IAO IEA IHR INH INR IOF IPNFZ IPY L7B LK8 M0L M1P M2P M2Q M3C M3E M3G M7P MK0 MV1 NAPCQ NMEPN NRXXU O9- OVD P2P PQEST PQQKQ PQUKI PRINS PROAC PSQYO QN7 QRP RIG RRCRK RRP SV3 TUS WH7 WOW X X7M ZGI ZXP --- -~X .55 .GJ 00T 08R 0R~ 36B 3O- 6J9 AAUGY ACGFO ACKIV AIAGR BCGST CCPQU DATHI EMOBN HZ~ ICQ IQODW ISN ISR ITC MVM NYCZX ONR PV9 QF4 QM4 QO4 RZL TEORI UAP UKHRP VQG ABJNI ALIPV CGR CUY CVF ECM EIF HMCUK NPM AAYXX CITATION 7QP 7QR 7TK 7XB 8FD 8FK FR3 K9. P64 Q9U RC3 7X8 |
ID | FETCH-LOGICAL-c531t-a4be0d17fd6c4bbe70b002d383a611195aed0ccc55a36583c004b38ef4ee99523 |
IEDL.DBID | BENPR |
ISSN | 0008-4212 |
IngestDate | Fri Jun 28 05:57:12 EDT 2024 Fri Aug 16 08:23:51 EDT 2024 Fri Jun 28 11:43:30 EDT 2024 Thu Oct 10 15:59:11 EDT 2024 Fri Aug 23 02:21:32 EDT 2024 Sat Sep 28 07:44:25 EDT 2024 Sun Oct 22 16:06:30 EDT 2023 Wed Apr 14 12:49:39 EDT 2021 Thu May 23 14:20:14 EDT 2019 |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 12 |
Keywords | Neuropeptide Y Feeding behavior Rat Rodentia Central nervous system Neuroendocrine regulation Hypothalamus Gene expression Neuropeptide Encephalon Feeding Vertebrata Mammalia Leptin Nutritional status |
Language | English |
License | CC BY 4.0 |
LinkModel | DirectLink |
MergedId | FETCHMERGED-LOGICAL-c531t-a4be0d17fd6c4bbe70b002d383a611195aed0ccc55a36583c004b38ef4ee99523 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 |
PMID | 15644956 |
PQID | 221698375 |
PQPubID | 23462 |
PageCount | 7 |
ParticipantIDs | proquest_miscellaneous_67215026 pascalfrancis_primary_16548822 proquest_miscellaneous_19410126 nrcresearch_primary_10_1139_y04_122 pubmed_primary_15644956 proquest_journals_221698375 crossref_primary_10_1139_y04_122 proquest_miscellaneous_954578523 |
PublicationCentury | 2000 |
PublicationDate | 2004-12-01 |
PublicationDateYYYYMMDD | 2004-12-01 |
PublicationDate_xml | – month: 12 year: 2004 text: 2004-12-01 day: 01 |
PublicationDecade | 2000 |
PublicationPlace | Ottawa, Canada |
PublicationPlace_xml | – name: Ottawa, Canada – name: Ottawa, ON – name: Canada – name: Ottawa |
PublicationTitle | Canadian journal of physiology and pharmacology |
PublicationTitleAlternate | Revue canadienne de physiologie et pharmacologie |
PublicationYear | 2004 |
Publisher | NRC Research Press National Research Council of Canada Canadian Science Publishing NRC Research Press |
Publisher_xml | – name: NRC Research Press – name: National Research Council of Canada – name: Canadian Science Publishing NRC Research Press |
References | Friedman J.M. (p_15/p_15_1) 2002; 60 Stephens T.W. (p_33/p_33_1) 1995; 377 Simmons D.M. (p_30/p_30_1) 1989; 12 Swart I. (p_34/p_34_1) 2002; 283 Zhang Y. (p_42/p_42_1) 1994; 372 Elmquist J.K. (p_13/p_13_1) 1998; 395 Overton J.M. (p_23/p_23_1) 2001; 37 Weigle D.S. (p_40/p_40_1) 1997; 82 Adam C.L. (p_1/p_1_1) 2002; 75 Bai F.L. (p_3/p_3_1) 1985; 331 Baskin D.G. (p_7/p_7_1) 1999; 48 Magoul R. (p_22/p_22_1) 2000; 11 De Balbian Verster F. (p_11/p_11_1) 1971; 10 Chronwall B.M. (p_9/p_9_1) 1985; 15 Rosene D.L. (p_27/p_27_1) 1986; 34 Stanley B.G. (p_32/p_32_1) 1986; 7 Larsen P.J. (p_21/p_21_1) 2000; 8 Wang T. (p_39/p_39_1) 1999; 65 Davies L. (p_10/p_10_1) 1994; 266 Tatemoto K. (p_35/p_35_1) 1982; 296 Kalra S.P. (p_18/p_18_1) 1988; 9 Rohner-Jeanrenaud F. (p_26/p_26_1) 2002; 26 Stanley B.G. (p_31/p_31_1) 1985; 82 Elias C.F. (p_12/p_12_1) 2001; 432 Schwartz M.W. (p_29/p_29_1) 1996; 45 Van Vugt D.A. (p_37/p_37_1) 1989; 50 Finn P.D. (p_14/p_14_1) 1998; 139 Campfield L.A. (p_8/p_8_1) 1995; 269 Ruffin M. (p_28/p_28_1) 2000; 874 Tsuruta Y. (p_36/p_36_1) 2002; 282 Kristensen P. (p_20/p_20_1) 1998; 393 Halaas J.L. (p_17/p_17_1) 1995; 269 Wang Q. (p_38/p_38_1) 1997; 46 Ghilardi N. (p_16/p_16_1) 1997; 11 Widdowson P.S. (p_41/p_41_1) 1997; 46 Baskin D.G. (p_6/p_6_1) 1999; 828 Barash I.A. (p_4/p_4_1) 1996; 137 Kalra S.P. (p_19/p_19_1) 1991; 88 Robson A.J. (p_25/p_25_1) 2002; 14 Baskin D.G. (p_5/p_5_1) 1998; 47 Ahima R.S. (p_2/p_2_1) 1999; 140 |
References_xml | – volume: 82 start-page: 3940 year: 1985 ident: p_31/p_31_1 publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.82.11.3940 contributor: fullname: Stanley B.G. – volume: 393 start-page: 72 year: 1998 ident: p_20/p_20_1 publication-title: Nature doi: 10.1038/29993 contributor: fullname: Kristensen P. – volume: 283 start-page: R1020 year: 2002 ident: p_34/p_34_1 publication-title: Am. J. Physiol. Regul. Integr. Comp. Physiol. doi: 10.1152/ajpregu.00501.2001 contributor: fullname: Swart I. – volume: 11 start-page: 3747 year: 2000 ident: p_22/p_22_1 publication-title: Neuroreport doi: 10.1097/00001756-200011270-00031 contributor: fullname: Magoul R. – volume: 269 start-page: 546 year: 1995 ident: p_8/p_8_1 publication-title: Science doi: 10.1126/science.7624778 contributor: fullname: Campfield L.A. – volume: 140 start-page: 4923 year: 1999 ident: p_2/p_2_1 publication-title: Endocrinology doi: 10.1210/endo.140.11.7105 contributor: fullname: Ahima R.S. – volume: 331 start-page: 172 year: 1985 ident: p_3/p_3_1 publication-title: Brain Res. doi: 10.1016/0006-8993(85)90730-9 contributor: fullname: Bai F.L. – volume: 139 start-page: 4652 year: 1998 ident: p_14/p_14_1 publication-title: Endocrinology doi: 10.1210/endo.139.11.6297 contributor: fullname: Finn P.D. – volume: 26 start-page: 143 year: 2002 ident: p_26/p_26_1 publication-title: Int. J. Obes. Relat. Metab. Disord. doi: 10.1038/sj.ijo.0801863 contributor: fullname: Rohner-Jeanrenaud F. – volume: 34 start-page: 1301 year: 1986 ident: p_27/p_27_1 publication-title: J. Histochem. Cytochem. doi: 10.1177/34.10.3745909 contributor: fullname: Rosene D.L. – volume: 46 start-page: 335 year: 1997 ident: p_38/p_38_1 publication-title: Diabetes doi: 10.2337/diab.46.3.335 contributor: fullname: Wang Q. – volume: 60 start-page: S1 year: 2002 ident: p_15/p_15_1 publication-title: Nutr. Rev. doi: 10.1301/002966402320634878 contributor: fullname: Friedman J.M. – volume: 296 start-page: 659 year: 1982 ident: p_35/p_35_1 publication-title: Nature doi: 10.1038/296659a0 contributor: fullname: Tatemoto K. – volume: 46 start-page: 1782 year: 1997 ident: p_41/p_41_1 publication-title: Diabetes doi: 10.2337/diab.46.11.1782 contributor: fullname: Widdowson P.S. – volume: 75 start-page: 250 year: 2002 ident: p_1/p_1_1 publication-title: Neuroendocrinology doi: 10.1159/000054716 contributor: fullname: Adam C.L. – volume: 269 start-page: 543 year: 1995 ident: p_17/p_17_1 publication-title: Science doi: 10.1126/science.7624777 contributor: fullname: Halaas J.L. – volume: 9 start-page: 723 year: 1988 ident: p_18/p_18_1 publication-title: Peptides doi: 10.1016/0196-9781(88)90112-X contributor: fullname: Kalra S.P. – volume: 377 start-page: 530 year: 1995 ident: p_33/p_33_1 publication-title: Nature doi: 10.1038/377530a0 contributor: fullname: Stephens T.W. – volume: 8 start-page: 590 year: 2000 ident: p_21/p_21_1 publication-title: Obes. Res. doi: 10.1038/oby.2000.76 contributor: fullname: Larsen P.J. – volume: 47 start-page: 538 year: 1998 ident: p_5/p_5_1 publication-title: Diabetes doi: 10.2337/diabetes.47.4.538 contributor: fullname: Baskin D.G. – volume: 10 start-page: 1395 year: 1971 ident: p_11/p_11_1 publication-title: Part I Physiol. Pharmacol. contributor: fullname: De Balbian Verster F. – volume: 37 start-page: 663 year: 2001 ident: p_23/p_23_1 publication-title: Hypertension doi: 10.1161/01.HYP.37.2.663 contributor: fullname: Overton J.M. – volume: 282 start-page: E967 year: 2002 ident: p_36/p_36_1 publication-title: Am. J. Physiol. Endocrinol. Metab. doi: 10.1152/ajpendo.00292.2001 contributor: fullname: Tsuruta Y. – volume: 50 start-page: 109 year: 1989 ident: p_37/p_37_1 publication-title: Neuroendocrinology doi: 10.1159/000125209 contributor: fullname: Van Vugt D.A. – volume: 372 start-page: 425 year: 1994 ident: p_42/p_42_1 publication-title: Nature doi: 10.1038/372425a0 contributor: fullname: Zhang Y. – volume: 45 start-page: 531 year: 1996 ident: p_29/p_29_1 publication-title: Diabetes doi: 10.2337/diab.45.4.531 contributor: fullname: Schwartz M.W. – volume: 14 start-page: 697 year: 2002 ident: p_25/p_25_1 publication-title: J. Neuroendocrinol. doi: 10.1046/j.1365-2826.2002.00830.x contributor: fullname: Robson A.J. – volume: 395 start-page: 535 year: 1998 ident: p_13/p_13_1 publication-title: J. Comp. Neurol. doi: 10.1002/(SICI)1096-9861(19980615)395:4<535::AID-CNE9>3.0.CO;2-2 contributor: fullname: Elmquist J.K. – volume: 828 start-page: 154 year: 1999 ident: p_6/p_6_1 publication-title: Brain Res. doi: 10.1016/S0006-8993(99)01252-4 contributor: fullname: Baskin D.G. – volume: 48 start-page: 828 year: 1999 ident: p_7/p_7_1 publication-title: Diabetes doi: 10.2337/diabetes.48.4.828 contributor: fullname: Baskin D.G. – volume: 65 start-page: 839 year: 1999 ident: p_39/p_39_1 publication-title: Physiol. Behav. doi: 10.1016/S0031-9384(98)00243-1 contributor: fullname: Wang T. – volume: 137 start-page: 3144 year: 1996 ident: p_4/p_4_1 publication-title: Endocrinology doi: 10.1210/endo.137.7.8770941 contributor: fullname: Barash I.A. – volume: 12 start-page: 169 year: 1989 ident: p_30/p_30_1 publication-title: J. Histotechnol. doi: 10.1179/014788889794651870 contributor: fullname: Simmons D.M. – volume: 266 start-page: R1687 year: 1994 ident: p_10/p_10_1 publication-title: Am. J. Physiol. contributor: fullname: Davies L. – volume: 11 start-page: 393 year: 1997 ident: p_16/p_16_1 publication-title: Mol. Endocrinol. doi: 10.1210/mend.11.4.9907 contributor: fullname: Ghilardi N. – volume: 7 start-page: 1189 year: 1986 ident: p_32/p_32_1 publication-title: Peptides doi: 10.1016/0196-9781(86)90149-X contributor: fullname: Stanley B.G. – volume: 88 start-page: 931 year: 1991 ident: p_19/p_19_1 publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.88.23.10931 contributor: fullname: Kalra S.P. – volume: 874 start-page: 30 year: 2000 ident: p_28/p_28_1 publication-title: Brain Res. doi: 10.1016/S0006-8993(00)02570-1 contributor: fullname: Ruffin M. – volume: 432 start-page: 1 year: 2001 ident: p_12/p_12_1 publication-title: J. Comp. Neurol. doi: 10.1002/cne.1085 contributor: fullname: Elias C.F. – volume: 15 start-page: 1159 year: 1985 ident: p_9/p_9_1 publication-title: Neuroscience doi: 10.1016/0306-4522(85)90260-X contributor: fullname: Chronwall B.M. – volume: 82 start-page: 561 year: 1997 ident: p_40/p_40_1 publication-title: J. Clin. Endocrinol. Metab. contributor: fullname: Weigle D.S. |
SSID | ssj0006838 |
Score | 1.8400191 |
Snippet | Adipocytes are the primary source of circulating leptin. Leptin inhibits eating, increases metabolism, and stimulates the reproductive axis. Numerous... |
SourceID | proquest crossref pubmed pascalfrancis nrcresearch |
SourceType | Aggregation Database Index Database Enrichment Source Publisher |
StartPage | 1128 |
SubjectTerms | Adipocytes Animals Appetite - physiology Arcuate nucleus Biological and medical sciences Body Weight - physiology Cell Count Cocaine- and amphetamine-regulated transcript protein Eating - physiology Fasting Fasting - physiology Feeding. Feeding behavior Fundamental and applied biological sciences. Psychology Gene expression Gene Expression - drug effects Histochemistry Hypothalamus Hypothalamus - drug effects Hypothalamus - physiology In Situ Hybridization Lateral Ventricles - physiology Leptin - pharmacology Leptin receptors Male Metabolism Nerve Tissue Proteins - metabolism Neuroendocrine system Neurons Neuropeptide Y Neuropeptide Y - metabolism Neuropeptides - biosynthesis Neuropeptides - genetics Nutritional status Perfusion Rats RNA, Complementary - biosynthesis RNA, Complementary - genetics Vertebrates: anatomy and physiology, studies on body, several organs or systems |
Title | Effect of leptin administration versus re-feeding on hypothalamic neuropeptide gene expression in fasted male rats |
URI | http://www.nrcresearchpress.com/doi/abs/10.1139/y04-122 https://www.ncbi.nlm.nih.gov/pubmed/15644956 https://www.proquest.com/docview/221698375 https://search.proquest.com/docview/19410126 https://search.proquest.com/docview/67215026 https://search.proquest.com/docview/954578523 |
Volume | 82 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3Nb9MwFLfYeoEDgo2PblCeBNpp0fLhOPEJtbBqQmKa0Cb1FvlTO2xpaFqJ_Pd7jt2WSpRr_OJEfn5-n_49Qr4USjKh8zTSLklIhWSRUIxFhS0EN7mkUrmA_s9rdnVHf8zyWajNaUNZ5fpM7A9qPVcuRn6Rpgnj6E3lX5vfkWsa5ZKroYPGARmkCXVZ2sHk8vrm1-YoZmXmj-K4jFzq09-aTdDqueh6vL50Rx29qBcqYOzcuyJJ0eI6Wd_gYr8F2mui6SvyMpiQMPY8f02emfqIHI9rdJ8fOziDvqizj5YfkbMbD03dncPt9qZVe96TbUCru2Oy8DDGMLfw4ApdahA7sLrgyjdWLSxMZL3CA3x43zXIafHgmtpDD43ZuJe1AdyXBsyfUGZbA05ohQutwiOqJMBJ2zfkbnp5--0qCv0YIoWSuowElSbWSWE1U1RKU8ROxWv0cQVLHHScMDpWSuW5yNCwyRQKoMxKY6kxnKPH-5Yc1vPavCcgjWEM94-1QtMySwRPhKAsi43MueDpkMCaLVXjYTeq3l3JeIWcq5BzQ_L5L3btp_r0L6owWjXaDsloh9HbmRh6c6Wb4nTN-SoIeFtttiN-YDOKkunSLaI281VbJZw68DS2n4Kh-53HjgL2UHA0cIsSl25I3vk9t_29HE1Z9G5P_vt7p-T5GpoyTj6Qw-ViZT6iGbWUI3JQzIoRGYwn3yfTURCdJ1UZI_w |
link.rule.ids | 315,786,790,12083,21416,27955,27956,31752,31753,33777,33778,43343,43838,74100,74657 |
linkProvider | ProQuest |
linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1Lb9NAEF5BOQAHBC2UUGhHAvVUq37srr0nVCGqAG3FIZVys_apHlrHxImE_z0ztpMQiXC1x2trZ2Znvt3xN4x9yq2R2ok0cnRIyLWRkbZSRnnItfLCcGNpQ__6Ro5v-fepmA61Oc1QVrlaE7uF2s0s7ZGfp2kiFaIp8bn-FVHTKDpcHTpoPGZPeJZxMvN8usZbsSyyfiGOi4gOPvt_ZhPMec7bjq0v3QpGz6u5HRh27qhEUjc4S6Fvb7E7_-zi0OVL9mJIIOGi1_gr9shX--zgokLw_NDCKXQlnd1e-T47_dkTU7dnMNn8Z9WcdWJryur2gM17EmOYBbinMpcK9BapLlDxxrKBuY9CH-4AL961NepZ31NLe-iIMWt62HlAq_Tgfw9FthXggEHTxio8YEACHLR5zW4vv06-jKOhG0Nk0U8XkebGxy7Jg5OWG-PzmAK8Q4SrZULEcdq72ForhM4wrcksup_JCh-490oh3n3D9qpZ5d8yMN5LidYTgna8yBKtEq25zGJvhNIqHTFYqaWse9KNsgMrmSpRcyVqbsQ-_qWu3VIn_5Ia7pa1CyN2vKXozUgSsVxBQxytNF8O7t2Ua2PEF6zvol_SYYuu_GzZlIniRJ0md0tIBN8iJgnYIaEwvc0LnLoRO-xtbvN5AhNZxLbv_vt5J-zpeHJ9VV59u_lxxJ6tSCrj5D3bW8yX_gMmVAtz3LnNH1xvIyo |
linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1Lb9QwELagSAgOCFooS6EdCdRTo3VeTnxCFbAqr6qHVtpb5Kd6aLNhsyuRf89M4t1lJZZrPHEij8cznz3-hrEPhdFC2TyJLB0SZkqLSBkhosIXSrpcZ9rQhv7PS3Fxk32b5tNAKdSGtMrVmtgv1HZmaI98nCSxkIim8rEPWRFXnycfm18RFZCig9ZQTeMhe4ROklMVh2K6xl5clOmwKPMyokPQ4f5sjPHPuOuZ-5Itx_S0npvAtnNL6ZKqxRHzQ6mL3bFo75Mmz9mzEEzC-aD9F-yBq_fZwXmNQPq-g1Po0zv7ffN9dno1kFR3Z3C9uXPVnvVia_rq7oDNB0JjmHm4o5SXGtQWwS5QIseyhbmL_OD6AB_edg3qXN1ReXvoSTIbetk6wBnqwP0OCbc1YIde0SYr3KNzAuy0fcluJl-uP11EoTJDZNBmF5HKtOM2LrwVJtPaFZycvUW0q0RMJHLKWW6MyXOVYoiTGjRFnZbOZ85Jidj3FdurZ7V7zUA7JwTOJO-Vzco0VjJWKhMpdzqXSiYjBiu1VM1AwFH1wCWVFWquQs2N2Pu_1LVb6uRfUqG1aqwfseMtRW96EojrSuriaKX5Kph6W60nJn5g3Yo2SgcvqnazZVvFMiMaNbFbQiAQzzlJwA4JiaFuUeLQjdjhMOc2v5djUIs4981_f--EPUaLqX58vfx-xJ6s-Cp5_JbtLeZL9w5jq4U-7q3mD8SHJ1Y |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Effect+of+leptin+administration+versus+re-feeding+on+hypothalamic+neuropeptide+gene+expression+in+fasted+male+rats&rft.jtitle=Canadian+journal+of+physiology+and+pharmacology&rft.au=McAlister%2C+Edward+D&rft.au=Van+Vugt%2C+Dean+A&rft.date=2004-12-01&rft.pub=NRC+Research+Press&rft.issn=0008-4212&rft.eissn=1205-7541&rft.volume=82&rft.issue=12&rft.spage=1128&rft.epage=1134&rft_id=info:doi/10.1139%2Fy04-122 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0008-4212&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0008-4212&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0008-4212&client=summon |