Interaction between Leptin and Growth Hormone (GH)/IGF-I Axis
In order to identify the mutual interaction between GH and leptin, we studied the effect of GH on fatty Zucker rats. GH administration at a high dose (5.0IU/kg) reduced % body fat after 7 days. The leptin mRNA level in subcutaneous fat tissue was not changed but that in epididymal fat tissue was dec...
Saved in:
| Published in | ENDOCRINE JOURNAL Vol. 46; no. Suppl; pp. S17 - S24 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Japan
The Japan Endocrine Society
1999
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 0918-8959 1348-4540 |
| DOI | 10.1507/endocrj.46.Suppl_S17 |
Cover
| Abstract | In order to identify the mutual interaction between GH and leptin, we studied the effect of GH on fatty Zucker rats. GH administration at a high dose (5.0IU/kg) reduced % body fat after 7 days. The leptin mRNA level in subcutaneous fat tissue was not changed but that in epididymal fat tissue was decreased by an even lower dose of GH (1.5IU/kg). IGF-I treatment (200μg/kg/day) did not change the % body fat or leptin mRNA level. These observations suggest that GH directly interacts with visceral fat and reduces fat mass and leptin expression. We also measured serum leptin levels in patients. The levels in patients with acromegaly were significantly lower than those in normal subjects with the same amount of body fat, but serum IGF-I and urinary C peptide excretion rates were higher in the acromegalic. These observations also suggests that GH directly interacts with adipose tissue and reduces leptin expression. Next we investigated the direct action of leptin on GH release from the pituitary. Leptin pretreatment of pituitary cells in culture or rats in a fasted or fed condition did not change GRH induced GH secretion. As indicated also by other recent studies, leptin may increase GRH or decrease somatostatin secretion by the hypothalamus. Thus GH interacts with fat tissues and leptin may be a good marker of the interaction. |
|---|---|
| AbstractList | In order to identify the mutual interaction between GH and leptin, we studied the effect of GH on fatty Zucker rats. GH administration at a high dose (5.0 IU/kg) reduced % body fat after 7 days. The leptin mRNA level in subcutaneous fat tissue was not changed but that in epididymal fat tissue was decreased by an even lower dose of GH (1.5 IU/kg). IGF-I treatment (200 μg/kg/day) did not change the % body fat or leptin mRNA level. These observations suggest that GH directly interacts with visceral fat and reduces fat mass and leptin expression. We also measured serum leptin levels in patients. The levels in patients with acromegaly were significantly lower than those in normal subjects with the same amount of body fat, but serum IGF-I and urinary C peptide excretion rates were higher in the acromegalic. These observations also suggests that GH directly interacts with adipose tissue and reduces leptin expression. Next we investigated the direct action of leptin on GH release from the pituitary. Leptin pretreatment of pituitary cells in culture or rats in a fasted or fed condition did not change GRH induced GH secretion. As indicated also by other recent studies, leptin may increase GRH or decrease somatostatin secretion by the hypothalamus. Thus GH interacts with fat tissues and leptin may be a good marker of the interaction. In order to identify the mutual interaction between GH and leptin, we studied the effect of GH on fatty Zucker rats. GH administration at a high dose (5.0 IU/kg) reduced % body fat after 7 days. The leptin mRNA level in subcutaneous fat tissue was not changed but that in epididymal fat tissue was decreased by an even lower dose of GH (1.5 IU/kg). IGF-I treatment (200 microg/kg/day) did not change the % body fat or leptin mRNA level. These observations suggest that GH directly interacts with visceral fat and reduces fat mass and leptin expression. We also measured serum leptin levels in patients. The levels in patients with acromegaly were significantly lower than those in normal subjects with the same amount of body fat, but serum IGF-I and urinary C peptide excretion rates were higher in the acromegalic. These observations also suggests that GH directly interacts with adipose tissue and reduces leptin expression. Next we investigated the direct action of leptin on GH release from the pituitary. Leptin pretreatment of pituitary cells in culture or rats in a fasted or fed condition did not change GRH induced GH secretion. As indicated also by other recent studies, leptin may increase GRH or decrease somatostatin secretion by the hypothalamus. Thus GH interacts with fat tissues and leptin may be a good marker of the interaction.In order to identify the mutual interaction between GH and leptin, we studied the effect of GH on fatty Zucker rats. GH administration at a high dose (5.0 IU/kg) reduced % body fat after 7 days. The leptin mRNA level in subcutaneous fat tissue was not changed but that in epididymal fat tissue was decreased by an even lower dose of GH (1.5 IU/kg). IGF-I treatment (200 microg/kg/day) did not change the % body fat or leptin mRNA level. These observations suggest that GH directly interacts with visceral fat and reduces fat mass and leptin expression. We also measured serum leptin levels in patients. The levels in patients with acromegaly were significantly lower than those in normal subjects with the same amount of body fat, but serum IGF-I and urinary C peptide excretion rates were higher in the acromegalic. These observations also suggests that GH directly interacts with adipose tissue and reduces leptin expression. Next we investigated the direct action of leptin on GH release from the pituitary. Leptin pretreatment of pituitary cells in culture or rats in a fasted or fed condition did not change GRH induced GH secretion. As indicated also by other recent studies, leptin may increase GRH or decrease somatostatin secretion by the hypothalamus. Thus GH interacts with fat tissues and leptin may be a good marker of the interaction. In order to identify the mutual interaction between GH and leptin, we studied the effect of GH on fatty Zucker rats. GH administration at a high dose (5.0IU/kg) reduced % body fat after 7 days. The leptin mRNA level in subcutaneous fat tissue was not changed but that in epididymal fat tissue was decreased by an even lower dose of GH (1.5IU/kg). IGF-I treatment (200μg/kg/day) did not change the % body fat or leptin mRNA level. These observations suggest that GH directly interacts with visceral fat and reduces fat mass and leptin expression. We also measured serum leptin levels in patients. The levels in patients with acromegaly were significantly lower than those in normal subjects with the same amount of body fat, but serum IGF-I and urinary C peptide excretion rates were higher in the acromegalic. These observations also suggests that GH directly interacts with adipose tissue and reduces leptin expression. Next we investigated the direct action of leptin on GH release from the pituitary. Leptin pretreatment of pituitary cells in culture or rats in a fasted or fed condition did not change GRH induced GH secretion. As indicated also by other recent studies, leptin may increase GRH or decrease somatostatin secretion by the hypothalamus. Thus GH interacts with fat tissues and leptin may be a good marker of the interaction. In order to identify the mutual interaction between GH and leptin, we studied the effect of GH on fatty Zucker rats. GH administration at a high dose (5.0 IU/kg) reduced % body fat after 7 days. The leptin mRNA level in subcutaneous fat tissue was not changed but that in epididymal fat tissue was decreased by an even lower dose of GH (1.5 IU/kg). IGF-I treatment (200 microg/kg/day) did not change the % body fat or leptin mRNA level. These observations suggest that GH directly interacts with visceral fat and reduces fat mass and leptin expression. We also measured serum leptin levels in patients. The levels in patients with acromegaly were significantly lower than those in normal subjects with the same amount of body fat, but serum IGF-I and urinary C peptide excretion rates were higher in the acromegalic. These observations also suggests that GH directly interacts with adipose tissue and reduces leptin expression. Next we investigated the direct action of leptin on GH release from the pituitary. Leptin pretreatment of pituitary cells in culture or rats in a fasted or fed condition did not change GRH induced GH secretion. As indicated also by other recent studies, leptin may increase GRH or decrease somatostatin secretion by the hypothalamus. Thus GH interacts with fat tissues and leptin may be a good marker of the interaction. |
| Author | ISOZAKI, OSAMU TSUSHIMA, TOSHIO SEKI, HITOSHI MIYAKAWA, MEGUMI DEMURA, HIROSHI |
| Author_xml | – sequence: 1 fullname: ISOZAKI, OSAMU organization: Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College – sequence: 1 fullname: TSUSHIMA, TOSHIO organization: Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College – sequence: 1 fullname: DEMURA, HIROSHI organization: Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College – sequence: 1 fullname: MIYAKAWA, MEGUMI organization: Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College – sequence: 1 fullname: SEKI, HITOSHI organization: Sumitomo Pharmaceuticals Research Center |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/12054113$$D View this record in MEDLINE/PubMed |
| BookMark | eNp9kEtv1DAUhS1URKeFf4BQVggWmdrxIzESi6piHtJIXRTWluPcUI8ydmo7Kvx7PMx0WrFgc-_mO-fcey7QmfMOEHpP8JxwXF-B67wJ2zkT87tpHAd1R-pXaEYoa0rGGT5DMyxJUzaSy3N0EeMWY0o5o2_QOakwZ4TQGfq6dgmCNsl6V7SQHgFcsYExWVdo1xXL4B_TfbHyYZfji0_L1eer9XJRrovrXza-Ra97PUR4d9yX6Mfi2_ebVbm5Xa5vrjel4ULUpewN5h3tNNC-7k3FSSU115oYySpZG0P6FkRnOOC-6WvWtEYL2TRcMyFaQ-kl-njwHYN_mCAmtbPRwDBoB36KSkhOsSA4gx-O4NTuoFNjsDsdfqunhzPw5QCY4GMM0Ctjk95_n4K2gyJY7dtVx3YVE-rUbhazf8Qn___LFgdZvsgaPXg3WAdq66fgcmvKPIi_OkWklApjJiLZL8UxqfOomGgobapsdHsw2sakf8IpXYdkzQBP6dmGPl_w8pQTae51yDj9A2CFtis |
| CitedBy_id | crossref_primary_10_1016_j_ghir_2015_07_002 crossref_primary_10_1016_j_molbrainres_2004_09_025 crossref_primary_10_1210_en_2012_2254 crossref_primary_10_1007_s11154_020_09560_x crossref_primary_10_1016_j_metabol_2024_156056 crossref_primary_10_1007_s00405_014_2946_1 crossref_primary_10_1016_j_jevs_2013_03_001 crossref_primary_10_1016_j_metabol_2024_155939 crossref_primary_10_1177_002215540405200214 crossref_primary_10_1111_jne_12883 crossref_primary_10_2527_2003_8192311x crossref_primary_10_1210_en_2013_1159 crossref_primary_10_1210_en_2010_0498 crossref_primary_10_1210_en_2014_1172 crossref_primary_10_1111_jne_12507 crossref_primary_10_2527_2004_82123486x crossref_primary_10_1007_s11102_008_0104_8 crossref_primary_10_1016_j_ygcen_2012_02_019 crossref_primary_10_1210_en_2015_1205 crossref_primary_10_1210_jc_2003_031799 crossref_primary_10_1210_en_2012_1331 crossref_primary_10_1210_endocr_bqaa204 crossref_primary_10_1183_09031936_03_00062403 |
| ContentType | Journal Article |
| Copyright | The Japan Endocrine Society |
| Copyright_xml | – notice: The Japan Endocrine Society |
| CorporateAuthor | Department of Medicine Institute of Clinical Endocrinology Tokyo Women's Medical College Sumitomo Pharmaceuticals Research Center |
| CorporateAuthor_xml | – name: Tokyo Women's Medical College – name: Sumitomo Pharmaceuticals Research Center – name: Institute of Clinical Endocrinology – name: Department of Medicine |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 |
| DOI | 10.1507/endocrj.46.Suppl_S17 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic MEDLINE |
| 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 |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1348-4540 |
| EndPage | S24 |
| ExternalDocumentID | 12054113 10_1507_endocrj_46_Suppl_S17 cq6endoc_1999_0046s1_004_5017_5024683382 article_endocrj1993_46_Suppl_46_Suppl_S17_article_char_en |
| Genre | Journal Article |
| GroupedDBID | --- .55 .GJ 29G 2WC 3O- 53G 5GY 5RE AAEJM AAFWJ ACPRK ADBBV AENEX AFPKN AJJEV ALMA_UNASSIGNED_HOLDINGS BAWUL BKOMP CS3 DIK DU5 E3Z EBD EBS EJD EMOBN F5P GROUPED_DOAJ JMI JSF JSH KQ8 MOJWN OK1 OVT P2P RJT RNS RPM RZJ SV3 TKC TR2 X7M XSB ZGI ZXP AAYXX CITATION ACRZS CGR CUY CVF ECM EIF M~E NPM 7X8 |
| ID | FETCH-LOGICAL-c5667-9fc05d3dae3f7fc25129a5aa1c94297cc1fbe6dc5e0f8f748bca69885a466bc33 |
| ISSN | 0918-8959 |
| IngestDate | Thu Jul 10 22:24:27 EDT 2025 Wed Feb 19 02:34:46 EST 2025 Tue Jul 01 01:17:11 EDT 2025 Thu Apr 24 23:02:31 EDT 2025 Thu Jul 10 16:15:05 EDT 2025 Wed Sep 03 06:30:27 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | Suppl |
| Language | English |
| LinkModel | OpenURL |
| MergedId | FETCHMERGED-LOGICAL-c5667-9fc05d3dae3f7fc25129a5aa1c94297cc1fbe6dc5e0f8f748bca69885a466bc33 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| OpenAccessLink | https://www.jstage.jst.go.jp/article/endocrj1993/46/Suppl/46_Suppl_S17/_article/-char/en |
| PMID | 12054113 |
| PQID | 69530610 |
| PQPubID | 23479 |
| ParticipantIDs | proquest_miscellaneous_69530610 pubmed_primary_12054113 crossref_citationtrail_10_1507_endocrj_46_Suppl_S17 crossref_primary_10_1507_endocrj_46_Suppl_S17 medicalonline_journals_cq6endoc_1999_0046s1_004_5017_5024683382 jstage_primary_article_endocrj1993_46_Suppl_46_Suppl_S17_article_char_en |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 1900 |
| PublicationDate | 1999-00-00 |
| PublicationDateYYYYMMDD | 1999-01-01 |
| PublicationDate_xml | – year: 1999 text: 1999-00-00 |
| PublicationDecade | 1990 |
| PublicationPlace | Japan |
| PublicationPlace_xml | – name: Japan |
| PublicationTitle | ENDOCRINE JOURNAL |
| PublicationTitleAlternate | Endocr J |
| PublicationYear | 1999 |
| Publisher | The Japan Endocrine Society |
| Publisher_xml | – name: The Japan Endocrine Society |
| References | 8) Isozaki O, Tsushima T, Nozoe Y, Demura H, Seki H (1988) Effects of growth hormone on leptin gene expression in rats. Endocr J 45 Suppl: S117-119. 9) Murakami T, Shima K (1995) Cloning of rat obese cDNA and its expression in obese rats. Biochem Biophys Res Commun 209: 944-952. 15) al-Shoumer KA, Anyaoku V, Richmond W, Shonston DG (1997) Elevated leptin concentrations in growth hormone-deficient hypopituitary adults. Clin Endocrinol 47: 153-159. 1) Thorner MO, Vance ML, Horvath E, Kovacs K (1992) The anterior pituitary. In: Wilson JD, Foster DW (eds) Williams Textbook of endocrinology. 8th ed, W.B. Saunders Company, Philadelphia, 221-310. 2) Goodman HM (1968) Multiple effects of growth hormone on lipolysis. Endocrinology 83: 300-308. 4) Deoer H, Block G-J, Van der Veen EA (1995) Clinical aspects of growth hormone deficiency in adults. Endocr Rev 16: 63-86. 6) Ahmad I, Steggles AW, Carrillo AJ, Finkelstein JA (1990) Developmental changes in levels of growth hormone mRNA in Zucker rats. J Cell Biochem 43:59-66. 7) Chua SCN Jr. Chung WK, Wu-Peng XS, Zhang Y, Liu SM, Tartaglia L, Leibel RL (1996) Phenotypes of mouse diabetes and rat fatty due to mutations in the OB (leptin) receptor. Science 271: 994-996. 11) Boni-Schnetzler M, Gosteli-Peter MA, Moritz W, Froesch ER, Zapf J (1996) Reduced ob mRNA in hypophysectomized rats is not restored by growth hormone (GH), but further suppressed by xogenously administered insulin-like growth factor (IGF)-I. Biochem Biophys Res Commun 225: 296-301. 14) Saladin R, De Vos P, Guerre-Millo M, Leturque A, Girard J, Staels B, Auwerx J (1995) Transient increase in obese gene expression after food intake or insulin administration. Nature 377: 527-529. 19) Gill MS, Toogood AA, O'Neill PA, Adams JE, Thorner MO, Shalet SM, Clayton PE (1997) Relationship between growth hormone (GH) status, serum leptin and body composition in healthy and GH deficient elderly subjects. Clin Endocrinol (Oxf) 47: 161-167. 17) Florkowski CM, Collier GR, Zimmet PZ, Livesey JH, Espiner EA, Donald RA (1996) Low-dose growth hormone replacement lowers plasma leptin and fat stores without affecting body mass index in adults with growth hormone deficiency. Clin Endocrinol (Oxf) 45: 769-773. 5) Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM (1994) Positional cloning of the mouse obese gene and its human homologue. Nature 372: 425-432. 18) Limone P, Oleandri SE, Ajmone Catt P, Grottoli S, Frangioni C, Avogadri E, Perrin M, Valetto MR, Maccario M (1997) The inhibitory effect of glucose on growth hormone secretion is lost in obesity but not in hypertension. J Endocrinol Invest 20: 616-620. 16) Nystrom F, Ekman B, Osterlund M, Lindstrom T, Ohman KP, Arngvist HJ (1997) Serum leptin concentrations in a normal population and in GH deficiency: Negative correlation with testosterone in men and effects of GH treatment. Clin Endocrinol (Oxf) 47: 191-198. 20) Carro E, Senaris R, Considine RV, Casanueva FF, Dieguez C (1997) Regulation of in vivo growth hormone secretion by leptin. Endocrinology 138: 2203-2206. 10) Makino R, Sekiya T, Hayashi K (1990) Evaluation of quantitative detection of mRNA by the reverse transcription-polymerase chain reaction. Technique 2: 295-301. 12) De Vos P, Paladin R, Auwerx J, Staels B (1995) Induction of ob gene expression by corticosteroids is accompanied by body weight loss and reduced food intake. J Biol Chem 270: 15958-15961. 13) Buchard C, Despres JP, Mauriege P (1993) Genetic and nongenetic determinants of regional fat distribution. Endocr Rev 14: 72-93. 3) Fain JN, Kovacev VP, Scow RO (1965) Effect of growth hormone and dexamethasone on lipolysis and metabolism in isolated fat cells of the rat. J Biol Chem 240: 3522-3529. |
| References_xml | – reference: 18) Limone P, Oleandri SE, Ajmone Catt P, Grottoli S, Frangioni C, Avogadri E, Perrin M, Valetto MR, Maccario M (1997) The inhibitory effect of glucose on growth hormone secretion is lost in obesity but not in hypertension. J Endocrinol Invest 20: 616-620. – reference: 3) Fain JN, Kovacev VP, Scow RO (1965) Effect of growth hormone and dexamethasone on lipolysis and metabolism in isolated fat cells of the rat. J Biol Chem 240: 3522-3529. – reference: 9) Murakami T, Shima K (1995) Cloning of rat obese cDNA and its expression in obese rats. Biochem Biophys Res Commun 209: 944-952. – reference: 17) Florkowski CM, Collier GR, Zimmet PZ, Livesey JH, Espiner EA, Donald RA (1996) Low-dose growth hormone replacement lowers plasma leptin and fat stores without affecting body mass index in adults with growth hormone deficiency. Clin Endocrinol (Oxf) 45: 769-773. – reference: 7) Chua SCN Jr. Chung WK, Wu-Peng XS, Zhang Y, Liu SM, Tartaglia L, Leibel RL (1996) Phenotypes of mouse diabetes and rat fatty due to mutations in the OB (leptin) receptor. Science 271: 994-996. – reference: 8) Isozaki O, Tsushima T, Nozoe Y, Demura H, Seki H (1988) Effects of growth hormone on leptin gene expression in rats. Endocr J 45 Suppl: S117-119. – reference: 2) Goodman HM (1968) Multiple effects of growth hormone on lipolysis. Endocrinology 83: 300-308. – reference: 11) Boni-Schnetzler M, Gosteli-Peter MA, Moritz W, Froesch ER, Zapf J (1996) Reduced ob mRNA in hypophysectomized rats is not restored by growth hormone (GH), but further suppressed by xogenously administered insulin-like growth factor (IGF)-I. Biochem Biophys Res Commun 225: 296-301. – reference: 6) Ahmad I, Steggles AW, Carrillo AJ, Finkelstein JA (1990) Developmental changes in levels of growth hormone mRNA in Zucker rats. J Cell Biochem 43:59-66. – reference: 14) Saladin R, De Vos P, Guerre-Millo M, Leturque A, Girard J, Staels B, Auwerx J (1995) Transient increase in obese gene expression after food intake or insulin administration. Nature 377: 527-529. – reference: 5) Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM (1994) Positional cloning of the mouse obese gene and its human homologue. Nature 372: 425-432. – reference: 19) Gill MS, Toogood AA, O'Neill PA, Adams JE, Thorner MO, Shalet SM, Clayton PE (1997) Relationship between growth hormone (GH) status, serum leptin and body composition in healthy and GH deficient elderly subjects. Clin Endocrinol (Oxf) 47: 161-167. – reference: 13) Buchard C, Despres JP, Mauriege P (1993) Genetic and nongenetic determinants of regional fat distribution. Endocr Rev 14: 72-93. – reference: 15) al-Shoumer KA, Anyaoku V, Richmond W, Shonston DG (1997) Elevated leptin concentrations in growth hormone-deficient hypopituitary adults. Clin Endocrinol 47: 153-159. – reference: 1) Thorner MO, Vance ML, Horvath E, Kovacs K (1992) The anterior pituitary. In: Wilson JD, Foster DW (eds) Williams Textbook of endocrinology. 8th ed, W.B. Saunders Company, Philadelphia, 221-310. – reference: 16) Nystrom F, Ekman B, Osterlund M, Lindstrom T, Ohman KP, Arngvist HJ (1997) Serum leptin concentrations in a normal population and in GH deficiency: Negative correlation with testosterone in men and effects of GH treatment. Clin Endocrinol (Oxf) 47: 191-198. – reference: 4) Deoer H, Block G-J, Van der Veen EA (1995) Clinical aspects of growth hormone deficiency in adults. Endocr Rev 16: 63-86. – reference: 20) Carro E, Senaris R, Considine RV, Casanueva FF, Dieguez C (1997) Regulation of in vivo growth hormone secretion by leptin. Endocrinology 138: 2203-2206. – reference: 10) Makino R, Sekiya T, Hayashi K (1990) Evaluation of quantitative detection of mRNA by the reverse transcription-polymerase chain reaction. Technique 2: 295-301. – reference: 12) De Vos P, Paladin R, Auwerx J, Staels B (1995) Induction of ob gene expression by corticosteroids is accompanied by body weight loss and reduced food intake. J Biol Chem 270: 15958-15961. |
| SSID | ssj0033543 ssib022572652 ssib044735826 ssib058492669 ssib002822051 ssib000750009 |
| Score | 1.6534377 |
| Snippet | In order to identify the mutual interaction between GH and leptin, we studied the effect of GH on fatty Zucker rats. GH administration at a high dose... In order to identify the mutual interaction between GH and leptin, we studied the effect of GH on fatty Zucker rats. GH administration at a high dose (5.0... |
| SourceID | proquest pubmed crossref medicalonline jstage |
| SourceType | Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | S17 |
| SubjectTerms | Acromegaly - blood Acromegaly - urine Adipose tissue Adipose Tissue - drug effects Adipose Tissue - metabolism Animals Body Composition C-Peptide - urine Female Gene Expression Regulation Growth Hormone - metabolism Growth Hormone - pharmacology Humans Insulin-Like Growth Factor I - metabolism Insulin-Like Growth Factor I - pharmacology Insulin-Like Growth Factor I - urine Leptin Leptin - biosynthesis Leptin - genetics Leptin - metabolism Male ob gene Obese Obesity - metabolism Rats Rats, Wistar Rats, Zucker Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - biosynthesis RNA, Messenger - genetics |
| Title | Interaction between Leptin and Growth Hormone (GH)/IGF-I Axis |
| URI | https://www.jstage.jst.go.jp/article/endocrj1993/46/Suppl/46_Suppl_S17/_article/-char/en http://mol.medicalonline.jp/library/journal/download?GoodsID=cq6endoc/1999/0046s1/004&name=5017-5024e https://www.ncbi.nlm.nih.gov/pubmed/12054113 https://www.proquest.com/docview/69530610 |
| Volume | 46 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| ispartofPNX | Endocrine Journal, 1999, Vol.46(Suppl), pp.S17-S24 |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1bb9MwFLZgIISEEHfCNQ88gKpsSew4zhNCwJqBBkJs0t4sx7Fpx9oO0grYr-f4kjSBTVxe3Cq-xuezc459Lgg9YZmo6kQXkSgqEFBkwqIqpioS1kwyxSbPaFu8o-U-eXOQHawDJ1rrkmW1KU9OtSv5H6rCM6CrsZL9B8p2jcID-A_0hRQoDOlf0dge5_lg363C1ZFRU3Eaxp9AxF5ORhNgSxeOlxyXIPlDfzvj7WhnJL5Pm8HJ_LxeSGMNOOr3bnGzOBEuvvX7TtRvVs1kOhMDRevd6Q_xWXwTg2PWV2q2stGMvCFE7Y3uiv4xIVCPFd5rt98xCR3ZmKO9je-js8D8bUPOrA6GsuM_3CQUPglQkTfD4jCtxzNLpCQFHjJx5qm_OMJus86jC2lOqQlX8fZDd2WEceZUJNsBeztJGMDWad0bb7G-wQFLcvEQuHLjbuHKzN2UOY8lZwsglhHZu4auegkifOHgcB2dU_Mb6NKu15G4ifqoCD0qQoeKEFAROlSEHhXh03H5bMviITR4uIX2t1_vvSwjHyQjksCJ51GhZZzVuBYK61xLw64WIhMikQWwGrmUia4UrWWmYs10TlglBS0YrFFCaSUxvo025tDdXRTGQiVU1gz2fEWAM2eaEJVgJnSGC6pVgHA7T1x6D_ImkMkRN5IkTDT3E80J5RYgHGARoKirdew8qPyhfOlI0JX266stbVRO1zX6VbuSxmIRigfo-YCI3K-ehssv1LbGDdq5OSRqEvPDM_hCQZISyjBmaYAet2TnsO-ayzQxV4tVw2mRgbSdxAG649CwfjkPq3tn5txHl533D3OS9wBtLL-u1EPgbZfVI4vpn_ZApKc |
| linkProvider | Colorado Alliance of Research Libraries |
| 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=Interaction+between+leptin+and+growth+hormone+%28GH%29%2FIGF-I+axis&rft.jtitle=Endocrine+journal&rft.au=Isozaki%2C+O&rft.au=Tsushima%2C+T&rft.au=Miyakawa%2C+M&rft.au=Demura%2C+H&rft.date=1999&rft.issn=0918-8959&rft.volume=46+Suppl&rft.spage=S17&rft_id=info:doi/10.1507%2Fendocrj.46.suppl_s17&rft_id=info%3Apmid%2F12054113&rft.externalDocID=12054113 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0918-8959&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0918-8959&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0918-8959&client=summon |