Ghrelin does not mediate the somatotroph and corticotroph responses to the stimulatory effect of glucagon or insulin-induced hypoglycaemia in humans
Summary objective Acylated ghrelin, a gastric peptide, possesses a potent GH‐ but also significant ACTH/cortisol‐releasing activity mediated by the activation of GH secretagogue receptors (GHS‐R) at the hypothalamus–pituitary level. The physiological role of ghrelin in the control of somatotroph an...
Gespeichert in:
| Veröffentlicht in: | Clinical endocrinology (Oxford) 2004-06, Vol.60 (6), p.699-704 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 704 |
|---|---|
| container_issue | 6 |
| container_start_page | 699 |
| container_title | Clinical endocrinology (Oxford) |
| container_volume | 60 |
| creator | Broglio, Fabio Prodam, Flavia Gottero, Cristina Destefanis, Silvia Me, Elisa Riganti, Fabrizio Giordano, Roberta Picu, Andreea Balbo, Marcella Van der Lely, Aart Jan Ghigo, Ezio Arvat, Emanuela |
| description | Summary
objective Acylated ghrelin, a gastric peptide, possesses a potent GH‐ but also significant ACTH/cortisol‐releasing activity mediated by the activation of GH secretagogue receptors (GHS‐R) at the hypothalamus–pituitary level. The physiological role of ghrelin in the control of somatotroph and corticotroph function is, however, largely unclear. Glucagon is known to induce a clear increase of GH, ACTH and cortisol levels in humans, at least after intramuscular administration. In fact, glucagon is considered to be a classical alternative to insulin‐induced hypoglycaemia (ITT) for the combined evaluation of the function of GH and the hypothalamus–pituitary–adrenal (HPA) axis. We aimed to clarify whether ghrelin mediate the GH and corticotroph responses to intramuscular glucagon or ITT, which has recently been reported able to induce a surprising ghrelin decrease.
subjects To this aim we enrolled six normal young male subjects [age (mean ± SD): 29·0 ± 8·0 years, body mass index (BMI) 21·9 ± 2·5 kg/m2].
design and measurements In all the subjects we studied ghrelin, GH, ACTH, cortisol and glucose levels after glucagon (GLU; 0·017 mg/kg intramuscularly), ITT (0·1 IU/kg insulin intravenously) or saline administration.
results Saline infusion was not followed by any significant variation in ghrelin, GH and glucose levels while ACTH and cortisol showed the expected spontaneous morning trend toward a decrease. GLU administration increased (P |
| doi_str_mv | 10.1111/j.1365-2265.2004.02038.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_198822607</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>656520631</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4608-930ab7cda5792845d9f1f2dc00db2a4bfc492d9bed085fae0e9abca8480d3a363</originalsourceid><addsrcrecordid>eNqNkc1u1DAUhS0EotPCKyALiWXCTZwfZ8ECDWWKqMoGBGJjObYz8ZDEwXbE5D144DokKiy5G1u-37nXOgchnECchHp9ihNS5FGaFnmcAmQxpEBofH6Edg-Nx2gHBCCCosgu0KVzJwDIKZRP0UWSJwUJtUO_D61VnR6wNMrhwXjcK6m5V9i3CjvTc2-8NWOL-SCxMNZrsT1Y5UYzuCDzZqW97qcuCOyMVdMo4bFp8LGbBD-aARuL9eCmsCzSg5yEkridR3PsZsFVr3no4nbq-eCeoScN75x6vp1X6Mv768_7m-j20-HD_u1tJLICaFQR4HUpJM_LKqVZLqsmaVIpAGSd8qxuRFalsqqVBJo3XIGqeC04zShIwklBrtDLde5ozc9JOc9OZrJDWMmSitLgIpQBoiskrHHOqoaNVvfcziwBtqTBTmwxnS2msyUN9icNdg7SF9v8qQ62_hVu9gfg1QZwJ3jXWD4I7f7hyopCmgfuzcr90p2a__sDbH99t9yCPlr12nl1ftBz-4MVJSlz9vXuwEry_Rt9d_OREXIPr6K4sw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>198822607</pqid></control><display><type>article</type><title>Ghrelin does not mediate the somatotroph and corticotroph responses to the stimulatory effect of glucagon or insulin-induced hypoglycaemia in humans</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Broglio, Fabio ; Prodam, Flavia ; Gottero, Cristina ; Destefanis, Silvia ; Me, Elisa ; Riganti, Fabrizio ; Giordano, Roberta ; Picu, Andreea ; Balbo, Marcella ; Van der Lely, Aart Jan ; Ghigo, Ezio ; Arvat, Emanuela</creator><creatorcontrib>Broglio, Fabio ; Prodam, Flavia ; Gottero, Cristina ; Destefanis, Silvia ; Me, Elisa ; Riganti, Fabrizio ; Giordano, Roberta ; Picu, Andreea ; Balbo, Marcella ; Van der Lely, Aart Jan ; Ghigo, Ezio ; Arvat, Emanuela</creatorcontrib><description>Summary
objective Acylated ghrelin, a gastric peptide, possesses a potent GH‐ but also significant ACTH/cortisol‐releasing activity mediated by the activation of GH secretagogue receptors (GHS‐R) at the hypothalamus–pituitary level. The physiological role of ghrelin in the control of somatotroph and corticotroph function is, however, largely unclear. Glucagon is known to induce a clear increase of GH, ACTH and cortisol levels in humans, at least after intramuscular administration. In fact, glucagon is considered to be a classical alternative to insulin‐induced hypoglycaemia (ITT) for the combined evaluation of the function of GH and the hypothalamus–pituitary–adrenal (HPA) axis. We aimed to clarify whether ghrelin mediate the GH and corticotroph responses to intramuscular glucagon or ITT, which has recently been reported able to induce a surprising ghrelin decrease.
subjects To this aim we enrolled six normal young male subjects [age (mean ± SD): 29·0 ± 8·0 years, body mass index (BMI) 21·9 ± 2·5 kg/m2].
design and measurements In all the subjects we studied ghrelin, GH, ACTH, cortisol and glucose levels after glucagon (GLU; 0·017 mg/kg intramuscularly), ITT (0·1 IU/kg insulin intravenously) or saline administration.
results Saline infusion was not followed by any significant variation in ghrelin, GH and glucose levels while ACTH and cortisol showed the expected spontaneous morning trend toward a decrease. GLU administration increased (P < 0·01) circulating GH, ACTH and cortisol as well as insulin and glucose levels. ITT induced an obvious increase (P < 0·01) of GH, ACTH and cortisol levels. The ITT‐induced increases in GH and ACTH, but not cortisol, levels were higher (P < 0·01) than those after GLU. Circulating ghrelin levels were not modified by GLU. On the other hand, ghrelin levels underwent a transient reduction (P < 0·01) after insulin‐induced hypoglycaemia.
conclusions Ghrelin does not mediate the GH and ACTH responses to glucagon or to the ITT. In fact, ghrelin levels are not modified at all by glucagon and transiently decrease during the ITT. These findings support the assumption that ghrelin does not play a major role in the physiological control of somatotroph and corticotroph function.</description><identifier>ISSN: 0300-0664</identifier><identifier>EISSN: 1365-2265</identifier><identifier>DOI: 10.1111/j.1365-2265.2004.02038.x</identifier><identifier>PMID: 15163333</identifier><identifier>CODEN: CLECAP</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Adrenocorticotropic Hormone - blood ; Adrenocorticotropic Hormone - secretion ; Adult ; Biological and medical sciences ; Blood Glucose - analysis ; Endocrinopathies ; Fundamental and applied biological sciences. Psychology ; Ghrelin ; Glucagon ; Growth Hormone - blood ; Growth Hormone - secretion ; Humans ; Hydrocortisone - blood ; Hypoglycemia - chemically induced ; Hypoglycemia - physiopathology ; Hypothalamo-Hypophyseal System - drug effects ; Hypothalamo-Hypophyseal System - physiopathology ; Insulin ; Male ; Medical sciences ; Peptide Hormones - blood ; Pituitary-Adrenal System - drug effects ; Pituitary-Adrenal System - physiopathology ; Vertebrates: endocrinology</subject><ispartof>Clinical endocrinology (Oxford), 2004-06, Vol.60 (6), p.699-704</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright Blackwell Scientific Publications Ltd. Jun 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4608-930ab7cda5792845d9f1f2dc00db2a4bfc492d9bed085fae0e9abca8480d3a363</citedby><cites>FETCH-LOGICAL-c4608-930ab7cda5792845d9f1f2dc00db2a4bfc492d9bed085fae0e9abca8480d3a363</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2265.2004.02038.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2265.2004.02038.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27902,27903,45552,45553</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15798025$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15163333$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Broglio, Fabio</creatorcontrib><creatorcontrib>Prodam, Flavia</creatorcontrib><creatorcontrib>Gottero, Cristina</creatorcontrib><creatorcontrib>Destefanis, Silvia</creatorcontrib><creatorcontrib>Me, Elisa</creatorcontrib><creatorcontrib>Riganti, Fabrizio</creatorcontrib><creatorcontrib>Giordano, Roberta</creatorcontrib><creatorcontrib>Picu, Andreea</creatorcontrib><creatorcontrib>Balbo, Marcella</creatorcontrib><creatorcontrib>Van der Lely, Aart Jan</creatorcontrib><creatorcontrib>Ghigo, Ezio</creatorcontrib><creatorcontrib>Arvat, Emanuela</creatorcontrib><title>Ghrelin does not mediate the somatotroph and corticotroph responses to the stimulatory effect of glucagon or insulin-induced hypoglycaemia in humans</title><title>Clinical endocrinology (Oxford)</title><addtitle>Clin Endocrinol (Oxf)</addtitle><description>Summary
objective Acylated ghrelin, a gastric peptide, possesses a potent GH‐ but also significant ACTH/cortisol‐releasing activity mediated by the activation of GH secretagogue receptors (GHS‐R) at the hypothalamus–pituitary level. The physiological role of ghrelin in the control of somatotroph and corticotroph function is, however, largely unclear. Glucagon is known to induce a clear increase of GH, ACTH and cortisol levels in humans, at least after intramuscular administration. In fact, glucagon is considered to be a classical alternative to insulin‐induced hypoglycaemia (ITT) for the combined evaluation of the function of GH and the hypothalamus–pituitary–adrenal (HPA) axis. We aimed to clarify whether ghrelin mediate the GH and corticotroph responses to intramuscular glucagon or ITT, which has recently been reported able to induce a surprising ghrelin decrease.
subjects To this aim we enrolled six normal young male subjects [age (mean ± SD): 29·0 ± 8·0 years, body mass index (BMI) 21·9 ± 2·5 kg/m2].
design and measurements In all the subjects we studied ghrelin, GH, ACTH, cortisol and glucose levels after glucagon (GLU; 0·017 mg/kg intramuscularly), ITT (0·1 IU/kg insulin intravenously) or saline administration.
results Saline infusion was not followed by any significant variation in ghrelin, GH and glucose levels while ACTH and cortisol showed the expected spontaneous morning trend toward a decrease. GLU administration increased (P < 0·01) circulating GH, ACTH and cortisol as well as insulin and glucose levels. ITT induced an obvious increase (P < 0·01) of GH, ACTH and cortisol levels. The ITT‐induced increases in GH and ACTH, but not cortisol, levels were higher (P < 0·01) than those after GLU. Circulating ghrelin levels were not modified by GLU. On the other hand, ghrelin levels underwent a transient reduction (P < 0·01) after insulin‐induced hypoglycaemia.
conclusions Ghrelin does not mediate the GH and ACTH responses to glucagon or to the ITT. In fact, ghrelin levels are not modified at all by glucagon and transiently decrease during the ITT. These findings support the assumption that ghrelin does not play a major role in the physiological control of somatotroph and corticotroph function.</description><subject>Adrenocorticotropic Hormone - blood</subject><subject>Adrenocorticotropic Hormone - secretion</subject><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - analysis</subject><subject>Endocrinopathies</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Ghrelin</subject><subject>Glucagon</subject><subject>Growth Hormone - blood</subject><subject>Growth Hormone - secretion</subject><subject>Humans</subject><subject>Hydrocortisone - blood</subject><subject>Hypoglycemia - chemically induced</subject><subject>Hypoglycemia - physiopathology</subject><subject>Hypothalamo-Hypophyseal System - drug effects</subject><subject>Hypothalamo-Hypophyseal System - physiopathology</subject><subject>Insulin</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Peptide Hormones - blood</subject><subject>Pituitary-Adrenal System - drug effects</subject><subject>Pituitary-Adrenal System - physiopathology</subject><subject>Vertebrates: endocrinology</subject><issn>0300-0664</issn><issn>1365-2265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhS0EotPCKyALiWXCTZwfZ8ECDWWKqMoGBGJjObYz8ZDEwXbE5D144DokKiy5G1u-37nXOgchnECchHp9ihNS5FGaFnmcAmQxpEBofH6Edg-Nx2gHBCCCosgu0KVzJwDIKZRP0UWSJwUJtUO_D61VnR6wNMrhwXjcK6m5V9i3CjvTc2-8NWOL-SCxMNZrsT1Y5UYzuCDzZqW97qcuCOyMVdMo4bFp8LGbBD-aARuL9eCmsCzSg5yEkridR3PsZsFVr3no4nbq-eCeoScN75x6vp1X6Mv768_7m-j20-HD_u1tJLICaFQR4HUpJM_LKqVZLqsmaVIpAGSd8qxuRFalsqqVBJo3XIGqeC04zShIwklBrtDLde5ozc9JOc9OZrJDWMmSitLgIpQBoiskrHHOqoaNVvfcziwBtqTBTmwxnS2msyUN9icNdg7SF9v8qQ62_hVu9gfg1QZwJ3jXWD4I7f7hyopCmgfuzcr90p2a__sDbH99t9yCPlr12nl1ftBz-4MVJSlz9vXuwEry_Rt9d_OREXIPr6K4sw</recordid><startdate>200406</startdate><enddate>200406</enddate><creator>Broglio, Fabio</creator><creator>Prodam, Flavia</creator><creator>Gottero, Cristina</creator><creator>Destefanis, Silvia</creator><creator>Me, Elisa</creator><creator>Riganti, Fabrizio</creator><creator>Giordano, Roberta</creator><creator>Picu, Andreea</creator><creator>Balbo, Marcella</creator><creator>Van der Lely, Aart Jan</creator><creator>Ghigo, Ezio</creator><creator>Arvat, Emanuela</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>K9.</scope><scope>NAPCQ</scope></search><sort><creationdate>200406</creationdate><title>Ghrelin does not mediate the somatotroph and corticotroph responses to the stimulatory effect of glucagon or insulin-induced hypoglycaemia in humans</title><author>Broglio, Fabio ; Prodam, Flavia ; Gottero, Cristina ; Destefanis, Silvia ; Me, Elisa ; Riganti, Fabrizio ; Giordano, Roberta ; Picu, Andreea ; Balbo, Marcella ; Van der Lely, Aart Jan ; Ghigo, Ezio ; Arvat, Emanuela</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4608-930ab7cda5792845d9f1f2dc00db2a4bfc492d9bed085fae0e9abca8480d3a363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adrenocorticotropic Hormone - blood</topic><topic>Adrenocorticotropic Hormone - secretion</topic><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - analysis</topic><topic>Endocrinopathies</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Ghrelin</topic><topic>Glucagon</topic><topic>Growth Hormone - blood</topic><topic>Growth Hormone - secretion</topic><topic>Humans</topic><topic>Hydrocortisone - blood</topic><topic>Hypoglycemia - chemically induced</topic><topic>Hypoglycemia - physiopathology</topic><topic>Hypothalamo-Hypophyseal System - drug effects</topic><topic>Hypothalamo-Hypophyseal System - physiopathology</topic><topic>Insulin</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Peptide Hormones - blood</topic><topic>Pituitary-Adrenal System - drug effects</topic><topic>Pituitary-Adrenal System - physiopathology</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Broglio, Fabio</creatorcontrib><creatorcontrib>Prodam, Flavia</creatorcontrib><creatorcontrib>Gottero, Cristina</creatorcontrib><creatorcontrib>Destefanis, Silvia</creatorcontrib><creatorcontrib>Me, Elisa</creatorcontrib><creatorcontrib>Riganti, Fabrizio</creatorcontrib><creatorcontrib>Giordano, Roberta</creatorcontrib><creatorcontrib>Picu, Andreea</creatorcontrib><creatorcontrib>Balbo, Marcella</creatorcontrib><creatorcontrib>Van der Lely, Aart Jan</creatorcontrib><creatorcontrib>Ghigo, Ezio</creatorcontrib><creatorcontrib>Arvat, Emanuela</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><jtitle>Clinical endocrinology (Oxford)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Broglio, Fabio</au><au>Prodam, Flavia</au><au>Gottero, Cristina</au><au>Destefanis, Silvia</au><au>Me, Elisa</au><au>Riganti, Fabrizio</au><au>Giordano, Roberta</au><au>Picu, Andreea</au><au>Balbo, Marcella</au><au>Van der Lely, Aart Jan</au><au>Ghigo, Ezio</au><au>Arvat, Emanuela</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ghrelin does not mediate the somatotroph and corticotroph responses to the stimulatory effect of glucagon or insulin-induced hypoglycaemia in humans</atitle><jtitle>Clinical endocrinology (Oxford)</jtitle><addtitle>Clin Endocrinol (Oxf)</addtitle><date>2004-06</date><risdate>2004</risdate><volume>60</volume><issue>6</issue><spage>699</spage><epage>704</epage><pages>699-704</pages><issn>0300-0664</issn><eissn>1365-2265</eissn><coden>CLECAP</coden><abstract>Summary
objective Acylated ghrelin, a gastric peptide, possesses a potent GH‐ but also significant ACTH/cortisol‐releasing activity mediated by the activation of GH secretagogue receptors (GHS‐R) at the hypothalamus–pituitary level. The physiological role of ghrelin in the control of somatotroph and corticotroph function is, however, largely unclear. Glucagon is known to induce a clear increase of GH, ACTH and cortisol levels in humans, at least after intramuscular administration. In fact, glucagon is considered to be a classical alternative to insulin‐induced hypoglycaemia (ITT) for the combined evaluation of the function of GH and the hypothalamus–pituitary–adrenal (HPA) axis. We aimed to clarify whether ghrelin mediate the GH and corticotroph responses to intramuscular glucagon or ITT, which has recently been reported able to induce a surprising ghrelin decrease.
subjects To this aim we enrolled six normal young male subjects [age (mean ± SD): 29·0 ± 8·0 years, body mass index (BMI) 21·9 ± 2·5 kg/m2].
design and measurements In all the subjects we studied ghrelin, GH, ACTH, cortisol and glucose levels after glucagon (GLU; 0·017 mg/kg intramuscularly), ITT (0·1 IU/kg insulin intravenously) or saline administration.
results Saline infusion was not followed by any significant variation in ghrelin, GH and glucose levels while ACTH and cortisol showed the expected spontaneous morning trend toward a decrease. GLU administration increased (P < 0·01) circulating GH, ACTH and cortisol as well as insulin and glucose levels. ITT induced an obvious increase (P < 0·01) of GH, ACTH and cortisol levels. The ITT‐induced increases in GH and ACTH, but not cortisol, levels were higher (P < 0·01) than those after GLU. Circulating ghrelin levels were not modified by GLU. On the other hand, ghrelin levels underwent a transient reduction (P < 0·01) after insulin‐induced hypoglycaemia.
conclusions Ghrelin does not mediate the GH and ACTH responses to glucagon or to the ITT. In fact, ghrelin levels are not modified at all by glucagon and transiently decrease during the ITT. These findings support the assumption that ghrelin does not play a major role in the physiological control of somatotroph and corticotroph function.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>15163333</pmid><doi>10.1111/j.1365-2265.2004.02038.x</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0300-0664 |
| ispartof | Clinical endocrinology (Oxford), 2004-06, Vol.60 (6), p.699-704 |
| issn | 0300-0664 1365-2265 |
| language | eng |
| recordid | cdi_proquest_journals_198822607 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Adrenocorticotropic Hormone - blood Adrenocorticotropic Hormone - secretion Adult Biological and medical sciences Blood Glucose - analysis Endocrinopathies Fundamental and applied biological sciences. Psychology Ghrelin Glucagon Growth Hormone - blood Growth Hormone - secretion Humans Hydrocortisone - blood Hypoglycemia - chemically induced Hypoglycemia - physiopathology Hypothalamo-Hypophyseal System - drug effects Hypothalamo-Hypophyseal System - physiopathology Insulin Male Medical sciences Peptide Hormones - blood Pituitary-Adrenal System - drug effects Pituitary-Adrenal System - physiopathology Vertebrates: endocrinology |
| title | Ghrelin does not mediate the somatotroph and corticotroph responses to the stimulatory effect of glucagon or insulin-induced hypoglycaemia in humans |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T09%3A31%3A43IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Ghrelin%20does%20not%20mediate%20the%20somatotroph%20and%20corticotroph%20responses%20to%20the%20stimulatory%20effect%20of%20glucagon%20or%20insulin-induced%20hypoglycaemia%20in%20humans&rft.jtitle=Clinical%20endocrinology%20(Oxford)&rft.au=Broglio,%20Fabio&rft.date=2004-06&rft.volume=60&rft.issue=6&rft.spage=699&rft.epage=704&rft.pages=699-704&rft.issn=0300-0664&rft.eissn=1365-2265&rft.coden=CLECAP&rft_id=info:doi/10.1111/j.1365-2265.2004.02038.x&rft_dat=%3Cproquest_cross%3E656520631%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=198822607&rft_id=info:pmid/15163333&rfr_iscdi=true |