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Low-dose glucocorticoid treatment affects multiple aspects of intermediary metabolism in healthy humans: a randomised controlled trial
Aim/hypothesis To assess whether low-dose glucocorticoid treatment induces adverse metabolic effects, as is evident for high glucocorticoid doses. Methods In a randomised placebo-controlled double-blind (participants and the investigators who performed the studies and assessed the outcomes were blin...
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Published in: | Diabetologia 2011-08, Vol.54 (8), p.2103-2112 |
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container_title | Diabetologia |
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creator | van Raalte, D. H. Brands, M. van der Zijl, N. J. Muskiet, M. H. Pouwels, P. J. W. Ackermans, M. T. Sauerwein, H. P. Serlie, M. J. Diamant, M. |
description | Aim/hypothesis
To assess whether low-dose glucocorticoid treatment induces adverse metabolic effects, as is evident for high glucocorticoid doses.
Methods
In a randomised placebo-controlled double-blind (participants and the investigators who performed the studies and assessed the outcomes were blinded) dose–response intervention study, 32 healthy men (age 22 ± 3 years; BMI 22.4 ± 1.7 kg/m
2
) were allocated to prednisolone 7.5 mg once daily (
n
= 12), prednisolone 30 mg once daily (
n
= 12), or placebo (
n
= 8) for 2 weeks using block randomisation. Main outcome measures were glucose, lipid and protein metabolism, measured by stable isotopes, before and at 2 weeks of treatment, in the fasted state and during a two-step hyperinsulinaemic clamp conducted in the Clinical Research Unit of the Academic Medical Centre, Amsterdam, the Netherlands
Results
Prednisolone, compared with placebo, dose dependently and significantly increased fasting plasma glucose levels, whereas only prednisolone 30 mg increased fasting insulin levels (29 ± 15 pmol/l). Prednisolone 7.5 mg and prednisolone 30 mg decreased the ability of insulin to suppress endogenous glucose production (by 17 ± 6% and 46 ± 7%, respectively, vs placebo). Peripheral glucose uptake was not reduced by prednisolone 7.5 mg, but was decreased by prednisolone 30 mg by 34 ± 6% (
p
|
doi_str_mv | 10.1007/s00125-011-2174-9 |
format | article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3131514</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2393527901</sourcerecordid><originalsourceid>FETCH-LOGICAL-c498t-d6822933854fae885efec137c040b422c2322cc46ba3616c99de026c9ba245bf3</originalsourceid><addsrcrecordid>eNp1kU2LFDEQhoMo7jj6A7xIEDxG89XptAdBFr9gwIuCt5BOV89kSXfGJL2yf8DfbdoZd_XgJQWpp6reqhehp4y-ZJS2rzKljDeEMkY4ayXp7qENk4ITKrm-jzZrmjCtvl2gRzlfUUpFI9VDdMFZo3jbNBv0cxd_kCFmwPuwuOhiKt5FP-CSwJYJ5oLtOIIrGU9LKP4YANt8_P0RR-znAmmCwdt0gycoto_B56n-4wPYUA43-LBMds6vscXJzkOcfIYBuziXFEOAdZC34TF6MNqQ4ck5btHX9---XH4ku88fPl2-3REnO13IoDTnnRC6kaMFrRuo0phoHZW0l5w7LurjpOqtUEy5rhuA8hp7y2XTj2KL3pz6Hpe-ynZ1v2SDOSY_1Q1MtN78m5n9wezjtRFMsKbedouenxuk-H2BXMxVXNJcNRtdD8pUq1eInSCXYs4JxtsBjJrVOXNyzlTnzOqc6WrNs7-V3Vb8saoCL86Azc6GsV7T-XzHSSF4q9rK8ROXa2reQ7pT-P_pvwCSlrTt</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>875516784</pqid></control><display><type>article</type><title>Low-dose glucocorticoid treatment affects multiple aspects of intermediary metabolism in healthy humans: a randomised controlled trial</title><source>Springer Nature:Jisc Collections:Springer Nature Read and Publish 2023-2025: Springer Reading List</source><creator>van Raalte, D. H. ; Brands, M. ; van der Zijl, N. J. ; Muskiet, M. H. ; Pouwels, P. J. W. ; Ackermans, M. T. ; Sauerwein, H. P. ; Serlie, M. J. ; Diamant, M.</creator><creatorcontrib>van Raalte, D. H. ; Brands, M. ; van der Zijl, N. J. ; Muskiet, M. H. ; Pouwels, P. J. W. ; Ackermans, M. T. ; Sauerwein, H. P. ; Serlie, M. J. ; Diamant, M.</creatorcontrib><description>Aim/hypothesis
To assess whether low-dose glucocorticoid treatment induces adverse metabolic effects, as is evident for high glucocorticoid doses.
Methods
In a randomised placebo-controlled double-blind (participants and the investigators who performed the studies and assessed the outcomes were blinded) dose–response intervention study, 32 healthy men (age 22 ± 3 years; BMI 22.4 ± 1.7 kg/m
2
) were allocated to prednisolone 7.5 mg once daily (
n
= 12), prednisolone 30 mg once daily (
n
= 12), or placebo (
n
= 8) for 2 weeks using block randomisation. Main outcome measures were glucose, lipid and protein metabolism, measured by stable isotopes, before and at 2 weeks of treatment, in the fasted state and during a two-step hyperinsulinaemic clamp conducted in the Clinical Research Unit of the Academic Medical Centre, Amsterdam, the Netherlands
Results
Prednisolone, compared with placebo, dose dependently and significantly increased fasting plasma glucose levels, whereas only prednisolone 30 mg increased fasting insulin levels (29 ± 15 pmol/l). Prednisolone 7.5 mg and prednisolone 30 mg decreased the ability of insulin to suppress endogenous glucose production (by 17 ± 6% and 46 ± 7%, respectively, vs placebo). Peripheral glucose uptake was not reduced by prednisolone 7.5 mg, but was decreased by prednisolone 30 mg by 34 ± 6% (
p
< 0.0001). Compared with placebo, prednisolone treatment tended to decrease lipolysis in the fasted state (
p
= 0.062), but both prednisolone 7.5 mg and prednisolone 30 mg decreased insulin-mediated suppression of lipolysis by 11 ± 5% and 34 ± 6%, respectively. Finally, prednisolone treatment increased whole-body proteolysis during hyperinsulinaemia, which tended to be driven by prednisolone 30 mg (5 ± 2%;
p
= 0.06). No side effects were reported by the study participants. All participants completed the study and were analysed.
Conclusions/interpretation
Not only at high doses but also at low doses, glucocorticoid therapy impaired intermediary metabolism by interfering with the metabolic actions of insulin on liver and adipose tissue. These data indicate that even low-dose glucocorticoids may impair glucose tolerance when administered chronically.
Trial registration:
ISRCTN83991850
Funding:
The study was funded by the Dutch Top Institute Pharma T1-106.</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-011-2174-9</identifier><identifier>PMID: 21562755</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Adult ; Biological and medical sciences ; Biological Transport - drug effects ; Blood Glucose - drug effects ; Body fat ; Diabetes ; Diabetes. Impaired glucose tolerance ; Disease ; Double-Blind Method ; Endocrine pancreas. Apud cells (diseases) ; Endocrinology ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Glucocorticoids - administration & dosage ; Glucocorticoids - adverse effects ; Glucocorticoids - pharmacology ; Glucose ; Human Physiology ; Humans ; Insulin - metabolism ; Insulin resistance ; Internal Medicine ; Lipolysis - drug effects ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Metabolic disorders ; Musculoskeletal system ; Prednisolone - administration & dosage ; Prednisolone - adverse effects ; Prednisolone - pharmacology ; Proteins ; Young Adult</subject><ispartof>Diabetologia, 2011-08, Vol.54 (8), p.2103-2112</ispartof><rights>The Author(s) 2011</rights><rights>2015 INIST-CNRS</rights><rights>Springer-Verlag 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c498t-d6822933854fae885efec137c040b422c2322cc46ba3616c99de026c9ba245bf3</citedby><cites>FETCH-LOGICAL-c498t-d6822933854fae885efec137c040b422c2322cc46ba3616c99de026c9ba245bf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24332767$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21562755$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van Raalte, D. H.</creatorcontrib><creatorcontrib>Brands, M.</creatorcontrib><creatorcontrib>van der Zijl, N. J.</creatorcontrib><creatorcontrib>Muskiet, M. H.</creatorcontrib><creatorcontrib>Pouwels, P. J. W.</creatorcontrib><creatorcontrib>Ackermans, M. T.</creatorcontrib><creatorcontrib>Sauerwein, H. P.</creatorcontrib><creatorcontrib>Serlie, M. J.</creatorcontrib><creatorcontrib>Diamant, M.</creatorcontrib><title>Low-dose glucocorticoid treatment affects multiple aspects of intermediary metabolism in healthy humans: a randomised controlled trial</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><addtitle>Diabetologia</addtitle><description>Aim/hypothesis
To assess whether low-dose glucocorticoid treatment induces adverse metabolic effects, as is evident for high glucocorticoid doses.
Methods
In a randomised placebo-controlled double-blind (participants and the investigators who performed the studies and assessed the outcomes were blinded) dose–response intervention study, 32 healthy men (age 22 ± 3 years; BMI 22.4 ± 1.7 kg/m
2
) were allocated to prednisolone 7.5 mg once daily (
n
= 12), prednisolone 30 mg once daily (
n
= 12), or placebo (
n
= 8) for 2 weeks using block randomisation. Main outcome measures were glucose, lipid and protein metabolism, measured by stable isotopes, before and at 2 weeks of treatment, in the fasted state and during a two-step hyperinsulinaemic clamp conducted in the Clinical Research Unit of the Academic Medical Centre, Amsterdam, the Netherlands
Results
Prednisolone, compared with placebo, dose dependently and significantly increased fasting plasma glucose levels, whereas only prednisolone 30 mg increased fasting insulin levels (29 ± 15 pmol/l). Prednisolone 7.5 mg and prednisolone 30 mg decreased the ability of insulin to suppress endogenous glucose production (by 17 ± 6% and 46 ± 7%, respectively, vs placebo). Peripheral glucose uptake was not reduced by prednisolone 7.5 mg, but was decreased by prednisolone 30 mg by 34 ± 6% (
p
< 0.0001). Compared with placebo, prednisolone treatment tended to decrease lipolysis in the fasted state (
p
= 0.062), but both prednisolone 7.5 mg and prednisolone 30 mg decreased insulin-mediated suppression of lipolysis by 11 ± 5% and 34 ± 6%, respectively. Finally, prednisolone treatment increased whole-body proteolysis during hyperinsulinaemia, which tended to be driven by prednisolone 30 mg (5 ± 2%;
p
= 0.06). No side effects were reported by the study participants. All participants completed the study and were analysed.
Conclusions/interpretation
Not only at high doses but also at low doses, glucocorticoid therapy impaired intermediary metabolism by interfering with the metabolic actions of insulin on liver and adipose tissue. These data indicate that even low-dose glucocorticoids may impair glucose tolerance when administered chronically.
Trial registration:
ISRCTN83991850
Funding:
The study was funded by the Dutch Top Institute Pharma T1-106.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Biological Transport - drug effects</subject><subject>Blood Glucose - drug effects</subject><subject>Body fat</subject><subject>Diabetes</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Disease</subject><subject>Double-Blind Method</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinology</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Glucocorticoids - administration & dosage</subject><subject>Glucocorticoids - adverse effects</subject><subject>Glucocorticoids - pharmacology</subject><subject>Glucose</subject><subject>Human Physiology</subject><subject>Humans</subject><subject>Insulin - metabolism</subject><subject>Insulin resistance</subject><subject>Internal Medicine</subject><subject>Lipolysis - drug effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Metabolic disorders</subject><subject>Musculoskeletal system</subject><subject>Prednisolone - administration & dosage</subject><subject>Prednisolone - adverse effects</subject><subject>Prednisolone - pharmacology</subject><subject>Proteins</subject><subject>Young Adult</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNp1kU2LFDEQhoMo7jj6A7xIEDxG89XptAdBFr9gwIuCt5BOV89kSXfGJL2yf8DfbdoZd_XgJQWpp6reqhehp4y-ZJS2rzKljDeEMkY4ayXp7qENk4ITKrm-jzZrmjCtvl2gRzlfUUpFI9VDdMFZo3jbNBv0cxd_kCFmwPuwuOhiKt5FP-CSwJYJ5oLtOIIrGU9LKP4YANt8_P0RR-znAmmCwdt0gycoto_B56n-4wPYUA43-LBMds6vscXJzkOcfIYBuziXFEOAdZC34TF6MNqQ4ck5btHX9---XH4ku88fPl2-3REnO13IoDTnnRC6kaMFrRuo0phoHZW0l5w7LurjpOqtUEy5rhuA8hp7y2XTj2KL3pz6Hpe-ynZ1v2SDOSY_1Q1MtN78m5n9wezjtRFMsKbedouenxuk-H2BXMxVXNJcNRtdD8pUq1eInSCXYs4JxtsBjJrVOXNyzlTnzOqc6WrNs7-V3Vb8saoCL86Azc6GsV7T-XzHSSF4q9rK8ROXa2reQ7pT-P_pvwCSlrTt</recordid><startdate>20110801</startdate><enddate>20110801</enddate><creator>van Raalte, D. H.</creator><creator>Brands, M.</creator><creator>van der Zijl, N. J.</creator><creator>Muskiet, M. H.</creator><creator>Pouwels, P. J. W.</creator><creator>Ackermans, M. T.</creator><creator>Sauerwein, H. P.</creator><creator>Serlie, M. J.</creator><creator>Diamant, M.</creator><general>Springer-Verlag</general><general>Springer</general><general>Springer Nature B.V</general><scope>C6C</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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20110801</creationdate><title>Low-dose glucocorticoid treatment affects multiple aspects of intermediary metabolism in healthy humans: a randomised controlled trial</title><author>van Raalte, D. H. ; Brands, M. ; van der Zijl, N. J. ; Muskiet, M. H. ; Pouwels, P. J. W. ; Ackermans, M. T. ; Sauerwein, H. P. ; Serlie, M. J. ; Diamant, M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c498t-d6822933854fae885efec137c040b422c2322cc46ba3616c99de026c9ba245bf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Biological Transport - drug effects</topic><topic>Blood Glucose - drug effects</topic><topic>Body fat</topic><topic>Diabetes</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Disease</topic><topic>Double-Blind Method</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinology</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Glucocorticoids - administration & dosage</topic><topic>Glucocorticoids - adverse effects</topic><topic>Glucocorticoids - pharmacology</topic><topic>Glucose</topic><topic>Human Physiology</topic><topic>Humans</topic><topic>Insulin - metabolism</topic><topic>Insulin resistance</topic><topic>Internal Medicine</topic><topic>Lipolysis - drug effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Metabolic disorders</topic><topic>Musculoskeletal system</topic><topic>Prednisolone - administration & dosage</topic><topic>Prednisolone - adverse effects</topic><topic>Prednisolone - pharmacology</topic><topic>Proteins</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>van Raalte, D. H.</creatorcontrib><creatorcontrib>Brands, M.</creatorcontrib><creatorcontrib>van der Zijl, N. J.</creatorcontrib><creatorcontrib>Muskiet, M. H.</creatorcontrib><creatorcontrib>Pouwels, P. J. W.</creatorcontrib><creatorcontrib>Ackermans, M. T.</creatorcontrib><creatorcontrib>Sauerwein, H. P.</creatorcontrib><creatorcontrib>Serlie, M. J.</creatorcontrib><creatorcontrib>Diamant, M.</creatorcontrib><collection>Springer Nature OA Free Journals</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>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>van Raalte, D. H.</au><au>Brands, M.</au><au>van der Zijl, N. J.</au><au>Muskiet, M. H.</au><au>Pouwels, P. J. W.</au><au>Ackermans, M. T.</au><au>Sauerwein, H. P.</au><au>Serlie, M. J.</au><au>Diamant, M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Low-dose glucocorticoid treatment affects multiple aspects of intermediary metabolism in healthy humans: a randomised controlled trial</atitle><jtitle>Diabetologia</jtitle><stitle>Diabetologia</stitle><addtitle>Diabetologia</addtitle><date>2011-08-01</date><risdate>2011</risdate><volume>54</volume><issue>8</issue><spage>2103</spage><epage>2112</epage><pages>2103-2112</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Aim/hypothesis
To assess whether low-dose glucocorticoid treatment induces adverse metabolic effects, as is evident for high glucocorticoid doses.
Methods
In a randomised placebo-controlled double-blind (participants and the investigators who performed the studies and assessed the outcomes were blinded) dose–response intervention study, 32 healthy men (age 22 ± 3 years; BMI 22.4 ± 1.7 kg/m
2
) were allocated to prednisolone 7.5 mg once daily (
n
= 12), prednisolone 30 mg once daily (
n
= 12), or placebo (
n
= 8) for 2 weeks using block randomisation. Main outcome measures were glucose, lipid and protein metabolism, measured by stable isotopes, before and at 2 weeks of treatment, in the fasted state and during a two-step hyperinsulinaemic clamp conducted in the Clinical Research Unit of the Academic Medical Centre, Amsterdam, the Netherlands
Results
Prednisolone, compared with placebo, dose dependently and significantly increased fasting plasma glucose levels, whereas only prednisolone 30 mg increased fasting insulin levels (29 ± 15 pmol/l). Prednisolone 7.5 mg and prednisolone 30 mg decreased the ability of insulin to suppress endogenous glucose production (by 17 ± 6% and 46 ± 7%, respectively, vs placebo). Peripheral glucose uptake was not reduced by prednisolone 7.5 mg, but was decreased by prednisolone 30 mg by 34 ± 6% (
p
< 0.0001). Compared with placebo, prednisolone treatment tended to decrease lipolysis in the fasted state (
p
= 0.062), but both prednisolone 7.5 mg and prednisolone 30 mg decreased insulin-mediated suppression of lipolysis by 11 ± 5% and 34 ± 6%, respectively. Finally, prednisolone treatment increased whole-body proteolysis during hyperinsulinaemia, which tended to be driven by prednisolone 30 mg (5 ± 2%;
p
= 0.06). No side effects were reported by the study participants. All participants completed the study and were analysed.
Conclusions/interpretation
Not only at high doses but also at low doses, glucocorticoid therapy impaired intermediary metabolism by interfering with the metabolic actions of insulin on liver and adipose tissue. These data indicate that even low-dose glucocorticoids may impair glucose tolerance when administered chronically.
Trial registration:
ISRCTN83991850
Funding:
The study was funded by the Dutch Top Institute Pharma T1-106.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>21562755</pmid><doi>10.1007/s00125-011-2174-9</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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source | Springer Nature:Jisc Collections:Springer Nature Read and Publish 2023-2025: Springer Reading List |
subjects | Adult Biological and medical sciences Biological Transport - drug effects Blood Glucose - drug effects Body fat Diabetes Diabetes. Impaired glucose tolerance Disease Double-Blind Method Endocrine pancreas. Apud cells (diseases) Endocrinology Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Glucocorticoids - administration & dosage Glucocorticoids - adverse effects Glucocorticoids - pharmacology Glucose Human Physiology Humans Insulin - metabolism Insulin resistance Internal Medicine Lipolysis - drug effects Male Medical sciences Medicine Medicine & Public Health Metabolic Diseases Metabolic disorders Musculoskeletal system Prednisolone - administration & dosage Prednisolone - adverse effects Prednisolone - pharmacology Proteins Young Adult |
title | Low-dose glucocorticoid treatment affects multiple aspects of intermediary metabolism in healthy humans: a randomised controlled trial |
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