Effects of fasting and glucocorticoids on hepatic gluconeogenesis assessed using two independent methods in vivo
1 Department of Surgery, Vanderbilt University, and the Nashville VA Medical Center; 2 Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee 37232; and 3 Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, New York, New...
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| Veröffentlicht in: | American journal of physiology: endocrinology and metabolism 2002-11, Vol.283 (5), p.E946-E957 |
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| creator | Goldstein, Richard E Rossetti, Luciano Palmer, Brett A. J Liu, Rong Massillon, Duna Scott, Melanie Neal, Doss Williams, Phillip Peeler, Benjamin Cherrington, Alan D |
| description | 1 Department of Surgery, Vanderbilt University, and
the Nashville VA Medical Center; 2 Department of
Molecular Physiology and Biophysics, Vanderbilt University,
Nashville, Tennessee 37232; and 3 Division of
Endocrinology, Department of Medicine, Albert Einstein College of
Medicine, New York, New York 10461
The purpose of this study was to
compare the assessment of gluconeogenesis (GNG) in the overnight- and
prolonged-fasted states and during chronic hypercortisolemia using the
arteriovenous difference and
[ 14 C]phospho enol pyruvate-liver biopsy
techniques as well as a combination of the two. Two weeks before a
study, catheters and flow probes were implanted in the hepatic and
portal veins and femoral artery of dogs. Animals were studied after an
18-h fast ( n = 8), a 42- or 66-h fast
( n = 7), and an 18-h fast plus a continuous infusion of
cortisol (3.0 µg · kg 1 · min 1 ) for
72 h ( n = 7). Each experiment consisted of an
80-min tracer ([3- 3 H]glucose and
[U- 14 C]alanine) and dye equilibration period ( 80 to 0 min) and a 45-min sampling period. In the cortisol-treated group,
plasma cortisol increased fivefold. In the overnight-fasted group,
total GNG flux rate (GNG flux ), conversion of glucose
6-phosphate to glucose (GNG G-6- P Glc ), glucose
cycling, and maximal GNG flux rate (GNG max ) were 0.95 ± 0.14, 0.65 ± 0.06, 0.62 ± 0.06, and 0.70 ± 0.09 mg · kg 1 · min 1 ,
respectively. In the prolonged-fasted group, they were 1.50 ± 0.18, 1.18 ± 0.13, 0.40 ± 0.07, and 1.28 ± 0.10 mg · kg 1 · min 1 , whereas in
the cortisol-treated group they were 1.64 ± 0.33, 0.99 ± 0.29, 1.32 ± 0.24, and 0.91 ± 0.13 mg · kg 1 · min 1 . These
results demonstrate that GNG G-6- P Glc and GNG max were almost identical. However, these rates were
15-38% lower than GNG flux generated by a
combination of the two methods. This difference was most apparent in
the steroid-treated group, where the combination of the two methods
(GNG flux ) detected a significant increase in gluconeogenic flux.
fasting; cortisol |
| doi_str_mv | 10.1152/ajpendo.00320.2002 |
| format | Article |
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the Nashville VA Medical Center; 2 Department of
Molecular Physiology and Biophysics, Vanderbilt University,
Nashville, Tennessee 37232; and 3 Division of
Endocrinology, Department of Medicine, Albert Einstein College of
Medicine, New York, New York 10461
The purpose of this study was to
compare the assessment of gluconeogenesis (GNG) in the overnight- and
prolonged-fasted states and during chronic hypercortisolemia using the
arteriovenous difference and
[ 14 C]phospho enol pyruvate-liver biopsy
techniques as well as a combination of the two. Two weeks before a
study, catheters and flow probes were implanted in the hepatic and
portal veins and femoral artery of dogs. Animals were studied after an
18-h fast ( n = 8), a 42- or 66-h fast
( n = 7), and an 18-h fast plus a continuous infusion of
cortisol (3.0 µg · kg 1 · min 1 ) for
72 h ( n = 7). Each experiment consisted of an
80-min tracer ([3- 3 H]glucose and
[U- 14 C]alanine) and dye equilibration period ( 80 to 0 min) and a 45-min sampling period. In the cortisol-treated group,
plasma cortisol increased fivefold. In the overnight-fasted group,
total GNG flux rate (GNG flux ), conversion of glucose
6-phosphate to glucose (GNG G-6- P Glc ), glucose
cycling, and maximal GNG flux rate (GNG max ) were 0.95 ± 0.14, 0.65 ± 0.06, 0.62 ± 0.06, and 0.70 ± 0.09 mg · kg 1 · min 1 ,
respectively. In the prolonged-fasted group, they were 1.50 ± 0.18, 1.18 ± 0.13, 0.40 ± 0.07, and 1.28 ± 0.10 mg · kg 1 · min 1 , whereas in
the cortisol-treated group they were 1.64 ± 0.33, 0.99 ± 0.29, 1.32 ± 0.24, and 0.91 ± 0.13 mg · kg 1 · min 1 . These
results demonstrate that GNG G-6- P Glc and GNG max were almost identical. However, these rates were
15-38% lower than GNG flux generated by a
combination of the two methods. This difference was most apparent in
the steroid-treated group, where the combination of the two methods
(GNG flux ) detected a significant increase in gluconeogenic flux.
fasting; cortisol</description><identifier>ISSN: 0193-1849</identifier><identifier>EISSN: 1522-1555</identifier><identifier>DOI: 10.1152/ajpendo.00320.2002</identifier><identifier>PMID: 12376321</identifier><language>eng</language><publisher>United States</publisher><subject>Amino Acids - metabolism ; Animals ; Biopsy ; Blood Glucose - metabolism ; Carbon Radioisotopes ; Dogs ; Fasting - physiology ; Female ; Gluconeogenesis - drug effects ; Gluconeogenesis - physiology ; Glucose-6-Phosphate - metabolism ; Glycerol - blood ; Hydrocortisone - blood ; Hydrocortisone - pharmacology ; Lactic Acid - blood ; Liver - cytology ; Liver - drug effects ; Liver - metabolism ; Male ; Phosphoenolpyruvate - pharmacokinetics ; Physiology - methods</subject><ispartof>American journal of physiology: endocrinology and metabolism, 2002-11, Vol.283 (5), p.E946-E957</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-8dd6a4641c2e395ae23a90b8fb099bbbc033b244056c43572772caac387d58763</citedby><cites>FETCH-LOGICAL-c387t-8dd6a4641c2e395ae23a90b8fb099bbbc033b244056c43572772caac387d58763</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12376321$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Goldstein, Richard E</creatorcontrib><creatorcontrib>Rossetti, Luciano</creatorcontrib><creatorcontrib>Palmer, Brett A. J</creatorcontrib><creatorcontrib>Liu, Rong</creatorcontrib><creatorcontrib>Massillon, Duna</creatorcontrib><creatorcontrib>Scott, Melanie</creatorcontrib><creatorcontrib>Neal, Doss</creatorcontrib><creatorcontrib>Williams, Phillip</creatorcontrib><creatorcontrib>Peeler, Benjamin</creatorcontrib><creatorcontrib>Cherrington, Alan D</creatorcontrib><title>Effects of fasting and glucocorticoids on hepatic gluconeogenesis assessed using two independent methods in vivo</title><title>American journal of physiology: endocrinology and metabolism</title><addtitle>Am J Physiol Endocrinol Metab</addtitle><description>1 Department of Surgery, Vanderbilt University, and
the Nashville VA Medical Center; 2 Department of
Molecular Physiology and Biophysics, Vanderbilt University,
Nashville, Tennessee 37232; and 3 Division of
Endocrinology, Department of Medicine, Albert Einstein College of
Medicine, New York, New York 10461
The purpose of this study was to
compare the assessment of gluconeogenesis (GNG) in the overnight- and
prolonged-fasted states and during chronic hypercortisolemia using the
arteriovenous difference and
[ 14 C]phospho enol pyruvate-liver biopsy
techniques as well as a combination of the two. Two weeks before a
study, catheters and flow probes were implanted in the hepatic and
portal veins and femoral artery of dogs. Animals were studied after an
18-h fast ( n = 8), a 42- or 66-h fast
( n = 7), and an 18-h fast plus a continuous infusion of
cortisol (3.0 µg · kg 1 · min 1 ) for
72 h ( n = 7). Each experiment consisted of an
80-min tracer ([3- 3 H]glucose and
[U- 14 C]alanine) and dye equilibration period ( 80 to 0 min) and a 45-min sampling period. In the cortisol-treated group,
plasma cortisol increased fivefold. In the overnight-fasted group,
total GNG flux rate (GNG flux ), conversion of glucose
6-phosphate to glucose (GNG G-6- P Glc ), glucose
cycling, and maximal GNG flux rate (GNG max ) were 0.95 ± 0.14, 0.65 ± 0.06, 0.62 ± 0.06, and 0.70 ± 0.09 mg · kg 1 · min 1 ,
respectively. In the prolonged-fasted group, they were 1.50 ± 0.18, 1.18 ± 0.13, 0.40 ± 0.07, and 1.28 ± 0.10 mg · kg 1 · min 1 , whereas in
the cortisol-treated group they were 1.64 ± 0.33, 0.99 ± 0.29, 1.32 ± 0.24, and 0.91 ± 0.13 mg · kg 1 · min 1 . These
results demonstrate that GNG G-6- P Glc and GNG max were almost identical. However, these rates were
15-38% lower than GNG flux generated by a
combination of the two methods. This difference was most apparent in
the steroid-treated group, where the combination of the two methods
(GNG flux ) detected a significant increase in gluconeogenic flux.
fasting; cortisol</description><subject>Amino Acids - metabolism</subject><subject>Animals</subject><subject>Biopsy</subject><subject>Blood Glucose - metabolism</subject><subject>Carbon Radioisotopes</subject><subject>Dogs</subject><subject>Fasting - physiology</subject><subject>Female</subject><subject>Gluconeogenesis - drug effects</subject><subject>Gluconeogenesis - physiology</subject><subject>Glucose-6-Phosphate - metabolism</subject><subject>Glycerol - blood</subject><subject>Hydrocortisone - blood</subject><subject>Hydrocortisone - pharmacology</subject><subject>Lactic Acid - blood</subject><subject>Liver - cytology</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Phosphoenolpyruvate - pharmacokinetics</subject><subject>Physiology - methods</subject><issn>0193-1849</issn><issn>1522-1555</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1r3DAYhEVoabZp_0AORafevNWHZVvHEHbTQqCX9Cxk6bWt4JVcS06y_z5yd0NOBYEQM88wGoSuKdlSKtgP_TiBt2FLCGdkywhhF2iTBVZQIcQHtCFU8oI2pbxEn2N8JITUomSf0CVlvK44oxs07boOTIo4dLjTMTnfY-0t7sfFBBPm5ExwNsseDzDp_DxJHkIPHqKLWMcI-Vi8xJVOzwE7b2HtBj7hA6Qh5ATn8ZN7Cl_Qx06PEb6e7yv0Z797uP1Z3P---3V7c18Y3tSpaKytdFmV1DDgUmhgXEvSNl1LpGzb1hDOW1aWRFSm5KJmdc2M1itsRZM_d4W-n3KnOfxdICZ1cNHAOOpcfYmqZrQmkvNsZCejmUOMM3Rqmt1Bz0dFiVp3Vued1b-d1bpzhr6d05f2APYdOQ-bDfJkGFw_PLsZ1DQcowtj6I9qv4zjA7ykt2TWcCXUTpaVmmyX2eL_7FuZd4a_Ap3uoe8</recordid><startdate>20021101</startdate><enddate>20021101</enddate><creator>Goldstein, Richard E</creator><creator>Rossetti, Luciano</creator><creator>Palmer, Brett A. J</creator><creator>Liu, Rong</creator><creator>Massillon, Duna</creator><creator>Scott, Melanie</creator><creator>Neal, Doss</creator><creator>Williams, Phillip</creator><creator>Peeler, Benjamin</creator><creator>Cherrington, Alan D</creator><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>7X8</scope></search><sort><creationdate>20021101</creationdate><title>Effects of fasting and glucocorticoids on hepatic gluconeogenesis assessed using two independent methods in vivo</title><author>Goldstein, Richard E ; Rossetti, Luciano ; Palmer, Brett A. J ; Liu, Rong ; Massillon, Duna ; Scott, Melanie ; Neal, Doss ; Williams, Phillip ; Peeler, Benjamin ; Cherrington, Alan D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-8dd6a4641c2e395ae23a90b8fb099bbbc033b244056c43572772caac387d58763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Amino Acids - metabolism</topic><topic>Animals</topic><topic>Biopsy</topic><topic>Blood Glucose - metabolism</topic><topic>Carbon Radioisotopes</topic><topic>Dogs</topic><topic>Fasting - physiology</topic><topic>Female</topic><topic>Gluconeogenesis - drug effects</topic><topic>Gluconeogenesis - physiology</topic><topic>Glucose-6-Phosphate - metabolism</topic><topic>Glycerol - blood</topic><topic>Hydrocortisone - blood</topic><topic>Hydrocortisone - pharmacology</topic><topic>Lactic Acid - blood</topic><topic>Liver - cytology</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>Phosphoenolpyruvate - pharmacokinetics</topic><topic>Physiology - methods</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Goldstein, Richard E</creatorcontrib><creatorcontrib>Rossetti, Luciano</creatorcontrib><creatorcontrib>Palmer, Brett A. J</creatorcontrib><creatorcontrib>Liu, Rong</creatorcontrib><creatorcontrib>Massillon, Duna</creatorcontrib><creatorcontrib>Scott, Melanie</creatorcontrib><creatorcontrib>Neal, Doss</creatorcontrib><creatorcontrib>Williams, Phillip</creatorcontrib><creatorcontrib>Peeler, Benjamin</creatorcontrib><creatorcontrib>Cherrington, Alan D</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology: endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Goldstein, Richard E</au><au>Rossetti, Luciano</au><au>Palmer, Brett A. J</au><au>Liu, Rong</au><au>Massillon, Duna</au><au>Scott, Melanie</au><au>Neal, Doss</au><au>Williams, Phillip</au><au>Peeler, Benjamin</au><au>Cherrington, Alan D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of fasting and glucocorticoids on hepatic gluconeogenesis assessed using two independent methods in vivo</atitle><jtitle>American journal of physiology: endocrinology and metabolism</jtitle><addtitle>Am J Physiol Endocrinol Metab</addtitle><date>2002-11-01</date><risdate>2002</risdate><volume>283</volume><issue>5</issue><spage>E946</spage><epage>E957</epage><pages>E946-E957</pages><issn>0193-1849</issn><eissn>1522-1555</eissn><abstract>1 Department of Surgery, Vanderbilt University, and
the Nashville VA Medical Center; 2 Department of
Molecular Physiology and Biophysics, Vanderbilt University,
Nashville, Tennessee 37232; and 3 Division of
Endocrinology, Department of Medicine, Albert Einstein College of
Medicine, New York, New York 10461
The purpose of this study was to
compare the assessment of gluconeogenesis (GNG) in the overnight- and
prolonged-fasted states and during chronic hypercortisolemia using the
arteriovenous difference and
[ 14 C]phospho enol pyruvate-liver biopsy
techniques as well as a combination of the two. Two weeks before a
study, catheters and flow probes were implanted in the hepatic and
portal veins and femoral artery of dogs. Animals were studied after an
18-h fast ( n = 8), a 42- or 66-h fast
( n = 7), and an 18-h fast plus a continuous infusion of
cortisol (3.0 µg · kg 1 · min 1 ) for
72 h ( n = 7). Each experiment consisted of an
80-min tracer ([3- 3 H]glucose and
[U- 14 C]alanine) and dye equilibration period ( 80 to 0 min) and a 45-min sampling period. In the cortisol-treated group,
plasma cortisol increased fivefold. In the overnight-fasted group,
total GNG flux rate (GNG flux ), conversion of glucose
6-phosphate to glucose (GNG G-6- P Glc ), glucose
cycling, and maximal GNG flux rate (GNG max ) were 0.95 ± 0.14, 0.65 ± 0.06, 0.62 ± 0.06, and 0.70 ± 0.09 mg · kg 1 · min 1 ,
respectively. In the prolonged-fasted group, they were 1.50 ± 0.18, 1.18 ± 0.13, 0.40 ± 0.07, and 1.28 ± 0.10 mg · kg 1 · min 1 , whereas in
the cortisol-treated group they were 1.64 ± 0.33, 0.99 ± 0.29, 1.32 ± 0.24, and 0.91 ± 0.13 mg · kg 1 · min 1 . These
results demonstrate that GNG G-6- P Glc and GNG max were almost identical. However, these rates were
15-38% lower than GNG flux generated by a
combination of the two methods. This difference was most apparent in
the steroid-treated group, where the combination of the two methods
(GNG flux ) detected a significant increase in gluconeogenic flux.
fasting; cortisol</abstract><cop>United States</cop><pmid>12376321</pmid><doi>10.1152/ajpendo.00320.2002</doi></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0193-1849 |
| ispartof | American journal of physiology: endocrinology and metabolism, 2002-11, Vol.283 (5), p.E946-E957 |
| issn | 0193-1849 1522-1555 |
| language | eng |
| recordid | cdi_pubmed_primary_12376321 |
| source | MEDLINE; American Physiological Society Paid; EZB-FREE-00999 freely available EZB journals |
| subjects | Amino Acids - metabolism Animals Biopsy Blood Glucose - metabolism Carbon Radioisotopes Dogs Fasting - physiology Female Gluconeogenesis - drug effects Gluconeogenesis - physiology Glucose-6-Phosphate - metabolism Glycerol - blood Hydrocortisone - blood Hydrocortisone - pharmacology Lactic Acid - blood Liver - cytology Liver - drug effects Liver - metabolism Male Phosphoenolpyruvate - pharmacokinetics Physiology - methods |
| title | Effects of fasting and glucocorticoids on hepatic gluconeogenesis assessed using two independent methods in vivo |
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