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Effect of hepatic denervation on peripheral insulin sensitivity in conscious dogs
1 Department of Molecular Physiology and Biophysics and 2 Diabetes Research and Training Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 We tested the hypothesis that the loss of hepatic nerves decreases peripheral insulin sensitivity. Surgical hepatic denervation (DN)...
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Published in: | American journal of physiology: endocrinology and metabolism 2002-02, Vol.282 (2), p.E286-E296 |
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container_title | American journal of physiology: endocrinology and metabolism |
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creator | Moore, Mary Courtney Satake, Shosuke Baranowski, Bryan Hsieh, Po-Shiuan Neal, Doss W Cherrington, Alan D |
description | 1 Department of Molecular Physiology and Biophysics and
2 Diabetes Research and Training Center, Vanderbilt
University School of Medicine, Nashville, Tennessee 37232
We tested the
hypothesis that the loss of hepatic nerves decreases peripheral insulin
sensitivity. Surgical hepatic denervation (DN) was performed in 22 dogs
~16 days before study; 7 dogs (Sham-Sal) had a sham procedure. A
euglycemic hyperinsulinemic (1 mU · kg 1 · min 1 ; arterial
insulin 35 ± 1 µU/ml in all dogs) clamp was performed in
conscious dogs. From 0 to 90 min of the clamp, all dogs received the
same treatment; then the DN dogs were divided into three groups. From
90 to 180 min, DN-PeA ( n = 7) and DN-PoA
( n = 7) groups received acetylcholine 2.5 µg · kg 1 · min 1 via
peripheral or portal vein, respectively, and DN-Sal ( n = 8) received no acetylcholine. During 150-180 min, the Sham-Sal, DN-Sal, DN-PeA, and DN-PoA groups exhibited glucose infusion rates of
12.4 ± 0.8, 9.3 ± 0.8 ( P |
doi_str_mv | 10.1152/ajpendo.00201.2001 |
format | article |
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2 Diabetes Research and Training Center, Vanderbilt
University School of Medicine, Nashville, Tennessee 37232
We tested the
hypothesis that the loss of hepatic nerves decreases peripheral insulin
sensitivity. Surgical hepatic denervation (DN) was performed in 22 dogs
~16 days before study; 7 dogs (Sham-Sal) had a sham procedure. A
euglycemic hyperinsulinemic (1 mU · kg 1 · min 1 ; arterial
insulin 35 ± 1 µU/ml in all dogs) clamp was performed in
conscious dogs. From 0 to 90 min of the clamp, all dogs received the
same treatment; then the DN dogs were divided into three groups. From
90 to 180 min, DN-PeA ( n = 7) and DN-PoA
( n = 7) groups received acetylcholine 2.5 µg · kg 1 · min 1 via
peripheral or portal vein, respectively, and DN-Sal ( n = 8) received no acetylcholine. During 150-180 min, the Sham-Sal, DN-Sal, DN-PeA, and DN-PoA groups exhibited glucose infusion rates of
12.4 ± 0.8, 9.3 ± 0.8 ( P < 0.05 vs.
Sham-Sal), 9.1 ± 0.1 ( P < 0.05 vs. Sham-Sal),
and 12.7 ± 1.6 mg · kg 1 · min 1 ; nonhepatic
glucose uptakes of 11.5 ± 0.9, 8.9 ± 0.7 ( P < 0.05 vs. Sham-Sal), 8.6 ± 0.9 ( P < 0.05 vs.
Sham-Sal), and 11.9 ± 1.7 mg · kg 1 · min 1 ; net
hindlimb glucose uptakes of 18.4 ± 2.1, 13.7 ± 1.1 ( P
< 0.05 vs. Sham-Sal), 17.5 ± 1.9, and 16.7 ± 3.2 mg/min; and glucose utilization rates of 14.4 ± 1.4, 10.4 ± 0.8 ( P < 0.05 vs. Sham-Sal), 9.8 ± 0.9 ( P
< 0.05 vs. Sham-Sal), and 13.6 ± 1.8 mg · kg 1 · min 1 ,
respectively. DN caused peripheral insulin resistance, and intraportal but not peripheral acetylcholine restored insulin sensitivity.
hepatic nerves; acetylcholine]]></description><identifier>ISSN: 0193-1849</identifier><identifier>EISSN: 1522-1555</identifier><identifier>DOI: 10.1152/ajpendo.00201.2001</identifier><identifier>PMID: 11788359</identifier><language>eng</language><publisher>United States</publisher><subject>Acetylcholine - administration & dosage ; Acetylcholine - pharmacology ; Animals ; Arteries ; Denervation ; Dogs ; Fatty Acids, Nonesterified - blood ; Female ; Gluconeogenesis - physiology ; Glucose - metabolism ; Glycerol - blood ; Hormones - blood ; Infusions, Intravenous ; Insulin - physiology ; Insulin Resistance - physiology ; Lactic Acid - blood ; Liver - innervation ; Liver Circulation - physiology ; Male ; Muscle, Skeletal - physiology ; Nervous System Physiological Phenomena ; Portal Vein</subject><ispartof>American journal of physiology: endocrinology and metabolism, 2002-02, Vol.282 (2), p.E286-E296</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c453t-76e47c94fc762490dbf168737b5f5d5f29c2daa6bfa5cc8c5d4ab3a12dcfb3fc3</citedby><cites>FETCH-LOGICAL-c453t-76e47c94fc762490dbf168737b5f5d5f29c2daa6bfa5cc8c5d4ab3a12dcfb3fc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11788359$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moore, Mary Courtney</creatorcontrib><creatorcontrib>Satake, Shosuke</creatorcontrib><creatorcontrib>Baranowski, Bryan</creatorcontrib><creatorcontrib>Hsieh, Po-Shiuan</creatorcontrib><creatorcontrib>Neal, Doss W</creatorcontrib><creatorcontrib>Cherrington, Alan D</creatorcontrib><title>Effect of hepatic denervation on peripheral insulin sensitivity in conscious dogs</title><title>American journal of physiology: endocrinology and metabolism</title><addtitle>Am J Physiol Endocrinol Metab</addtitle><description><![CDATA[1 Department of Molecular Physiology and Biophysics and
2 Diabetes Research and Training Center, Vanderbilt
University School of Medicine, Nashville, Tennessee 37232
We tested the
hypothesis that the loss of hepatic nerves decreases peripheral insulin
sensitivity. Surgical hepatic denervation (DN) was performed in 22 dogs
~16 days before study; 7 dogs (Sham-Sal) had a sham procedure. A
euglycemic hyperinsulinemic (1 mU · kg 1 · min 1 ; arterial
insulin 35 ± 1 µU/ml in all dogs) clamp was performed in
conscious dogs. From 0 to 90 min of the clamp, all dogs received the
same treatment; then the DN dogs were divided into three groups. From
90 to 180 min, DN-PeA ( n = 7) and DN-PoA
( n = 7) groups received acetylcholine 2.5 µg · kg 1 · min 1 via
peripheral or portal vein, respectively, and DN-Sal ( n = 8) received no acetylcholine. During 150-180 min, the Sham-Sal, DN-Sal, DN-PeA, and DN-PoA groups exhibited glucose infusion rates of
12.4 ± 0.8, 9.3 ± 0.8 ( P < 0.05 vs.
Sham-Sal), 9.1 ± 0.1 ( P < 0.05 vs. Sham-Sal),
and 12.7 ± 1.6 mg · kg 1 · min 1 ; nonhepatic
glucose uptakes of 11.5 ± 0.9, 8.9 ± 0.7 ( P < 0.05 vs. Sham-Sal), 8.6 ± 0.9 ( P < 0.05 vs.
Sham-Sal), and 11.9 ± 1.7 mg · kg 1 · min 1 ; net
hindlimb glucose uptakes of 18.4 ± 2.1, 13.7 ± 1.1 ( P
< 0.05 vs. Sham-Sal), 17.5 ± 1.9, and 16.7 ± 3.2 mg/min; and glucose utilization rates of 14.4 ± 1.4, 10.4 ± 0.8 ( P < 0.05 vs. Sham-Sal), 9.8 ± 0.9 ( P
< 0.05 vs. Sham-Sal), and 13.6 ± 1.8 mg · kg 1 · min 1 ,
respectively. DN caused peripheral insulin resistance, and intraportal but not peripheral acetylcholine restored insulin sensitivity.
hepatic nerves; acetylcholine]]></description><subject>Acetylcholine - administration & dosage</subject><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Arteries</subject><subject>Denervation</subject><subject>Dogs</subject><subject>Fatty Acids, Nonesterified - blood</subject><subject>Female</subject><subject>Gluconeogenesis - physiology</subject><subject>Glucose - metabolism</subject><subject>Glycerol - blood</subject><subject>Hormones - blood</subject><subject>Infusions, Intravenous</subject><subject>Insulin - physiology</subject><subject>Insulin Resistance - physiology</subject><subject>Lactic Acid - blood</subject><subject>Liver - innervation</subject><subject>Liver Circulation - physiology</subject><subject>Male</subject><subject>Muscle, Skeletal - physiology</subject><subject>Nervous System Physiological Phenomena</subject><subject>Portal Vein</subject><issn>0193-1849</issn><issn>1522-1555</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNp1kF1r2zAUhkXZaNN2f6AXxVe7c6ZPy74cIf2AwBi010KWjmIVx_IkO1v-_ZQlpVcDgcTR-7wcHoTuCF4SIug3_TbCYMMSY4rJkmJMLtAif9CSCCE-oQUmDStJzZsrdJ3SG8ZYCk4v0RUhsq6ZaBbo59o5MFMRXNHBqCdvCgsDxH1-hqHIZ4Toxw6i7gs_pLn3Q5FgSH7yez8d8qwwYUjGhzkVNmzTLfrsdJ_gy_m-Qa8P65fVU7n58fi8-r4pDRdsKmUFXJqGOyMryhtsW0eqWjLZCiescLQx1GpdtU4LY2ojLNct04Ra41rmDLtBX0-9Ywy_ZkiT2vlkoO_1AHkXJQmTVcV5DtJT0MSQUgSnxuh3Oh4UweooUp1Fqn8i1VFkhu7P7XO7A_uBnM3lQHMKdH7b_fYR1Ngdkg992B7Uw9z3L_Bnem-mNVVUrWldqdG6zJb_Z9-X-WDYX2FDl-s</recordid><startdate>20020201</startdate><enddate>20020201</enddate><creator>Moore, Mary Courtney</creator><creator>Satake, Shosuke</creator><creator>Baranowski, Bryan</creator><creator>Hsieh, Po-Shiuan</creator><creator>Neal, Doss W</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>20020201</creationdate><title>Effect of hepatic denervation on peripheral insulin sensitivity in conscious dogs</title><author>Moore, Mary Courtney ; Satake, Shosuke ; Baranowski, Bryan ; Hsieh, Po-Shiuan ; Neal, Doss W ; Cherrington, Alan D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c453t-76e47c94fc762490dbf168737b5f5d5f29c2daa6bfa5cc8c5d4ab3a12dcfb3fc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Acetylcholine - administration & dosage</topic><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Arteries</topic><topic>Denervation</topic><topic>Dogs</topic><topic>Fatty Acids, Nonesterified - blood</topic><topic>Female</topic><topic>Gluconeogenesis - physiology</topic><topic>Glucose - metabolism</topic><topic>Glycerol - blood</topic><topic>Hormones - blood</topic><topic>Infusions, Intravenous</topic><topic>Insulin - physiology</topic><topic>Insulin Resistance - physiology</topic><topic>Lactic Acid - blood</topic><topic>Liver - innervation</topic><topic>Liver Circulation - physiology</topic><topic>Male</topic><topic>Muscle, Skeletal - physiology</topic><topic>Nervous System Physiological Phenomena</topic><topic>Portal Vein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moore, Mary Courtney</creatorcontrib><creatorcontrib>Satake, Shosuke</creatorcontrib><creatorcontrib>Baranowski, Bryan</creatorcontrib><creatorcontrib>Hsieh, Po-Shiuan</creatorcontrib><creatorcontrib>Neal, Doss W</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>Moore, Mary Courtney</au><au>Satake, Shosuke</au><au>Baranowski, Bryan</au><au>Hsieh, Po-Shiuan</au><au>Neal, Doss W</au><au>Cherrington, Alan D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of hepatic denervation on peripheral insulin sensitivity in conscious dogs</atitle><jtitle>American journal of physiology: endocrinology and metabolism</jtitle><addtitle>Am J Physiol Endocrinol Metab</addtitle><date>2002-02-01</date><risdate>2002</risdate><volume>282</volume><issue>2</issue><spage>E286</spage><epage>E296</epage><pages>E286-E296</pages><issn>0193-1849</issn><eissn>1522-1555</eissn><abstract><![CDATA[1 Department of Molecular Physiology and Biophysics and
2 Diabetes Research and Training Center, Vanderbilt
University School of Medicine, Nashville, Tennessee 37232
We tested the
hypothesis that the loss of hepatic nerves decreases peripheral insulin
sensitivity. Surgical hepatic denervation (DN) was performed in 22 dogs
~16 days before study; 7 dogs (Sham-Sal) had a sham procedure. A
euglycemic hyperinsulinemic (1 mU · kg 1 · min 1 ; arterial
insulin 35 ± 1 µU/ml in all dogs) clamp was performed in
conscious dogs. From 0 to 90 min of the clamp, all dogs received the
same treatment; then the DN dogs were divided into three groups. From
90 to 180 min, DN-PeA ( n = 7) and DN-PoA
( n = 7) groups received acetylcholine 2.5 µg · kg 1 · min 1 via
peripheral or portal vein, respectively, and DN-Sal ( n = 8) received no acetylcholine. During 150-180 min, the Sham-Sal, DN-Sal, DN-PeA, and DN-PoA groups exhibited glucose infusion rates of
12.4 ± 0.8, 9.3 ± 0.8 ( P < 0.05 vs.
Sham-Sal), 9.1 ± 0.1 ( P < 0.05 vs. Sham-Sal),
and 12.7 ± 1.6 mg · kg 1 · min 1 ; nonhepatic
glucose uptakes of 11.5 ± 0.9, 8.9 ± 0.7 ( P < 0.05 vs. Sham-Sal), 8.6 ± 0.9 ( P < 0.05 vs.
Sham-Sal), and 11.9 ± 1.7 mg · kg 1 · min 1 ; net
hindlimb glucose uptakes of 18.4 ± 2.1, 13.7 ± 1.1 ( P
< 0.05 vs. Sham-Sal), 17.5 ± 1.9, and 16.7 ± 3.2 mg/min; and glucose utilization rates of 14.4 ± 1.4, 10.4 ± 0.8 ( P < 0.05 vs. Sham-Sal), 9.8 ± 0.9 ( P
< 0.05 vs. Sham-Sal), and 13.6 ± 1.8 mg · kg 1 · min 1 ,
respectively. DN caused peripheral insulin resistance, and intraportal but not peripheral acetylcholine restored insulin sensitivity.
hepatic nerves; acetylcholine]]></abstract><cop>United States</cop><pmid>11788359</pmid><doi>10.1152/ajpendo.00201.2001</doi></addata></record> |
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identifier | ISSN: 0193-1849 |
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source | American Physiological Society Journals |
subjects | Acetylcholine - administration & dosage Acetylcholine - pharmacology Animals Arteries Denervation Dogs Fatty Acids, Nonesterified - blood Female Gluconeogenesis - physiology Glucose - metabolism Glycerol - blood Hormones - blood Infusions, Intravenous Insulin - physiology Insulin Resistance - physiology Lactic Acid - blood Liver - innervation Liver Circulation - physiology Male Muscle, Skeletal - physiology Nervous System Physiological Phenomena Portal Vein |
title | Effect of hepatic denervation on peripheral insulin sensitivity in conscious dogs |
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