Insulin resistance induced by sucrose feeding in rats is due to an impairment of the hepatic parasympathetic nerves
A considerable proportion of whole-body insulin-stimulated glucose uptake is dependent upon the hepatic insulin-sensitising substance (HISS) in a pathway mediated by the hepatic parasympathetic nerves (HPNs). We tested the hypothesis that a high-sucrose diet leads to the impairment of the HPN-depend...
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| Veröffentlicht in: | Diabetologia 2005-05, Vol.48 (5), p.976-983 |
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| creator | RIBEIRO, R. T LAUTT, W. W LEGARE, D. J MACEDO, M P |
| description | A considerable proportion of whole-body insulin-stimulated glucose uptake is dependent upon the hepatic insulin-sensitising substance (HISS) in a pathway mediated by the hepatic parasympathetic nerves (HPNs). We tested the hypothesis that a high-sucrose diet leads to the impairment of the HPN-dependent component of insulin action.
We quantified insulin sensitivity using the rapid insulin sensitivity test, a modified euglycaemic clamp. Quantification of the HPN-dependent component was achieved by administration of a muscarinic receptor antagonist (atropine, 3 mg/kg).
Insulin sensitivity was higher in standard-fed than in sucrose-fed Wistar rats (305.6+/-34.1 vs 193.9+/-13.7 mg glucose/kg body weight; p |
| doi_str_mv | 10.1007/s00125-005-1714-6 |
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We quantified insulin sensitivity using the rapid insulin sensitivity test, a modified euglycaemic clamp. Quantification of the HPN-dependent component was achieved by administration of a muscarinic receptor antagonist (atropine, 3 mg/kg).
Insulin sensitivity was higher in standard-fed than in sucrose-fed Wistar rats (305.6+/-34.1 vs 193.9+/-13.7 mg glucose/kg body weight; p<0.005) and Sprague-Dawley rats (196.4+/-5.9 vs 95.5+/-16.3 mg glucose/kg body weight; p<0.01). The HPN-independent component was similar in the two diet groups. Insulin resistance was entirely due to an impairment of the HPN-dependent component in both Wistar rats (164.3+/-28.1 [standard-fed] vs 26.5+/-7.5 [sucrose-fed] mg glucose/kg body weight; p<0.0001) and Sprague-Dawley rats (111.7+/-9.5 vs 35.3+/-21.4 mg glucose/kg body weight; p<0.01). Furthermore, HPN-dependent insulin resistance in Sprague-Dawley rats was already evident after 2 weeks of a high-sucrose diet (28.5+/-7.6 [2 weeks], 35.3+/-21.4 [6 weeks], 17.9+/-5.4 [9 weeks] mg glucose/kg body weight) and was independent of the nature of sucrose supplementation (12.3+/-4.7 [solid] and 17.9+/-5.4 [liquid] mg glucose/kg body weight).
Our results support the hypothesis that insulin resistance caused by sucrose feeding is due to an impairment of the HPN-dependent component of insulin action, leading to a dysfunction of the HISS pathway.</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-005-1714-6</identifier><identifier>PMID: 15830187</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Animals ; Atropine - pharmacology ; Biological and medical sciences ; Blood Glucose - drug effects ; Blood Glucose - metabolism ; Denervation ; Diabetes ; Diabetes. Impaired glucose tolerance ; Dietary Sucrose - pharmacology ; Dietary Supplements ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Fundamental and applied biological sciences. Psychology ; Glucose ; Hypotheses ; Injections, Intravenous ; Insulin - administration & dosage ; Insulin - pharmacology ; Insulin resistance ; Insulin Resistance - physiology ; Kinetics ; Laboratory animals ; Liver - innervation ; Liver diseases ; Male ; Medical sciences ; Mice ; Models, Animal ; Musculoskeletal system ; Parasympathetic Nervous System - physiopathology ; Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Striated muscle. Tendons ; Sucrose ; Vertebrates: nervous system and sense organs ; Vertebrates: osteoarticular system, musculoskeletal system</subject><ispartof>Diabetologia, 2005-05, Vol.48 (5), p.976-983</ispartof><rights>2005 INIST-CNRS</rights><rights>Springer-Verlag 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c520t-aeb931042b15f1c883c44fdebcd30709e2c9b0bb17556144a3d4682aa29f14dc3</citedby><cites>FETCH-LOGICAL-c520t-aeb931042b15f1c883c44fdebcd30709e2c9b0bb17556144a3d4682aa29f14dc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16801144$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15830187$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>RIBEIRO, R. T</creatorcontrib><creatorcontrib>LAUTT, W. W</creatorcontrib><creatorcontrib>LEGARE, D. J</creatorcontrib><creatorcontrib>MACEDO, M P</creatorcontrib><title>Insulin resistance induced by sucrose feeding in rats is due to an impairment of the hepatic parasympathetic nerves</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><description>A considerable proportion of whole-body insulin-stimulated glucose uptake is dependent upon the hepatic insulin-sensitising substance (HISS) in a pathway mediated by the hepatic parasympathetic nerves (HPNs). We tested the hypothesis that a high-sucrose diet leads to the impairment of the HPN-dependent component of insulin action.
We quantified insulin sensitivity using the rapid insulin sensitivity test, a modified euglycaemic clamp. Quantification of the HPN-dependent component was achieved by administration of a muscarinic receptor antagonist (atropine, 3 mg/kg).
Insulin sensitivity was higher in standard-fed than in sucrose-fed Wistar rats (305.6+/-34.1 vs 193.9+/-13.7 mg glucose/kg body weight; p<0.005) and Sprague-Dawley rats (196.4+/-5.9 vs 95.5+/-16.3 mg glucose/kg body weight; p<0.01). The HPN-independent component was similar in the two diet groups. Insulin resistance was entirely due to an impairment of the HPN-dependent component in both Wistar rats (164.3+/-28.1 [standard-fed] vs 26.5+/-7.5 [sucrose-fed] mg glucose/kg body weight; p<0.0001) and Sprague-Dawley rats (111.7+/-9.5 vs 35.3+/-21.4 mg glucose/kg body weight; p<0.01). Furthermore, HPN-dependent insulin resistance in Sprague-Dawley rats was already evident after 2 weeks of a high-sucrose diet (28.5+/-7.6 [2 weeks], 35.3+/-21.4 [6 weeks], 17.9+/-5.4 [9 weeks] mg glucose/kg body weight) and was independent of the nature of sucrose supplementation (12.3+/-4.7 [solid] and 17.9+/-5.4 [liquid] mg glucose/kg body weight).
Our results support the hypothesis that insulin resistance caused by sucrose feeding is due to an impairment of the HPN-dependent component of insulin action, leading to a dysfunction of the HISS pathway.</description><subject>Animals</subject><subject>Atropine - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - drug effects</subject><subject>Blood Glucose - metabolism</subject><subject>Denervation</subject><subject>Diabetes</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Dietary Sucrose - pharmacology</subject><subject>Dietary Supplements</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glucose</subject><subject>Hypotheses</subject><subject>Injections, Intravenous</subject><subject>Insulin - administration & dosage</subject><subject>Insulin - pharmacology</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - physiology</subject><subject>Kinetics</subject><subject>Laboratory animals</subject><subject>Liver - innervation</subject><subject>Liver diseases</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Models, Animal</subject><subject>Musculoskeletal system</subject><subject>Parasympathetic Nervous System - physiopathology</subject><subject>Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rats, Wistar</subject><subject>Striated muscle. Tendons</subject><subject>Sucrose</subject><subject>Vertebrates: nervous system and sense organs</subject><subject>Vertebrates: osteoarticular system, musculoskeletal system</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkV2L1TAQhoMo7nH1B3gjQdC7aiYfbXojyOLHwoI3Ct6FNJ3uydKmx0y7cP69Kefgqldh8j4zzDsvYy9BvAMhmvckBEhTCWEqaEBX9SO2A61kJbS0j9lukyuw9c8L9ozoTgihjK6fsgswVgmwzY7RdaJ1jIlnpEiLTwF5TP0asOfdkdMa8kzIB8Q-plu-gX4hHon3K_Jl5j7xOB18zBOmhc8DX_bI93jwSwz84LOnY5HL51YnzPdIz9mTwY-EL87vJfvx-dP3q6_Vzbcv11cfb6pgpFgqj12roFjpwAwQrFVB66HHLvRKNKJFGdpOdB00xtSgtVe9rq30XrYD6D6oS_bhNPewdhP2oSyY_egOOU4-H93so_tXSXHvbud7J1tprG3LgLfnAXn-tSItbooUcBx9wnklVzdWAoAt4Ov_wLt5zamYcxKU1a1qTIHgBG0npYzDn01AuC1Pd8rTlTzdlqerS8-rvy08dJwDLMCbM-Ap-HHIJcFID1xtBZTbqN9Pr6qu</recordid><startdate>20050501</startdate><enddate>20050501</enddate><creator>RIBEIRO, R. 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J ; MACEDO, M P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c520t-aeb931042b15f1c883c44fdebcd30709e2c9b0bb17556144a3d4682aa29f14dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Atropine - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - drug effects</topic><topic>Blood Glucose - metabolism</topic><topic>Denervation</topic><topic>Diabetes</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Dietary Sucrose - pharmacology</topic><topic>Dietary Supplements</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glucose</topic><topic>Hypotheses</topic><topic>Injections, Intravenous</topic><topic>Insulin - administration & dosage</topic><topic>Insulin - pharmacology</topic><topic>Insulin resistance</topic><topic>Insulin Resistance - physiology</topic><topic>Kinetics</topic><topic>Laboratory animals</topic><topic>Liver - innervation</topic><topic>Liver diseases</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Models, Animal</topic><topic>Musculoskeletal system</topic><topic>Parasympathetic Nervous System - physiopathology</topic><topic>Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rats, Wistar</topic><topic>Striated muscle. 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T</au><au>LAUTT, W. W</au><au>LEGARE, D. J</au><au>MACEDO, M P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Insulin resistance induced by sucrose feeding in rats is due to an impairment of the hepatic parasympathetic nerves</atitle><jtitle>Diabetologia</jtitle><addtitle>Diabetologia</addtitle><date>2005-05-01</date><risdate>2005</risdate><volume>48</volume><issue>5</issue><spage>976</spage><epage>983</epage><pages>976-983</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>A considerable proportion of whole-body insulin-stimulated glucose uptake is dependent upon the hepatic insulin-sensitising substance (HISS) in a pathway mediated by the hepatic parasympathetic nerves (HPNs). We tested the hypothesis that a high-sucrose diet leads to the impairment of the HPN-dependent component of insulin action.
We quantified insulin sensitivity using the rapid insulin sensitivity test, a modified euglycaemic clamp. Quantification of the HPN-dependent component was achieved by administration of a muscarinic receptor antagonist (atropine, 3 mg/kg).
Insulin sensitivity was higher in standard-fed than in sucrose-fed Wistar rats (305.6+/-34.1 vs 193.9+/-13.7 mg glucose/kg body weight; p<0.005) and Sprague-Dawley rats (196.4+/-5.9 vs 95.5+/-16.3 mg glucose/kg body weight; p<0.01). The HPN-independent component was similar in the two diet groups. Insulin resistance was entirely due to an impairment of the HPN-dependent component in both Wistar rats (164.3+/-28.1 [standard-fed] vs 26.5+/-7.5 [sucrose-fed] mg glucose/kg body weight; p<0.0001) and Sprague-Dawley rats (111.7+/-9.5 vs 35.3+/-21.4 mg glucose/kg body weight; p<0.01). Furthermore, HPN-dependent insulin resistance in Sprague-Dawley rats was already evident after 2 weeks of a high-sucrose diet (28.5+/-7.6 [2 weeks], 35.3+/-21.4 [6 weeks], 17.9+/-5.4 [9 weeks] mg glucose/kg body weight) and was independent of the nature of sucrose supplementation (12.3+/-4.7 [solid] and 17.9+/-5.4 [liquid] mg glucose/kg body weight).
Our results support the hypothesis that insulin resistance caused by sucrose feeding is due to an impairment of the HPN-dependent component of insulin action, leading to a dysfunction of the HISS pathway.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>15830187</pmid><doi>10.1007/s00125-005-1714-6</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Diabetologia, 2005-05, Vol.48 (5), p.976-983 |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Atropine - pharmacology Biological and medical sciences Blood Glucose - drug effects Blood Glucose - metabolism Denervation Diabetes Diabetes. Impaired glucose tolerance Dietary Sucrose - pharmacology Dietary Supplements Endocrine pancreas. Apud cells (diseases) Endocrinopathies Fundamental and applied biological sciences. Psychology Glucose Hypotheses Injections, Intravenous Insulin - administration & dosage Insulin - pharmacology Insulin resistance Insulin Resistance - physiology Kinetics Laboratory animals Liver - innervation Liver diseases Male Medical sciences Mice Models, Animal Musculoskeletal system Parasympathetic Nervous System - physiopathology Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ Rats Rats, Sprague-Dawley Rats, Wistar Striated muscle. Tendons Sucrose Vertebrates: nervous system and sense organs Vertebrates: osteoarticular system, musculoskeletal system |
| title | Insulin resistance induced by sucrose feeding in rats is due to an impairment of the hepatic parasympathetic nerves |
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