Hyperinsulinaemia during exercise does not suppress hepatic glycogen concentrations in patients with type 1 diabetes: a magnetic resonance spectroscopy study
Aims/hypothesis We compared in vivo changes in liver glycogen concentration during exercise between patients with type 1 diabetes and healthy volunteers. Methods We studied seven men with type 1 diabetes (mean ± SEM diabetes duration 10 ± 2 years, age 33 ± 3 years, BMI 24 ± 1 kg/m², HbA₁c 8.1 ± 0.2%...
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| creator | Chokkalingam, K Tsintzas, K Snaar, J. E. M Norton, L Solanky, B Leverton, E Morris, P Mansell, P Macdonald, I. A |
| description | Aims/hypothesis We compared in vivo changes in liver glycogen concentration during exercise between patients with type 1 diabetes and healthy volunteers. Methods We studied seven men with type 1 diabetes (mean ± SEM diabetes duration 10 ± 2 years, age 33 ± 3 years, BMI 24 ± 1 kg/m², HbA₁c 8.1 ± 0.2% and VO₂ peak 43 ± 2 ml [kg lean body mass]-¹ min-¹) and five non-diabetic controls (mean ± SEM age 30 ± 3 years, BMI 22 ± 1 kg/m², HbA₁c 5.4 ± 0.1% and VO₂ peak 52 ± 4 ml [kg lean body mass]-¹ min-¹, before and after a standardised breakfast and after three bouts (EX1, EX2, EX3) of 40 min of cycling at 60% VO₂ peak. ¹³C Magnetic resonance spectroscopy of liver glycogen was acquired in a 3.0 T magnet using a surface coil. Whole-body substrate oxidation was determined using indirect calorimetry. Results Blood glucose and serum insulin concentrations were significantly higher (p < 0.05) in the fasting state, during the postprandial period and during EX1 and EX2 in subjects with type 1 diabetes compared with controls. Serum insulin concentration was still different between groups during EX3 (p < 0.05), but blood glucose concentration was similar. There was no difference between groups in liver glycogen concentration before or after the three bouts of exercise, despite the relative hyperinsulinaemia in type 1 diabetes. There were also no differences in substrate oxidation rates between groups. Conclusions/interpretation In patients with type 1 diabetes, hyperinsulinaemic and hyperglycaemic conditions during moderate exercise did not suppress hepatic glycogen concentrations. These findings do not support the hypothesis that exercise-induced hypoglycaemia in patients with type 1 diabetes is due to suppression of hepatic glycogen mobilisation. |
| doi_str_mv | 10.1007/s00125-007-0747-4 |
| format | Article |
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E. M ; Norton, L ; Solanky, B ; Leverton, E ; Morris, P ; Mansell, P ; Macdonald, I. A</creator><creatorcontrib>Chokkalingam, K ; Tsintzas, K ; Snaar, J. E. M ; Norton, L ; Solanky, B ; Leverton, E ; Morris, P ; Mansell, P ; Macdonald, I. A</creatorcontrib><description>Aims/hypothesis We compared in vivo changes in liver glycogen concentration during exercise between patients with type 1 diabetes and healthy volunteers. Methods We studied seven men with type 1 diabetes (mean ± SEM diabetes duration 10 ± 2 years, age 33 ± 3 years, BMI 24 ± 1 kg/m², HbA₁c 8.1 ± 0.2% and VO₂ peak 43 ± 2 ml [kg lean body mass]-¹ min-¹) and five non-diabetic controls (mean ± SEM age 30 ± 3 years, BMI 22 ± 1 kg/m², HbA₁c 5.4 ± 0.1% and VO₂ peak 52 ± 4 ml [kg lean body mass]-¹ min-¹, before and after a standardised breakfast and after three bouts (EX1, EX2, EX3) of 40 min of cycling at 60% VO₂ peak. ¹³C Magnetic resonance spectroscopy of liver glycogen was acquired in a 3.0 T magnet using a surface coil. Whole-body substrate oxidation was determined using indirect calorimetry. Results Blood glucose and serum insulin concentrations were significantly higher (p < 0.05) in the fasting state, during the postprandial period and during EX1 and EX2 in subjects with type 1 diabetes compared with controls. Serum insulin concentration was still different between groups during EX3 (p < 0.05), but blood glucose concentration was similar. There was no difference between groups in liver glycogen concentration before or after the three bouts of exercise, despite the relative hyperinsulinaemia in type 1 diabetes. There were also no differences in substrate oxidation rates between groups. Conclusions/interpretation In patients with type 1 diabetes, hyperinsulinaemic and hyperglycaemic conditions during moderate exercise did not suppress hepatic glycogen concentrations. These findings do not support the hypothesis that exercise-induced hypoglycaemia in patients with type 1 diabetes is due to suppression of hepatic glycogen mobilisation.</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-007-0747-4</identifier><identifier>PMID: 17639304</identifier><language>eng</language><publisher>Berlin: Berlin/Heidelberg : Springer-Verlag</publisher><subject>Adult ; Biological and medical sciences ; Blood Glucose - drug effects ; Blood Glucose - metabolism ; Body mass index ; Diabetes ; Diabetes Mellitus, Type 1 - metabolism ; Diabetes Mellitus, Type 1 - physiopathology ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; exercise ; Exercise - physiology ; Glucagon ; Glucose ; Humans ; hyperinsulinemia ; Hyperinsulinism - etiology ; Hypoglycemia ; Hypotheses ; Infusions, Intravenous ; Insulin ; Insulin - administration & dosage ; Insulin - blood ; Insulin - pharmacology ; insulin-dependent diabetes mellitus ; Liver ; Liver Glycogen - metabolism ; Magnetic resonance spectroscopy ; Magnetic Resonance Spectroscopy - methods ; Male ; Medical sciences ; Metabolism ; Oxidation ; Physiology ; Reference Values ; Spectrum analysis</subject><ispartof>Diabetologia, 2007-09, Vol.50 (9), p.1921-1929</ispartof><rights>2007 INIST-CNRS</rights><rights>Springer-Verlag 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c423t-ba875c14e4ed98983b97071109382d7ff25b4cc879fc80508acce4c3763ab8783</citedby><cites>FETCH-LOGICAL-c423t-ba875c14e4ed98983b97071109382d7ff25b4cc879fc80508acce4c3763ab8783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18994157$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17639304$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chokkalingam, K</creatorcontrib><creatorcontrib>Tsintzas, K</creatorcontrib><creatorcontrib>Snaar, J. E. M</creatorcontrib><creatorcontrib>Norton, L</creatorcontrib><creatorcontrib>Solanky, B</creatorcontrib><creatorcontrib>Leverton, E</creatorcontrib><creatorcontrib>Morris, P</creatorcontrib><creatorcontrib>Mansell, P</creatorcontrib><creatorcontrib>Macdonald, I. A</creatorcontrib><title>Hyperinsulinaemia during exercise does not suppress hepatic glycogen concentrations in patients with type 1 diabetes: a magnetic resonance spectroscopy study</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><description>Aims/hypothesis We compared in vivo changes in liver glycogen concentration during exercise between patients with type 1 diabetes and healthy volunteers. Methods We studied seven men with type 1 diabetes (mean ± SEM diabetes duration 10 ± 2 years, age 33 ± 3 years, BMI 24 ± 1 kg/m², HbA₁c 8.1 ± 0.2% and VO₂ peak 43 ± 2 ml [kg lean body mass]-¹ min-¹) and five non-diabetic controls (mean ± SEM age 30 ± 3 years, BMI 22 ± 1 kg/m², HbA₁c 5.4 ± 0.1% and VO₂ peak 52 ± 4 ml [kg lean body mass]-¹ min-¹, before and after a standardised breakfast and after three bouts (EX1, EX2, EX3) of 40 min of cycling at 60% VO₂ peak. ¹³C Magnetic resonance spectroscopy of liver glycogen was acquired in a 3.0 T magnet using a surface coil. Whole-body substrate oxidation was determined using indirect calorimetry. Results Blood glucose and serum insulin concentrations were significantly higher (p < 0.05) in the fasting state, during the postprandial period and during EX1 and EX2 in subjects with type 1 diabetes compared with controls. Serum insulin concentration was still different between groups during EX3 (p < 0.05), but blood glucose concentration was similar. There was no difference between groups in liver glycogen concentration before or after the three bouts of exercise, despite the relative hyperinsulinaemia in type 1 diabetes. There were also no differences in substrate oxidation rates between groups. Conclusions/interpretation In patients with type 1 diabetes, hyperinsulinaemic and hyperglycaemic conditions during moderate exercise did not suppress hepatic glycogen concentrations. These findings do not support the hypothesis that exercise-induced hypoglycaemia in patients with type 1 diabetes is due to suppression of hepatic glycogen mobilisation.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - drug effects</subject><subject>Blood Glucose - metabolism</subject><subject>Body mass index</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Diabetes Mellitus, Type 1 - physiopathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>exercise</subject><subject>Exercise - physiology</subject><subject>Glucagon</subject><subject>Glucose</subject><subject>Humans</subject><subject>hyperinsulinemia</subject><subject>Hyperinsulinism - etiology</subject><subject>Hypoglycemia</subject><subject>Hypotheses</subject><subject>Infusions, Intravenous</subject><subject>Insulin</subject><subject>Insulin - administration & dosage</subject><subject>Insulin - blood</subject><subject>Insulin - pharmacology</subject><subject>insulin-dependent diabetes mellitus</subject><subject>Liver</subject><subject>Liver Glycogen - metabolism</subject><subject>Magnetic resonance spectroscopy</subject><subject>Magnetic Resonance Spectroscopy - methods</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolism</subject><subject>Oxidation</subject><subject>Physiology</subject><subject>Reference Values</subject><subject>Spectrum analysis</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpdkdGK1TAQhoso7tnVB_BGg7DeVZMmbZK9k0VdYcELXfAupOm0m6VNaqZF-zC-qynnwIJXmUy--Wcyf1G8YvQ9o1R-QEpZVZc5LKkUshRPigMTvCqpqNTT4rA_l0w1P8-Kc8QHSimvRfO8OGOy4ZpTcSj-3mwzJB9wHX2wMHlLujXfBwJ_IDmPQLoISEJcCK7znACR3MNsF-_IMG4uDhCIi8FBWFLOxoDEB7IDOYPkt1_uyZKbEEY6b1tYAK-IJZMdAuwiWTEGm-sJzuCWFNHFeSO4rN32onjW2xHh5em8KO4-f_pxfVPefvvy9frjbelExZeytUrWjgkQ0GmlFW-1pJIxqrmqOtn3Vd0K55TUvVO0pso6B8LxvAXbKqn4RfHuqDun-GsFXMzk0cE42gBxRdMoxkXDd_Dtf-BDXFPIs5mKcSUE1XWG2BFy-TOYoDdz8pNNm2HU7MaZo3FmD3fjjMg1r0_CaztB91hxcioDlyfAorNjn_LKPD5ySmvBapm5N0eut9HYIWXm7ntFGc_NdMNow_8BRPmtRg</recordid><startdate>20070901</startdate><enddate>20070901</enddate><creator>Chokkalingam, K</creator><creator>Tsintzas, K</creator><creator>Snaar, J. 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E. M ; Norton, L ; Solanky, B ; Leverton, E ; Morris, P ; Mansell, P ; Macdonald, I. A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c423t-ba875c14e4ed98983b97071109382d7ff25b4cc879fc80508acce4c3763ab8783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - drug effects</topic><topic>Blood Glucose - metabolism</topic><topic>Body mass index</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Diabetes Mellitus, Type 1 - physiopathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>exercise</topic><topic>Exercise - physiology</topic><topic>Glucagon</topic><topic>Glucose</topic><topic>Humans</topic><topic>hyperinsulinemia</topic><topic>Hyperinsulinism - etiology</topic><topic>Hypoglycemia</topic><topic>Hypotheses</topic><topic>Infusions, Intravenous</topic><topic>Insulin</topic><topic>Insulin - administration & dosage</topic><topic>Insulin - blood</topic><topic>Insulin - pharmacology</topic><topic>insulin-dependent diabetes mellitus</topic><topic>Liver</topic><topic>Liver Glycogen - metabolism</topic><topic>Magnetic resonance spectroscopy</topic><topic>Magnetic Resonance Spectroscopy - methods</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolism</topic><topic>Oxidation</topic><topic>Physiology</topic><topic>Reference Values</topic><topic>Spectrum analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chokkalingam, K</creatorcontrib><creatorcontrib>Tsintzas, K</creatorcontrib><creatorcontrib>Snaar, J. 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A</creatorcontrib><collection>AGRIS</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>MEDLINE - Academic</collection><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chokkalingam, K</au><au>Tsintzas, K</au><au>Snaar, J. E. M</au><au>Norton, L</au><au>Solanky, B</au><au>Leverton, E</au><au>Morris, P</au><au>Mansell, P</au><au>Macdonald, I. A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperinsulinaemia during exercise does not suppress hepatic glycogen concentrations in patients with type 1 diabetes: a magnetic resonance spectroscopy study</atitle><jtitle>Diabetologia</jtitle><addtitle>Diabetologia</addtitle><date>2007-09-01</date><risdate>2007</risdate><volume>50</volume><issue>9</issue><spage>1921</spage><epage>1929</epage><pages>1921-1929</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Aims/hypothesis We compared in vivo changes in liver glycogen concentration during exercise between patients with type 1 diabetes and healthy volunteers. Methods We studied seven men with type 1 diabetes (mean ± SEM diabetes duration 10 ± 2 years, age 33 ± 3 years, BMI 24 ± 1 kg/m², HbA₁c 8.1 ± 0.2% and VO₂ peak 43 ± 2 ml [kg lean body mass]-¹ min-¹) and five non-diabetic controls (mean ± SEM age 30 ± 3 years, BMI 22 ± 1 kg/m², HbA₁c 5.4 ± 0.1% and VO₂ peak 52 ± 4 ml [kg lean body mass]-¹ min-¹, before and after a standardised breakfast and after three bouts (EX1, EX2, EX3) of 40 min of cycling at 60% VO₂ peak. ¹³C Magnetic resonance spectroscopy of liver glycogen was acquired in a 3.0 T magnet using a surface coil. Whole-body substrate oxidation was determined using indirect calorimetry. Results Blood glucose and serum insulin concentrations were significantly higher (p < 0.05) in the fasting state, during the postprandial period and during EX1 and EX2 in subjects with type 1 diabetes compared with controls. Serum insulin concentration was still different between groups during EX3 (p < 0.05), but blood glucose concentration was similar. There was no difference between groups in liver glycogen concentration before or after the three bouts of exercise, despite the relative hyperinsulinaemia in type 1 diabetes. There were also no differences in substrate oxidation rates between groups. Conclusions/interpretation In patients with type 1 diabetes, hyperinsulinaemic and hyperglycaemic conditions during moderate exercise did not suppress hepatic glycogen concentrations. These findings do not support the hypothesis that exercise-induced hypoglycaemia in patients with type 1 diabetes is due to suppression of hepatic glycogen mobilisation.</abstract><cop>Berlin</cop><pub>Berlin/Heidelberg : Springer-Verlag</pub><pmid>17639304</pmid><doi>10.1007/s00125-007-0747-4</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Biological and medical sciences Blood Glucose - drug effects Blood Glucose - metabolism Body mass index Diabetes Diabetes Mellitus, Type 1 - metabolism Diabetes Mellitus, Type 1 - physiopathology Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance exercise Exercise - physiology Glucagon Glucose Humans hyperinsulinemia Hyperinsulinism - etiology Hypoglycemia Hypotheses Infusions, Intravenous Insulin Insulin - administration & dosage Insulin - blood Insulin - pharmacology insulin-dependent diabetes mellitus Liver Liver Glycogen - metabolism Magnetic resonance spectroscopy Magnetic Resonance Spectroscopy - methods Male Medical sciences Metabolism Oxidation Physiology Reference Values Spectrum analysis |
| title | Hyperinsulinaemia during exercise does not suppress hepatic glycogen concentrations in patients with type 1 diabetes: a magnetic resonance spectroscopy study |
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