Skeletal Muscle Mitochondrial Capacity and Insulin Resistance in Type 2 Diabetes
Maximal mitochondrial ATP synthesis, measured by dynamic 31P magnetic resonance spectroscopy, is reduced in type 2 diabetes but is not associated with insulin resistance. Objective: The objective of this study was to determine the role of maximum mitochondrial capacity on the variation in insulin se...
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| Veröffentlicht in: | The journal of clinical endocrinology and metabolism 2011-04, Vol.96 (4), p.1160-1168 |
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| creator | Bajpeyi, Sudip Pasarica, Magdalena Moro, Cedric Conley, Kevin Jubrias, Sharon Sereda, Olga Burk, David H Zhang, Zhengyu Gupta, Alok Kjems, Lise Smith, Steven R |
| description | Maximal mitochondrial ATP synthesis, measured by dynamic 31P magnetic resonance spectroscopy, is reduced in type 2 diabetes but is not associated with insulin resistance.
Objective:
The objective of this study was to determine the role of maximum mitochondrial capacity on the variation in insulin sensitivity within a population of patients with type 2 diabetes mellitus (T2DM).
Research Design and Methods:
Fifty-eight participants enrolled in a cross-sectional design: eight active controls [maximum aerobic capacity (VO2max) > 40 ml/kg · min], 17 healthy sedentary controls without a family history (FH−) and seven with a family history (FH+) of diabetes, four obese participants, and 21 patients with T2DM. Mitochondrial capacity was measured noninvasively using 31P magnetic resonance spectroscopy of the vastus lateralis. Maximal ATP synthetic rate (ATPmax) was determined from the rate of phosphocreatine (PCr) recovery after short-term isometric exercise.
Results:
ATPmax was lower (P < 0.001) in T2DM and higher (P < 0.001) in active as compared with healthy sedentary FH− (active, 1.01 ± 0.2; FH−, 0.7 ± 0.2; FH+, 0.6 ± 0.1; obese, 0.6 ± 0.1; T2DM, 0.5 ± 0.2 mm ATP/sec; ANOVA P < 0.0001). Insulin sensitivity, measured by euglycemic-hyperinsulinemic (80 mIU/m2 · min) clamp was also reduced in T2DM (P < 0.001) (active, 12.0 ± 3.2; FH−, 7.8 ± 2.2; FH+, 6.8 ± 3.5; obese, 3.1 ± 1.0; T2DM, 3.4 ± 1.6; mg/kg estimated metabolic body size · min; ANOVA P < 0.0001). Unexpectedly, there was a broad range of ATPmax within the T2DM population where 52% of subjects with T2DM had ATPmax values that were within the range observed in healthy sedentary controls. In addition, 24% of the T2DM subjects overlapped with the active control group (range, 0.65–1.27 mm ATP/sec). In contrast to the positive correlation between ATPmax and M-value in the whole population (r2 = 0.35; P < 0.0001), there was no correlation between ATPmax and M-value in the patients with T2DM (r2 = 0.004; P = 0.79).
Conclusions:
Mitochondrial capacity is not associated with insulin action in T2DM. |
| doi_str_mv | 10.1210/jc.2010-1621 |
| format | Article |
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Objective:
The objective of this study was to determine the role of maximum mitochondrial capacity on the variation in insulin sensitivity within a population of patients with type 2 diabetes mellitus (T2DM).
Research Design and Methods:
Fifty-eight participants enrolled in a cross-sectional design: eight active controls [maximum aerobic capacity (VO2max) > 40 ml/kg · min], 17 healthy sedentary controls without a family history (FH−) and seven with a family history (FH+) of diabetes, four obese participants, and 21 patients with T2DM. Mitochondrial capacity was measured noninvasively using 31P magnetic resonance spectroscopy of the vastus lateralis. Maximal ATP synthetic rate (ATPmax) was determined from the rate of phosphocreatine (PCr) recovery after short-term isometric exercise.
Results:
ATPmax was lower (P < 0.001) in T2DM and higher (P < 0.001) in active as compared with healthy sedentary FH− (active, 1.01 ± 0.2; FH−, 0.7 ± 0.2; FH+, 0.6 ± 0.1; obese, 0.6 ± 0.1; T2DM, 0.5 ± 0.2 mm ATP/sec; ANOVA P < 0.0001). Insulin sensitivity, measured by euglycemic-hyperinsulinemic (80 mIU/m2 · min) clamp was also reduced in T2DM (P < 0.001) (active, 12.0 ± 3.2; FH−, 7.8 ± 2.2; FH+, 6.8 ± 3.5; obese, 3.1 ± 1.0; T2DM, 3.4 ± 1.6; mg/kg estimated metabolic body size · min; ANOVA P < 0.0001). Unexpectedly, there was a broad range of ATPmax within the T2DM population where 52% of subjects with T2DM had ATPmax values that were within the range observed in healthy sedentary controls. In addition, 24% of the T2DM subjects overlapped with the active control group (range, 0.65–1.27 mm ATP/sec). In contrast to the positive correlation between ATPmax and M-value in the whole population (r2 = 0.35; P < 0.0001), there was no correlation between ATPmax and M-value in the patients with T2DM (r2 = 0.004; P = 0.79).
Conclusions:
Mitochondrial capacity is not associated with insulin action in T2DM.]]></description><identifier>ISSN: 0021-972X</identifier><identifier>EISSN: 1945-7197</identifier><identifier>DOI: 10.1210/jc.2010-1621</identifier><identifier>PMID: 21307136</identifier><identifier>CODEN: JCEMAZ</identifier><language>eng</language><publisher>Bethesda, MD: Endocrine Society</publisher><subject>Adult ; Biological and medical sciences ; Cross-Sectional Studies ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - metabolism ; Diabetes Mellitus, Type 2 - pathology ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrine Research ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Exercise Test ; Feeding. Feeding behavior ; Female ; Fundamental and applied biological sciences. Psychology ; Humans ; Insulin Resistance - physiology ; Male ; Medical sciences ; Middle Aged ; Mitochondria, Muscle - metabolism ; Motor Activity - physiology ; Muscle, Skeletal - metabolism ; Muscle, Skeletal - pathology ; Obesity - complications ; Obesity - metabolism ; Obesity - pathology ; Sedentary Lifestyle ; Validation Studies as Topic ; Vertebrates: anatomy and physiology, studies on body, several organs or systems ; Vertebrates: endocrinology ; Young Adult</subject><ispartof>The journal of clinical endocrinology and metabolism, 2011-04, Vol.96 (4), p.1160-1168</ispartof><rights>Copyright © 2011 by The Endocrine Society</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5687-6b413c12788462540ed22616121b9ef54b76c0b6a77363560c6b93ba8d6d15643</citedby><cites>FETCH-LOGICAL-c5687-6b413c12788462540ed22616121b9ef54b76c0b6a77363560c6b93ba8d6d15643</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=24084443$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21307136$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bajpeyi, Sudip</creatorcontrib><creatorcontrib>Pasarica, Magdalena</creatorcontrib><creatorcontrib>Moro, Cedric</creatorcontrib><creatorcontrib>Conley, Kevin</creatorcontrib><creatorcontrib>Jubrias, Sharon</creatorcontrib><creatorcontrib>Sereda, Olga</creatorcontrib><creatorcontrib>Burk, David H</creatorcontrib><creatorcontrib>Zhang, Zhengyu</creatorcontrib><creatorcontrib>Gupta, Alok</creatorcontrib><creatorcontrib>Kjems, Lise</creatorcontrib><creatorcontrib>Smith, Steven R</creatorcontrib><title>Skeletal Muscle Mitochondrial Capacity and Insulin Resistance in Type 2 Diabetes</title><title>The journal of clinical endocrinology and metabolism</title><addtitle>J Clin Endocrinol Metab</addtitle><description><![CDATA[Maximal mitochondrial ATP synthesis, measured by dynamic 31P magnetic resonance spectroscopy, is reduced in type 2 diabetes but is not associated with insulin resistance.
Objective:
The objective of this study was to determine the role of maximum mitochondrial capacity on the variation in insulin sensitivity within a population of patients with type 2 diabetes mellitus (T2DM).
Research Design and Methods:
Fifty-eight participants enrolled in a cross-sectional design: eight active controls [maximum aerobic capacity (VO2max) > 40 ml/kg · min], 17 healthy sedentary controls without a family history (FH−) and seven with a family history (FH+) of diabetes, four obese participants, and 21 patients with T2DM. Mitochondrial capacity was measured noninvasively using 31P magnetic resonance spectroscopy of the vastus lateralis. Maximal ATP synthetic rate (ATPmax) was determined from the rate of phosphocreatine (PCr) recovery after short-term isometric exercise.
Results:
ATPmax was lower (P < 0.001) in T2DM and higher (P < 0.001) in active as compared with healthy sedentary FH− (active, 1.01 ± 0.2; FH−, 0.7 ± 0.2; FH+, 0.6 ± 0.1; obese, 0.6 ± 0.1; T2DM, 0.5 ± 0.2 mm ATP/sec; ANOVA P < 0.0001). Insulin sensitivity, measured by euglycemic-hyperinsulinemic (80 mIU/m2 · min) clamp was also reduced in T2DM (P < 0.001) (active, 12.0 ± 3.2; FH−, 7.8 ± 2.2; FH+, 6.8 ± 3.5; obese, 3.1 ± 1.0; T2DM, 3.4 ± 1.6; mg/kg estimated metabolic body size · min; ANOVA P < 0.0001). Unexpectedly, there was a broad range of ATPmax within the T2DM population where 52% of subjects with T2DM had ATPmax values that were within the range observed in healthy sedentary controls. In addition, 24% of the T2DM subjects overlapped with the active control group (range, 0.65–1.27 mm ATP/sec). In contrast to the positive correlation between ATPmax and M-value in the whole population (r2 = 0.35; P < 0.0001), there was no correlation between ATPmax and M-value in the patients with T2DM (r2 = 0.004; P = 0.79).
Conclusions:
Mitochondrial capacity is not associated with insulin action in T2DM.]]></description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Cross-Sectional Studies</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - pathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrine Research</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Exercise Test</subject><subject>Feeding. Feeding behavior</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Insulin Resistance - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mitochondria, Muscle - metabolism</subject><subject>Motor Activity - physiology</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Muscle, Skeletal - pathology</subject><subject>Obesity - complications</subject><subject>Obesity - metabolism</subject><subject>Obesity - pathology</subject><subject>Sedentary Lifestyle</subject><subject>Validation Studies as Topic</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><subject>Vertebrates: endocrinology</subject><subject>Young Adult</subject><issn>0021-972X</issn><issn>1945-7197</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkcuLFDEQh4Mo7rh68yx9ES_2Wnl00n0RZHwt7KLoCt5COl3jZDaTtEm3y_z3ZpxxVTAQQlW-ev4IeUzhjDIKLzb2jAGFmkpG75AF7URTK9qpu2QBwGjdKfb1hDzIeQNAhWj4fXLCKAdFuVyQj5-v0eNkfHU5Z-uxunRTtOsYhuSKc2lGY920q0wYqvOQZ-9C9Qmzy5MJFqtiXe1GrFj12pkeJ8wPyb2V8RkfHd9T8uXtm6vl-_riw7vz5auL2jayVbXsBeWWMtW2QrJGAA6MSSrLSH2Hq0b0SlropVGKS95IsLLveG_aQQ60kYKfkpeHvOPcb3GwGKZkvB6T25q009E4_e9PcGv9Lf7QZXJgDSsJnh0TpPh9xjzprcsWvTcB45x1W3qBVv4inx9Im2LOCVe3VSjovQZ6Y_VeA73XoOBP_u7sFv699AI8PQImW-NXqazS5T-cgFYIwQsnDtxN9BOmfO3nG0x6jcZPaw3lCKnaulSmIIpVl8tVCeOHMAxDtMkFHBPmrDdxTqFI8v-ufwLdNq5i</recordid><startdate>201104</startdate><enddate>201104</enddate><creator>Bajpeyi, Sudip</creator><creator>Pasarica, Magdalena</creator><creator>Moro, Cedric</creator><creator>Conley, Kevin</creator><creator>Jubrias, Sharon</creator><creator>Sereda, Olga</creator><creator>Burk, David H</creator><creator>Zhang, Zhengyu</creator><creator>Gupta, Alok</creator><creator>Kjems, Lise</creator><creator>Smith, Steven R</creator><general>Endocrine Society</general><general>Copyright by The Endocrine Society</general><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>201104</creationdate><title>Skeletal Muscle Mitochondrial Capacity and Insulin Resistance in Type 2 Diabetes</title><author>Bajpeyi, Sudip ; Pasarica, Magdalena ; Moro, Cedric ; Conley, Kevin ; Jubrias, Sharon ; Sereda, Olga ; Burk, David H ; Zhang, Zhengyu ; Gupta, Alok ; Kjems, Lise ; Smith, Steven R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5687-6b413c12788462540ed22616121b9ef54b76c0b6a77363560c6b93ba8d6d15643</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Cross-Sectional Studies</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diabetes Mellitus, Type 2 - pathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrine Research</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Exercise Test</topic><topic>Feeding. Feeding behavior</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Insulin Resistance - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mitochondria, Muscle - metabolism</topic><topic>Motor Activity - physiology</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Muscle, Skeletal - pathology</topic><topic>Obesity - complications</topic><topic>Obesity - metabolism</topic><topic>Obesity - pathology</topic><topic>Sedentary Lifestyle</topic><topic>Validation Studies as Topic</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><topic>Vertebrates: endocrinology</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bajpeyi, Sudip</creatorcontrib><creatorcontrib>Pasarica, Magdalena</creatorcontrib><creatorcontrib>Moro, Cedric</creatorcontrib><creatorcontrib>Conley, Kevin</creatorcontrib><creatorcontrib>Jubrias, Sharon</creatorcontrib><creatorcontrib>Sereda, Olga</creatorcontrib><creatorcontrib>Burk, David H</creatorcontrib><creatorcontrib>Zhang, Zhengyu</creatorcontrib><creatorcontrib>Gupta, Alok</creatorcontrib><creatorcontrib>Kjems, Lise</creatorcontrib><creatorcontrib>Smith, Steven R</creatorcontrib><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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The journal of clinical endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bajpeyi, Sudip</au><au>Pasarica, Magdalena</au><au>Moro, Cedric</au><au>Conley, Kevin</au><au>Jubrias, Sharon</au><au>Sereda, Olga</au><au>Burk, David H</au><au>Zhang, Zhengyu</au><au>Gupta, Alok</au><au>Kjems, Lise</au><au>Smith, Steven R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Skeletal Muscle Mitochondrial Capacity and Insulin Resistance in Type 2 Diabetes</atitle><jtitle>The journal of clinical endocrinology and metabolism</jtitle><addtitle>J Clin Endocrinol Metab</addtitle><date>2011-04</date><risdate>2011</risdate><volume>96</volume><issue>4</issue><spage>1160</spage><epage>1168</epage><pages>1160-1168</pages><issn>0021-972X</issn><eissn>1945-7197</eissn><coden>JCEMAZ</coden><abstract><![CDATA[Maximal mitochondrial ATP synthesis, measured by dynamic 31P magnetic resonance spectroscopy, is reduced in type 2 diabetes but is not associated with insulin resistance.
Objective:
The objective of this study was to determine the role of maximum mitochondrial capacity on the variation in insulin sensitivity within a population of patients with type 2 diabetes mellitus (T2DM).
Research Design and Methods:
Fifty-eight participants enrolled in a cross-sectional design: eight active controls [maximum aerobic capacity (VO2max) > 40 ml/kg · min], 17 healthy sedentary controls without a family history (FH−) and seven with a family history (FH+) of diabetes, four obese participants, and 21 patients with T2DM. Mitochondrial capacity was measured noninvasively using 31P magnetic resonance spectroscopy of the vastus lateralis. Maximal ATP synthetic rate (ATPmax) was determined from the rate of phosphocreatine (PCr) recovery after short-term isometric exercise.
Results:
ATPmax was lower (P < 0.001) in T2DM and higher (P < 0.001) in active as compared with healthy sedentary FH− (active, 1.01 ± 0.2; FH−, 0.7 ± 0.2; FH+, 0.6 ± 0.1; obese, 0.6 ± 0.1; T2DM, 0.5 ± 0.2 mm ATP/sec; ANOVA P < 0.0001). Insulin sensitivity, measured by euglycemic-hyperinsulinemic (80 mIU/m2 · min) clamp was also reduced in T2DM (P < 0.001) (active, 12.0 ± 3.2; FH−, 7.8 ± 2.2; FH+, 6.8 ± 3.5; obese, 3.1 ± 1.0; T2DM, 3.4 ± 1.6; mg/kg estimated metabolic body size · min; ANOVA P < 0.0001). Unexpectedly, there was a broad range of ATPmax within the T2DM population where 52% of subjects with T2DM had ATPmax values that were within the range observed in healthy sedentary controls. In addition, 24% of the T2DM subjects overlapped with the active control group (range, 0.65–1.27 mm ATP/sec). In contrast to the positive correlation between ATPmax and M-value in the whole population (r2 = 0.35; P < 0.0001), there was no correlation between ATPmax and M-value in the patients with T2DM (r2 = 0.004; P = 0.79).
Conclusions:
Mitochondrial capacity is not associated with insulin action in T2DM.]]></abstract><cop>Bethesda, MD</cop><pub>Endocrine Society</pub><pmid>21307136</pmid><doi>10.1210/jc.2010-1621</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The journal of clinical endocrinology and metabolism, 2011-04, Vol.96 (4), p.1160-1168 |
| issn | 0021-972X 1945-7197 |
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| source | MEDLINE; Journals@Ovid Complete; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adult Biological and medical sciences Cross-Sectional Studies Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - metabolism Diabetes Mellitus, Type 2 - pathology Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrine Research Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Exercise Test Feeding. Feeding behavior Female Fundamental and applied biological sciences. Psychology Humans Insulin Resistance - physiology Male Medical sciences Middle Aged Mitochondria, Muscle - metabolism Motor Activity - physiology Muscle, Skeletal - metabolism Muscle, Skeletal - pathology Obesity - complications Obesity - metabolism Obesity - pathology Sedentary Lifestyle Validation Studies as Topic Vertebrates: anatomy and physiology, studies on body, several organs or systems Vertebrates: endocrinology Young Adult |
| title | Skeletal Muscle Mitochondrial Capacity and Insulin Resistance in Type 2 Diabetes |
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