Mitochondrial function assessed by 31 P MRS and BOLD MRI in non‐obese type 2 diabetic rats
The study aims to characterize age‐associated changes in skeletal muscle bioenergetics by evaluating the response to ischemia‐reperfusion in the skeletal muscle of the Goto‐Kakizaki ( GK ) rats, a rat model of non‐obese type 2 diabetes (T2D). 31 P magnetic resonance spectroscopy ( MRS ) and blood ox...
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creator | Liu, Yuchi Mei, Xunbai Li, Jielei Lai, Nicola Yu, Xin |
description | The study aims to characterize age‐associated changes in skeletal muscle bioenergetics by evaluating the response to ischemia‐reperfusion in the skeletal muscle of the Goto‐Kakizaki (
GK
) rats, a rat model of non‐obese type 2 diabetes (T2D).
31
P magnetic resonance spectroscopy (
MRS
) and blood oxygen level‐dependent (
BOLD
)
MRI
was performed on the hindlimb of young (12 weeks) and adult (20 weeks)
GK
and Wistar (control) rats.
31
P‐
MRS
and
BOLD
‐
MRI
data were acquired continuously during an ischemia and reperfusion protocol to quantify changes in phosphate metabolites and muscle oxygenation. The time constant of phosphocreatine recovery, an index of mitochondrial oxidative capacity, was not statistically different between
GK
rats (60.8 ± 13.9 sec in young group, 83.7 ± 13.0 sec in adult group) and their age‐matched controls (62.4 ± 11.6 sec in young group, 77.5 ± 7.1 sec in adult group). During ischemia, baseline‐normalized
BOLD
‐
MRI
signal was significantly lower in
GK
rats than in their age‐matched controls. These results suggest that insulin resistance leads to alterations in tissue metabolism without impaired mitochondrial oxidative capacity in
GK
rats. |
doi_str_mv | 10.14814/phy2.12890 |
format | Article |
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GK
) rats, a rat model of non‐obese type 2 diabetes (T2D).
31
P magnetic resonance spectroscopy (
MRS
) and blood oxygen level‐dependent (
BOLD
)
MRI
was performed on the hindlimb of young (12 weeks) and adult (20 weeks)
GK
and Wistar (control) rats.
31
P‐
MRS
and
BOLD
‐
MRI
data were acquired continuously during an ischemia and reperfusion protocol to quantify changes in phosphate metabolites and muscle oxygenation. The time constant of phosphocreatine recovery, an index of mitochondrial oxidative capacity, was not statistically different between
GK
rats (60.8 ± 13.9 sec in young group, 83.7 ± 13.0 sec in adult group) and their age‐matched controls (62.4 ± 11.6 sec in young group, 77.5 ± 7.1 sec in adult group). During ischemia, baseline‐normalized
BOLD
‐
MRI
signal was significantly lower in
GK
rats than in their age‐matched controls. These results suggest that insulin resistance leads to alterations in tissue metabolism without impaired mitochondrial oxidative capacity in
GK
rats.</description><identifier>EISSN: 2051-817X</identifier><identifier>DOI: 10.14814/phy2.12890</identifier><language>eng</language><publisher>Oxford: John Wiley & Sons, Inc</publisher><subject>Bioenergetics ; Body temperature ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Experiments ; Functional magnetic resonance imaging ; Glucose ; Insulin ; Insulin resistance ; Ischemia ; Laboratories ; Magnetic resonance spectroscopy ; Metabolism ; Metabolites ; Mitochondria ; Musculoskeletal system ; NMR ; Nuclear magnetic resonance ; Obesity ; Oxidative metabolism ; Phosphocreatine ; Reperfusion ; Skeletal muscle ; Spectrum analysis ; Studies</subject><ispartof>Physiological reports, 2016-08, Vol.4 (15)</ispartof><rights>2016. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1069-c9ee3da2702120aee5577be80a6a302d96792156246fd196e34f50cb2e7c07613</citedby><cites>FETCH-LOGICAL-c1069-c9ee3da2702120aee5577be80a6a302d96792156246fd196e34f50cb2e7c07613</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,27901,27902</link.rule.ids></links><search><creatorcontrib>Liu, Yuchi</creatorcontrib><creatorcontrib>Mei, Xunbai</creatorcontrib><creatorcontrib>Li, Jielei</creatorcontrib><creatorcontrib>Lai, Nicola</creatorcontrib><creatorcontrib>Yu, Xin</creatorcontrib><title>Mitochondrial function assessed by 31 P MRS and BOLD MRI in non‐obese type 2 diabetic rats</title><title>Physiological reports</title><description>The study aims to characterize age‐associated changes in skeletal muscle bioenergetics by evaluating the response to ischemia‐reperfusion in the skeletal muscle of the Goto‐Kakizaki (
GK
) rats, a rat model of non‐obese type 2 diabetes (T2D).
31
P magnetic resonance spectroscopy (
MRS
) and blood oxygen level‐dependent (
BOLD
)
MRI
was performed on the hindlimb of young (12 weeks) and adult (20 weeks)
GK
and Wistar (control) rats.
31
P‐
MRS
and
BOLD
‐
MRI
data were acquired continuously during an ischemia and reperfusion protocol to quantify changes in phosphate metabolites and muscle oxygenation. The time constant of phosphocreatine recovery, an index of mitochondrial oxidative capacity, was not statistically different between
GK
rats (60.8 ± 13.9 sec in young group, 83.7 ± 13.0 sec in adult group) and their age‐matched controls (62.4 ± 11.6 sec in young group, 77.5 ± 7.1 sec in adult group). During ischemia, baseline‐normalized
BOLD
‐
MRI
signal was significantly lower in
GK
rats than in their age‐matched controls. These results suggest that insulin resistance leads to alterations in tissue metabolism without impaired mitochondrial oxidative capacity in
GK
rats.</description><subject>Bioenergetics</subject><subject>Body temperature</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Experiments</subject><subject>Functional magnetic resonance imaging</subject><subject>Glucose</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Ischemia</subject><subject>Laboratories</subject><subject>Magnetic resonance spectroscopy</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Mitochondria</subject><subject>Musculoskeletal system</subject><subject>NMR</subject><subject>Nuclear magnetic resonance</subject><subject>Obesity</subject><subject>Oxidative metabolism</subject><subject>Phosphocreatine</subject><subject>Reperfusion</subject><subject>Skeletal muscle</subject><subject>Spectrum analysis</subject><subject>Studies</subject><issn>2051-817X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNotkN1KwzAcxYMgOOaufIGAl9L5T9ImzaXOr8HGxA_wQihp-i_rmElNuove-Qg-o09i3YQDhwOHc-BHyBmDKUtzll62655PGc81HJERh4wlOVNvJ2QS4wYAGAihIR2R92XTebv2rgqN2dJ652zXeEdNjDioomVPBaOPdPn0TI2r6PVqcTOEOW0cdd79fH37EiPSrm-Rclo1psSusTSYLp6S49psI07-fUxe725fZg_JYnU_n10tEstA6sRqRFEZroAzDgYxy5QqMQcjjQBeaak0Z5nkqawrpiWKtM7AlhyVBSWZGJPzw24b_OcOY1ds_C644bLgXAOXXOV6aF0cWjb4GAPWRRuaDxP6gkGxp1b8USv21MQv2spfrQ</recordid><startdate>201608</startdate><enddate>201608</enddate><creator>Liu, Yuchi</creator><creator>Mei, Xunbai</creator><creator>Li, Jielei</creator><creator>Lai, Nicola</creator><creator>Yu, Xin</creator><general>John Wiley & Sons, Inc</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>201608</creationdate><title>Mitochondrial function assessed by 31 P MRS and BOLD MRI in non‐obese type 2 diabetic rats</title><author>Liu, Yuchi ; Mei, Xunbai ; Li, Jielei ; Lai, Nicola ; Yu, Xin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1069-c9ee3da2702120aee5577be80a6a302d96792156246fd196e34f50cb2e7c07613</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Bioenergetics</topic><topic>Body temperature</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Experiments</topic><topic>Functional magnetic resonance imaging</topic><topic>Glucose</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Ischemia</topic><topic>Laboratories</topic><topic>Magnetic resonance spectroscopy</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Mitochondria</topic><topic>Musculoskeletal system</topic><topic>NMR</topic><topic>Nuclear magnetic resonance</topic><topic>Obesity</topic><topic>Oxidative metabolism</topic><topic>Phosphocreatine</topic><topic>Reperfusion</topic><topic>Skeletal muscle</topic><topic>Spectrum analysis</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Yuchi</creatorcontrib><creatorcontrib>Mei, Xunbai</creatorcontrib><creatorcontrib>Li, Jielei</creatorcontrib><creatorcontrib>Lai, Nicola</creatorcontrib><creatorcontrib>Yu, Xin</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Biological Science Database</collection><collection>Publicly Available Content 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><jtitle>Physiological reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Yuchi</au><au>Mei, Xunbai</au><au>Li, Jielei</au><au>Lai, Nicola</au><au>Yu, Xin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitochondrial function assessed by 31 P MRS and BOLD MRI in non‐obese type 2 diabetic rats</atitle><jtitle>Physiological reports</jtitle><date>2016-08</date><risdate>2016</risdate><volume>4</volume><issue>15</issue><eissn>2051-817X</eissn><abstract>The study aims to characterize age‐associated changes in skeletal muscle bioenergetics by evaluating the response to ischemia‐reperfusion in the skeletal muscle of the Goto‐Kakizaki (
GK
) rats, a rat model of non‐obese type 2 diabetes (T2D).
31
P magnetic resonance spectroscopy (
MRS
) and blood oxygen level‐dependent (
BOLD
)
MRI
was performed on the hindlimb of young (12 weeks) and adult (20 weeks)
GK
and Wistar (control) rats.
31
P‐
MRS
and
BOLD
‐
MRI
data were acquired continuously during an ischemia and reperfusion protocol to quantify changes in phosphate metabolites and muscle oxygenation. The time constant of phosphocreatine recovery, an index of mitochondrial oxidative capacity, was not statistically different between
GK
rats (60.8 ± 13.9 sec in young group, 83.7 ± 13.0 sec in adult group) and their age‐matched controls (62.4 ± 11.6 sec in young group, 77.5 ± 7.1 sec in adult group). During ischemia, baseline‐normalized
BOLD
‐
MRI
signal was significantly lower in
GK
rats than in their age‐matched controls. These results suggest that insulin resistance leads to alterations in tissue metabolism without impaired mitochondrial oxidative capacity in
GK
rats.</abstract><cop>Oxford</cop><pub>John Wiley & Sons, Inc</pub><doi>10.14814/phy2.12890</doi><oa>free_for_read</oa></addata></record> |
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subjects | Bioenergetics Body temperature Diabetes Diabetes mellitus Diabetes mellitus (non-insulin dependent) Experiments Functional magnetic resonance imaging Glucose Insulin Insulin resistance Ischemia Laboratories Magnetic resonance spectroscopy Metabolism Metabolites Mitochondria Musculoskeletal system NMR Nuclear magnetic resonance Obesity Oxidative metabolism Phosphocreatine Reperfusion Skeletal muscle Spectrum analysis Studies |
title | Mitochondrial function assessed by 31 P MRS and BOLD MRI in non‐obese type 2 diabetic rats |
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