Glycolysis/gluconeogenesis- and tricarboxylic acid cycle-related metabolites, Mediterranean diet, and type 2 diabetes
Background: Glycolysis/gluconeogenesis and tricarboxylic acid (TCA) cycle metabolites have been associated with type 2 diabetes (T2D). However, the associations of these metabolites with T2D incidence and the potential effect of dietary interventions remain unclear. Objectives: We aimed to evaluate...
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creator | Guasch-Ferre, Marta Santos, Jose L. Martinez-Gonzalez, Miguel A. Clish, Clary B. Razquin, Cristina Wang, Dong Liang, Liming Li, Jun Dennis, Courtney Corella, Dolores Munoz-Bravo, Carlos Romaguera, Dora Estruch, Ramon Manuel Santos-Lozano, Jose Castaner, Olga Alonso-Gomez, Angel Serra-Majem, Luis Ros, Emilio Canudas, Silvia Asensio, Eva M. Fito, Montserrat Pierce, Kerry Alfredo Martinez, J. Salas-Salvado, Jordi Toledo, Estefania Hu, Frank B. Ruiz-Canela, Miguel |
description | Background: Glycolysis/gluconeogenesis and tricarboxylic acid (TCA) cycle metabolites have been associated with type 2 diabetes (T2D). However, the associations of these metabolites with T2D incidence and the potential effect of dietary interventions remain unclear.
Objectives: We aimed to evaluate the association of baseline and 1-y changes in glycolysis/gluconeogenesis and TCA cycle metabolites with insulin resistance and T2D incidence, and the potential modifying effect of Mediterranean diet (MedDiet) interventions.
Methods: We included 251 incident T2D cases and 638 noncases in a nested case-cohort study within the PREDIMED Study during median follow-up of 3.8 y. Participants were allocated to MedDiet + extra-virgin olive oil. MedDiet + nuts, or control diet. Plasma metabolites were measured using a targeted approach by LC-tandem MS. We tested the associations of baseline and 1-y changes in glycolysis/gluconeogenesis and TCA cycle metabolites with subsequent T2D risk using weighted Cox regression models and adjusting for potential confounders. We designed a weighted score combining all these metabolites and applying the leave-oneout cross-validation approach.
Results: Baseline circulating concentrations of hexose monophosphate. pyruvate, lactate, alanine, glycerol-3 phosphate, and isocitrate were significantly associated with higher T21) risk (17-44% higher risk for each 1-SD increment). The weighted score including all metabolites was associated with a 30% (95% CI: 1.12, 1.51) higher relative risk of T2D for each 1-SD increment. Baseline lactate and alanine were associated with baseline and 1-y changes of homeostasis model assessment of insulin resistance. One-year increases in most metabolites and in the weighted score were associated with higher relative risk of T2D after 1-y of follow-up. Lower risks were observed in the MedDiet groups than in the control group although no significant interactions were found after adjusting for multiple comparisons.
Conclusions: We identified a panel of glycolysis/gluconeogenesisrelated metabolites that was significantly associated with T2D risk in a Mediterranean population at high cardiovascular disease risk. A MedDiet could counteract the detrimental effects of these metabolites. |
doi_str_mv | 10.1093/ajcn/ngaa016 |
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fullrecord | <record><control><sourceid>webofscience</sourceid><recordid>TN_cdi_webofscience_primary_000525318600015</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>000525318600015</sourcerecordid><originalsourceid>FETCH-LOGICAL-c128t-27bf2541f64651fd49946199eefb6e51217f9be3d431b62ebcc865d4b5ed294c3</originalsourceid><addsrcrecordid>eNqNkMtOwzAURC0EoqWw4wOyp6F-J16iCApSERtYV37cVK5cu0pcQf4eS-UDWM3cuUezGITuCX4kWLGV3tu4ijutMZEXaE4Ua2tGcXOJ5hhjWisixQzdjOMeY0J5K6_RrPwl5qqZo9M6TDaFafTjahdONkVIO4hQ7rrS0VV58FYPJv1MwdtKW-8qO9kA9QBBZ3DVAbI2KfgM47J6B1fMMOgIOlbOQ16eW6YjVLQE2kABb9FVr8MId3-6QF8vz5_da735WL91T5vaEtrmmjamp4KTXnIpSO-4UlwSpQB6I0EQSppeGWCOM2IkBWNtK4XjRoCjilu2QA_n3m8wqR-th2hhexz8QQ_TtswjqGCklcURUej2_3Tns84-xS6dYma_65F2ag</addsrcrecordid><sourcetype>Enrichment Source</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Glycolysis/gluconeogenesis- and tricarboxylic acid cycle-related metabolites, Mediterranean diet, and type 2 diabetes</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Web of Science - Science Citation Index Expanded - 2020<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" /></source><source>Alma/SFX Local Collection</source><creator>Guasch-Ferre, Marta ; Santos, Jose L. ; Martinez-Gonzalez, Miguel A. ; Clish, Clary B. ; Razquin, Cristina ; Wang, Dong ; Liang, Liming ; Li, Jun ; Dennis, Courtney ; Corella, Dolores ; Munoz-Bravo, Carlos ; Romaguera, Dora ; Estruch, Ramon ; Manuel Santos-Lozano, Jose ; Castaner, Olga ; Alonso-Gomez, Angel ; Serra-Majem, Luis ; Ros, Emilio ; Canudas, Silvia ; Asensio, Eva M. ; Fito, Montserrat ; Pierce, Kerry ; Alfredo Martinez, J. ; Salas-Salvado, Jordi ; Toledo, Estefania ; Hu, Frank B. ; Ruiz-Canela, Miguel</creator><creatorcontrib>Guasch-Ferre, Marta ; Santos, Jose L. ; Martinez-Gonzalez, Miguel A. ; Clish, Clary B. ; Razquin, Cristina ; Wang, Dong ; Liang, Liming ; Li, Jun ; Dennis, Courtney ; Corella, Dolores ; Munoz-Bravo, Carlos ; Romaguera, Dora ; Estruch, Ramon ; Manuel Santos-Lozano, Jose ; Castaner, Olga ; Alonso-Gomez, Angel ; Serra-Majem, Luis ; Ros, Emilio ; Canudas, Silvia ; Asensio, Eva M. ; Fito, Montserrat ; Pierce, Kerry ; Alfredo Martinez, J. ; Salas-Salvado, Jordi ; Toledo, Estefania ; Hu, Frank B. ; Ruiz-Canela, Miguel</creatorcontrib><description>Background: Glycolysis/gluconeogenesis and tricarboxylic acid (TCA) cycle metabolites have been associated with type 2 diabetes (T2D). However, the associations of these metabolites with T2D incidence and the potential effect of dietary interventions remain unclear.
Objectives: We aimed to evaluate the association of baseline and 1-y changes in glycolysis/gluconeogenesis and TCA cycle metabolites with insulin resistance and T2D incidence, and the potential modifying effect of Mediterranean diet (MedDiet) interventions.
Methods: We included 251 incident T2D cases and 638 noncases in a nested case-cohort study within the PREDIMED Study during median follow-up of 3.8 y. Participants were allocated to MedDiet + extra-virgin olive oil. MedDiet + nuts, or control diet. Plasma metabolites were measured using a targeted approach by LC-tandem MS. We tested the associations of baseline and 1-y changes in glycolysis/gluconeogenesis and TCA cycle metabolites with subsequent T2D risk using weighted Cox regression models and adjusting for potential confounders. We designed a weighted score combining all these metabolites and applying the leave-oneout cross-validation approach.
Results: Baseline circulating concentrations of hexose monophosphate. pyruvate, lactate, alanine, glycerol-3 phosphate, and isocitrate were significantly associated with higher T21) risk (17-44% higher risk for each 1-SD increment). The weighted score including all metabolites was associated with a 30% (95% CI: 1.12, 1.51) higher relative risk of T2D for each 1-SD increment. Baseline lactate and alanine were associated with baseline and 1-y changes of homeostasis model assessment of insulin resistance. One-year increases in most metabolites and in the weighted score were associated with higher relative risk of T2D after 1-y of follow-up. Lower risks were observed in the MedDiet groups than in the control group although no significant interactions were found after adjusting for multiple comparisons.
Conclusions: We identified a panel of glycolysis/gluconeogenesisrelated metabolites that was significantly associated with T2D risk in a Mediterranean population at high cardiovascular disease risk. A MedDiet could counteract the detrimental effects of these metabolites.</description><identifier>ISSN: 0002-9165</identifier><identifier>EISSN: 1938-3207</identifier><identifier>DOI: 10.1093/ajcn/ngaa016</identifier><identifier>PMID: 32060497</identifier><language>eng</language><publisher>NEW YORK: Elsevier</publisher><subject>Life Sciences & Biomedicine ; Nutrition & Dietetics ; Science & Technology</subject><ispartof>The American journal of clinical nutrition, 2020-04, Vol.111 (4), p.835-844</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>58</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000525318600015</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c128t-27bf2541f64651fd49946199eefb6e51217f9be3d431b62ebcc865d4b5ed294c3</citedby><cites>FETCH-LOGICAL-c128t-27bf2541f64651fd49946199eefb6e51217f9be3d431b62ebcc865d4b5ed294c3</cites><orcidid>0000-0003-2700-7459 ; 0000-0002-0897-3048 ; 0000-0002-7684-2787 ; 0000-0001-8259-9245 ; 0000-0001-8525-1404 ; 0000-0003-2895-0369 ; 0000-0002-5630-1588 ; 0000-0003-3480-2645 ; 0000-0002-6263-4434</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,27931,27932,28255</link.rule.ids></links><search><creatorcontrib>Guasch-Ferre, Marta</creatorcontrib><creatorcontrib>Santos, Jose L.</creatorcontrib><creatorcontrib>Martinez-Gonzalez, Miguel A.</creatorcontrib><creatorcontrib>Clish, Clary B.</creatorcontrib><creatorcontrib>Razquin, Cristina</creatorcontrib><creatorcontrib>Wang, Dong</creatorcontrib><creatorcontrib>Liang, Liming</creatorcontrib><creatorcontrib>Li, Jun</creatorcontrib><creatorcontrib>Dennis, Courtney</creatorcontrib><creatorcontrib>Corella, Dolores</creatorcontrib><creatorcontrib>Munoz-Bravo, Carlos</creatorcontrib><creatorcontrib>Romaguera, Dora</creatorcontrib><creatorcontrib>Estruch, Ramon</creatorcontrib><creatorcontrib>Manuel Santos-Lozano, Jose</creatorcontrib><creatorcontrib>Castaner, Olga</creatorcontrib><creatorcontrib>Alonso-Gomez, Angel</creatorcontrib><creatorcontrib>Serra-Majem, Luis</creatorcontrib><creatorcontrib>Ros, Emilio</creatorcontrib><creatorcontrib>Canudas, Silvia</creatorcontrib><creatorcontrib>Asensio, Eva M.</creatorcontrib><creatorcontrib>Fito, Montserrat</creatorcontrib><creatorcontrib>Pierce, Kerry</creatorcontrib><creatorcontrib>Alfredo Martinez, J.</creatorcontrib><creatorcontrib>Salas-Salvado, Jordi</creatorcontrib><creatorcontrib>Toledo, Estefania</creatorcontrib><creatorcontrib>Hu, Frank B.</creatorcontrib><creatorcontrib>Ruiz-Canela, Miguel</creatorcontrib><title>Glycolysis/gluconeogenesis- and tricarboxylic acid cycle-related metabolites, Mediterranean diet, and type 2 diabetes</title><title>The American journal of clinical nutrition</title><addtitle>AM J CLIN NUTR</addtitle><description>Background: Glycolysis/gluconeogenesis and tricarboxylic acid (TCA) cycle metabolites have been associated with type 2 diabetes (T2D). However, the associations of these metabolites with T2D incidence and the potential effect of dietary interventions remain unclear.
Objectives: We aimed to evaluate the association of baseline and 1-y changes in glycolysis/gluconeogenesis and TCA cycle metabolites with insulin resistance and T2D incidence, and the potential modifying effect of Mediterranean diet (MedDiet) interventions.
Methods: We included 251 incident T2D cases and 638 noncases in a nested case-cohort study within the PREDIMED Study during median follow-up of 3.8 y. Participants were allocated to MedDiet + extra-virgin olive oil. MedDiet + nuts, or control diet. Plasma metabolites were measured using a targeted approach by LC-tandem MS. We tested the associations of baseline and 1-y changes in glycolysis/gluconeogenesis and TCA cycle metabolites with subsequent T2D risk using weighted Cox regression models and adjusting for potential confounders. We designed a weighted score combining all these metabolites and applying the leave-oneout cross-validation approach.
Results: Baseline circulating concentrations of hexose monophosphate. pyruvate, lactate, alanine, glycerol-3 phosphate, and isocitrate were significantly associated with higher T21) risk (17-44% higher risk for each 1-SD increment). The weighted score including all metabolites was associated with a 30% (95% CI: 1.12, 1.51) higher relative risk of T2D for each 1-SD increment. Baseline lactate and alanine were associated with baseline and 1-y changes of homeostasis model assessment of insulin resistance. One-year increases in most metabolites and in the weighted score were associated with higher relative risk of T2D after 1-y of follow-up. Lower risks were observed in the MedDiet groups than in the control group although no significant interactions were found after adjusting for multiple comparisons.
Conclusions: We identified a panel of glycolysis/gluconeogenesisrelated metabolites that was significantly associated with T2D risk in a Mediterranean population at high cardiovascular disease risk. A MedDiet could counteract the detrimental effects of these metabolites.</description><subject>Life Sciences & Biomedicine</subject><subject>Nutrition & Dietetics</subject><subject>Science & Technology</subject><issn>0002-9165</issn><issn>1938-3207</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>AOWDO</sourceid><recordid>eNqNkMtOwzAURC0EoqWw4wOyp6F-J16iCApSERtYV37cVK5cu0pcQf4eS-UDWM3cuUezGITuCX4kWLGV3tu4ijutMZEXaE4Ua2tGcXOJ5hhjWisixQzdjOMeY0J5K6_RrPwl5qqZo9M6TDaFafTjahdONkVIO4hQ7rrS0VV58FYPJv1MwdtKW-8qO9kA9QBBZ3DVAbI2KfgM47J6B1fMMOgIOlbOQ16eW6YjVLQE2kABb9FVr8MId3-6QF8vz5_da735WL91T5vaEtrmmjamp4KTXnIpSO-4UlwSpQB6I0EQSppeGWCOM2IkBWNtK4XjRoCjilu2QA_n3m8wqR-th2hhexz8QQ_TtswjqGCklcURUej2_3Tns84-xS6dYma_65F2ag</recordid><startdate>20200401</startdate><enddate>20200401</enddate><creator>Guasch-Ferre, Marta</creator><creator>Santos, Jose L.</creator><creator>Martinez-Gonzalez, Miguel A.</creator><creator>Clish, Clary B.</creator><creator>Razquin, Cristina</creator><creator>Wang, Dong</creator><creator>Liang, Liming</creator><creator>Li, Jun</creator><creator>Dennis, Courtney</creator><creator>Corella, Dolores</creator><creator>Munoz-Bravo, Carlos</creator><creator>Romaguera, Dora</creator><creator>Estruch, Ramon</creator><creator>Manuel Santos-Lozano, Jose</creator><creator>Castaner, Olga</creator><creator>Alonso-Gomez, Angel</creator><creator>Serra-Majem, Luis</creator><creator>Ros, Emilio</creator><creator>Canudas, Silvia</creator><creator>Asensio, Eva M.</creator><creator>Fito, Montserrat</creator><creator>Pierce, Kerry</creator><creator>Alfredo Martinez, J.</creator><creator>Salas-Salvado, Jordi</creator><creator>Toledo, Estefania</creator><creator>Hu, Frank B.</creator><creator>Ruiz-Canela, Miguel</creator><general>Elsevier</general><scope>AOWDO</scope><scope>BLEPL</scope><scope>DTL</scope><orcidid>https://orcid.org/0000-0003-2700-7459</orcidid><orcidid>https://orcid.org/0000-0002-0897-3048</orcidid><orcidid>https://orcid.org/0000-0002-7684-2787</orcidid><orcidid>https://orcid.org/0000-0001-8259-9245</orcidid><orcidid>https://orcid.org/0000-0001-8525-1404</orcidid><orcidid>https://orcid.org/0000-0003-2895-0369</orcidid><orcidid>https://orcid.org/0000-0002-5630-1588</orcidid><orcidid>https://orcid.org/0000-0003-3480-2645</orcidid><orcidid>https://orcid.org/0000-0002-6263-4434</orcidid></search><sort><creationdate>20200401</creationdate><title>Glycolysis/gluconeogenesis- and tricarboxylic acid cycle-related metabolites, Mediterranean diet, and type 2 diabetes</title><author>Guasch-Ferre, Marta ; Santos, Jose L. ; Martinez-Gonzalez, Miguel A. ; Clish, Clary B. ; Razquin, Cristina ; Wang, Dong ; Liang, Liming ; Li, Jun ; Dennis, Courtney ; Corella, Dolores ; Munoz-Bravo, Carlos ; Romaguera, Dora ; Estruch, Ramon ; Manuel Santos-Lozano, Jose ; Castaner, Olga ; Alonso-Gomez, Angel ; Serra-Majem, Luis ; Ros, Emilio ; Canudas, Silvia ; Asensio, Eva M. ; Fito, Montserrat ; Pierce, Kerry ; Alfredo Martinez, J. ; Salas-Salvado, Jordi ; Toledo, Estefania ; Hu, Frank B. ; Ruiz-Canela, Miguel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c128t-27bf2541f64651fd49946199eefb6e51217f9be3d431b62ebcc865d4b5ed294c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Life Sciences & Biomedicine</topic><topic>Nutrition & Dietetics</topic><topic>Science & Technology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guasch-Ferre, Marta</creatorcontrib><creatorcontrib>Santos, Jose L.</creatorcontrib><creatorcontrib>Martinez-Gonzalez, Miguel A.</creatorcontrib><creatorcontrib>Clish, Clary B.</creatorcontrib><creatorcontrib>Razquin, Cristina</creatorcontrib><creatorcontrib>Wang, Dong</creatorcontrib><creatorcontrib>Liang, Liming</creatorcontrib><creatorcontrib>Li, Jun</creatorcontrib><creatorcontrib>Dennis, Courtney</creatorcontrib><creatorcontrib>Corella, Dolores</creatorcontrib><creatorcontrib>Munoz-Bravo, Carlos</creatorcontrib><creatorcontrib>Romaguera, Dora</creatorcontrib><creatorcontrib>Estruch, Ramon</creatorcontrib><creatorcontrib>Manuel Santos-Lozano, Jose</creatorcontrib><creatorcontrib>Castaner, Olga</creatorcontrib><creatorcontrib>Alonso-Gomez, Angel</creatorcontrib><creatorcontrib>Serra-Majem, Luis</creatorcontrib><creatorcontrib>Ros, Emilio</creatorcontrib><creatorcontrib>Canudas, Silvia</creatorcontrib><creatorcontrib>Asensio, Eva M.</creatorcontrib><creatorcontrib>Fito, Montserrat</creatorcontrib><creatorcontrib>Pierce, Kerry</creatorcontrib><creatorcontrib>Alfredo Martinez, J.</creatorcontrib><creatorcontrib>Salas-Salvado, Jordi</creatorcontrib><creatorcontrib>Toledo, Estefania</creatorcontrib><creatorcontrib>Hu, Frank B.</creatorcontrib><creatorcontrib>Ruiz-Canela, Miguel</creatorcontrib><collection>Web of Science - Science Citation Index Expanded - 2020</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><jtitle>The American journal of clinical nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guasch-Ferre, Marta</au><au>Santos, Jose L.</au><au>Martinez-Gonzalez, Miguel A.</au><au>Clish, Clary B.</au><au>Razquin, Cristina</au><au>Wang, Dong</au><au>Liang, Liming</au><au>Li, Jun</au><au>Dennis, Courtney</au><au>Corella, Dolores</au><au>Munoz-Bravo, Carlos</au><au>Romaguera, Dora</au><au>Estruch, Ramon</au><au>Manuel Santos-Lozano, Jose</au><au>Castaner, Olga</au><au>Alonso-Gomez, Angel</au><au>Serra-Majem, Luis</au><au>Ros, Emilio</au><au>Canudas, Silvia</au><au>Asensio, Eva M.</au><au>Fito, Montserrat</au><au>Pierce, Kerry</au><au>Alfredo Martinez, J.</au><au>Salas-Salvado, Jordi</au><au>Toledo, Estefania</au><au>Hu, Frank B.</au><au>Ruiz-Canela, Miguel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glycolysis/gluconeogenesis- and tricarboxylic acid cycle-related metabolites, Mediterranean diet, and type 2 diabetes</atitle><jtitle>The American journal of clinical nutrition</jtitle><stitle>AM J CLIN NUTR</stitle><date>2020-04-01</date><risdate>2020</risdate><volume>111</volume><issue>4</issue><spage>835</spage><epage>844</epage><pages>835-844</pages><issn>0002-9165</issn><eissn>1938-3207</eissn><abstract>Background: Glycolysis/gluconeogenesis and tricarboxylic acid (TCA) cycle metabolites have been associated with type 2 diabetes (T2D). However, the associations of these metabolites with T2D incidence and the potential effect of dietary interventions remain unclear.
Objectives: We aimed to evaluate the association of baseline and 1-y changes in glycolysis/gluconeogenesis and TCA cycle metabolites with insulin resistance and T2D incidence, and the potential modifying effect of Mediterranean diet (MedDiet) interventions.
Methods: We included 251 incident T2D cases and 638 noncases in a nested case-cohort study within the PREDIMED Study during median follow-up of 3.8 y. Participants were allocated to MedDiet + extra-virgin olive oil. MedDiet + nuts, or control diet. Plasma metabolites were measured using a targeted approach by LC-tandem MS. We tested the associations of baseline and 1-y changes in glycolysis/gluconeogenesis and TCA cycle metabolites with subsequent T2D risk using weighted Cox regression models and adjusting for potential confounders. We designed a weighted score combining all these metabolites and applying the leave-oneout cross-validation approach.
Results: Baseline circulating concentrations of hexose monophosphate. pyruvate, lactate, alanine, glycerol-3 phosphate, and isocitrate were significantly associated with higher T21) risk (17-44% higher risk for each 1-SD increment). The weighted score including all metabolites was associated with a 30% (95% CI: 1.12, 1.51) higher relative risk of T2D for each 1-SD increment. Baseline lactate and alanine were associated with baseline and 1-y changes of homeostasis model assessment of insulin resistance. One-year increases in most metabolites and in the weighted score were associated with higher relative risk of T2D after 1-y of follow-up. Lower risks were observed in the MedDiet groups than in the control group although no significant interactions were found after adjusting for multiple comparisons.
Conclusions: We identified a panel of glycolysis/gluconeogenesisrelated metabolites that was significantly associated with T2D risk in a Mediterranean population at high cardiovascular disease risk. A MedDiet could counteract the detrimental effects of these metabolites.</abstract><cop>NEW YORK</cop><pub>Elsevier</pub><pmid>32060497</pmid><doi>10.1093/ajcn/ngaa016</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-2700-7459</orcidid><orcidid>https://orcid.org/0000-0002-0897-3048</orcidid><orcidid>https://orcid.org/0000-0002-7684-2787</orcidid><orcidid>https://orcid.org/0000-0001-8259-9245</orcidid><orcidid>https://orcid.org/0000-0001-8525-1404</orcidid><orcidid>https://orcid.org/0000-0003-2895-0369</orcidid><orcidid>https://orcid.org/0000-0002-5630-1588</orcidid><orcidid>https://orcid.org/0000-0003-3480-2645</orcidid><orcidid>https://orcid.org/0000-0002-6263-4434</orcidid></addata></record> |
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subjects | Life Sciences & Biomedicine Nutrition & Dietetics Science & Technology |
title | Glycolysis/gluconeogenesis- and tricarboxylic acid cycle-related metabolites, Mediterranean diet, and type 2 diabetes |
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