Glycolysis/gluconeogenesis- and tricarboxylic acid cycle-related metabolites, Mediterranean diet, and type 2 diabetes.


Journal

The American journal of clinical nutrition
ISSN: 1938-3207
Titre abrégé: Am J Clin Nutr
Pays: United States
ID NLM: 0376027

Informations de publication

Date de publication:
01 04 2020
Historique:
received: 21 03 2019
accepted: 23 01 2020
pubmed: 16 2 2020
medline: 21 5 2020
entrez: 16 2 2020
Statut: ppublish

Résumé

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. 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. 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-one-out cross-validation approach. Baseline circulating concentrations of hexose monophosphate, pyruvate, lactate, alanine, glycerol-3 phosphate, and isocitrate were significantly associated with higher T2D 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. We identified a panel of glycolysis/gluconeogenesis-related 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.This trial was registered at controlled-trials.com as ISRCTN35739639.

Sections du résumé

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-one-out cross-validation approach.
RESULTS
Baseline circulating concentrations of hexose monophosphate, pyruvate, lactate, alanine, glycerol-3 phosphate, and isocitrate were significantly associated with higher T2D 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/gluconeogenesis-related 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.This trial was registered at controlled-trials.com as ISRCTN35739639.

Identifiants

pubmed: 32060497
pii: S0002-9165(22)01071-1
doi: 10.1093/ajcn/nqaa016
pmc: PMC7138680
doi:

Banques de données

ISRCTN
['ISRCTN35739639']

Types de publication

Journal Article Randomized Controlled Trial Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

835-844

Subventions

Organisme : NIDDK NIH HHS
ID : K99 DK119412
Pays : United States
Organisme : NIDDK NIH HHS
ID : K99 DK122128
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK102896
Pays : United States

Informations de copyright

Copyright © The Author(s) 2020.

Références

Obes Rev. 2015 Feb;16 Suppl 1:55-66
pubmed: 25614204
Clin Chem. 2015 Mar;61(3):487-97
pubmed: 25524438
J Clin Invest. 2019 Nov 1;129(11):4671-4675
pubmed: 31545298
Cell Metab. 2010 Apr 7;11(4):311-9
pubmed: 20374963
Mol Syst Biol. 2008;4:214
pubmed: 18682704
Diabetologia. 2018 Jun;61(6):1315-1324
pubmed: 29626220
Int J Epidemiol. 2012 Apr;41(2):377-85
pubmed: 21172932
Curr Diab Rep. 2016 Aug;16(8):74
pubmed: 27319324
PLoS One. 2014 Jan 17;9(1):e85082
pubmed: 24465478
Int J Mol Sci. 2013 Apr 24;14(5):8869-89
pubmed: 23615475
Diabetes Care. 2011 Jan;34 Suppl 1:S62-9
pubmed: 21193628
Biochem J. 2011 Apr 1;435(1):277-84
pubmed: 21208194
J Clin Epidemiol. 1999 Dec;52(12):1165-72
pubmed: 10580779
Ann Epidemiol. 2013 Dec;23(12):791-796.e4
pubmed: 24176820
Am J Physiol Endocrinol Metab. 2002 Aug;283(2):E233-40
pubmed: 12110527
Diabetes. 2013 Aug;62(8):2689-98
pubmed: 23382451
Metabolism. 1992 Jan;41(1):22-7
pubmed: 1538640
Endocr Connect. 2015 Mar;4(1):R1-R15
pubmed: 25385852
Diabetes. 2013 Feb;62(2):639-48
pubmed: 23043162
Cell. 1998 Mar 6;92(5):593-6
pubmed: 9506512
PLoS One. 2016 Dec 21;11(12):e0168352
pubmed: 28002466
Ann Intern Med. 2014 Jan 7;160(1):1-10
pubmed: 24573661
PLoS One. 2010 Nov 11;5(11):e13953
pubmed: 21085649
Diabetes Obes Metab. 2019 Feb;21(2):397-401
pubmed: 30146690
Clin Chem. 2018 Oct;64(10):1541-1542
pubmed: 30087141
Diabetes Care. 2012 Aug;35(8):1749-56
pubmed: 22563043
Sci Rep. 2019 Mar 25;9(1):5053
pubmed: 30911015
Diabetes. 2013 Dec;62(12):4270-6
pubmed: 23884885
N Engl J Med. 2018 Jun 21;378(25):e34
pubmed: 29897866
Arch Physiol Biochem. 2012 Jul;118(3):156-89
pubmed: 22385297
Am J Epidemiol. 1994 Jun 15;139(12):1197-209
pubmed: 8209878
J Diabetes Res. 2015;2015:102054
pubmed: 25961050
PLoS One. 2013;8(1):e55113
pubmed: 23383072
Annu Rev Biochem. 1975;44:933-55
pubmed: 1094924
Nat Med. 2011 Apr;17(4):448-53
pubmed: 21423183
Nat Commun. 2015 Apr 13;6:6791
pubmed: 25864806
Diabetes Care. 2018 Jan;41(Suppl 1):S13-S27
pubmed: 29222373
Diabetes Care. 2016 May;39(5):833-46
pubmed: 27208380
Nature. 2017 Nov 2;551(7678):115-118
pubmed: 29045397
Biometrics. 1986 Jun;42(2):301-10
pubmed: 3741972
Cell Metab. 2017 Aug 1;26(2):281-283
pubmed: 28768165
Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11168-72
pubmed: 9326580
Obesity (Silver Spring). 2018 Apr;26(4):683-688
pubmed: 29476613
Cell Metab. 2018 Apr 3;27(4):757-785
pubmed: 29617642
Mol Genet Metab. 2008 May;94(1):16-37
pubmed: 18243024
Nat Rev Endocrinol. 2019 Oct;15(10):569-589
pubmed: 31439934
Diabetologia. 2018 Jul;61(7):1560-1571
pubmed: 29663011
J Clin Invest. 2019 Nov 1;129(11):4563-4566
pubmed: 31545302
Int J Epidemiol. 2010 Dec;39(6):1647-55
pubmed: 20797988
Islets. 2010 Mar-Apr;2(2):89-95
pubmed: 21099300
J Biol Chem. 2007 May 18;282(20):14807-15
pubmed: 17389595

Auteurs

Marta Guasch-Ferré (M)

Department of Nutrition, Harvard TH Chan School of Public Health, Boston, MA, USA.
Human Nutrition Unit, Faculty of Medicine and Health Sciences, Pere Virgili Health Research Institute, Rovira i Virgili University, Reus, Spain.
Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.

José L Santos (JL)

Department of Nutrition, Diabetes and Metabolism, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.

Miguel A Martínez-González (MA)

Department of Nutrition, Harvard TH Chan School of Public Health, Boston, MA, USA.
Department of Preventive Medicine and Public Health, IdiSNA (Health Research Institute of Navarra), University of Navarra, Pamplona, Spain.
The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.

Clary B Clish (CB)

Broad Institute of MIT and Harvard University, Cambridge, MA, USA.

Cristina Razquin (C)

Department of Preventive Medicine and Public Health, IdiSNA (Health Research Institute of Navarra), University of Navarra, Pamplona, Spain.
The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.

Dong Wang (D)

Department of Nutrition, Harvard TH Chan School of Public Health, Boston, MA, USA.

Liming Liang (L)

Department of Biostatistics, Harvard TH Chan School of Public Health, Boston, MA, USA.

Jun Li (J)

Department of Nutrition, Harvard TH Chan School of Public Health, Boston, MA, USA.

Courtney Dennis (C)

Broad Institute of MIT and Harvard University, Cambridge, MA, USA.

Dolores Corella (D)

The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.
Department of Preventive Medicine, University of Valencia, Valencia, Spain.

Carlos Muñoz-Bravo (C)

Department of Public Health and Psychiatry, University of Málaga, Málaga, Spain.

Dora Romaguera (D)

The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.
Health Research Institute of the Balearic Islands (IdISBa), University Hospital Son Espases, Mallorca, Spain.

Ramón Estruch (R)

The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.
Department of Internal Medicine, Department of Endocrinology and Nutrition Biomedical Research Institute August Pi Sunyer (IDI-BAPS), Hospital Clinic, University of Barcelona, Barcelona, Spain.

José Manuel Santos-Lozano (JM)

The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.
Department of Family Medicine, Primary Care Division of Sevilla, San Pablo Health Center, Sevilla, Spain.

Olga Castañer (O)

The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.
Cardiovascular and Nutrition Research Group, Hospital del Mar Research Institute (IMIM), Barcelona, Spain.

Angel Alonso-Gómez (A)

The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.
Bioaraba Health Research Institute; Osakidetza Baseque Health Service, Araba University Hospital; Unibersity of the Basque Country UPV/EHU; Vitoria-Gasteiz, Spain.

Luis Serra-Majem (L)

The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.
Research Institute of Biomedical and Health Sciences (IUIBS), University of Las Palmas de Gran Canaria and Service of Preventive Medicine, Complejo Hospitalario Universitario Insular Materno Infantil (CHUIMI), Canary Health Service, Las Palmas de Gran Canaria, Spain.

Emilio Ros (E)

The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.
Lipid Clinic, Department of Endocrinology and Nutrition Biomedical Research Institute August Pi Sunyer (IDI-BAPS), Hospital Clinic, University of Barcelona, Barcelona, Spain.

Sílvia Canudas (S)

Human Nutrition Unit, Faculty of Medicine and Health Sciences, Pere Virgili Health Research Institute, Rovira i Virgili University, Reus, Spain.
The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.

Eva M Asensio (EM)

Department of Preventive Medicine, University of Valencia, Valencia, Spain.

Montserrat Fitó (M)

The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.
Cardiovascular and Nutrition Research Group, Hospital del Mar Research Institute (IMIM), Barcelona, Spain.

Kerry Pierce (K)

Broad Institute of MIT and Harvard University, Cambridge, MA, USA.

J Alfredo Martínez (JA)

The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.
Department of Nutrition, Food Sciences, and Physiology, Center for Nutrition Research, University of Navarra, Pamplona, IMDEA Food, Madrid, Spain.

Jordi Salas-Salvadó (J)

Human Nutrition Unit, Faculty of Medicine and Health Sciences, Pere Virgili Health Research Institute, Rovira i Virgili University, Reus, Spain.
The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.

Estefanía Toledo (E)

Department of Preventive Medicine and Public Health, IdiSNA (Health Research Institute of Navarra), University of Navarra, Pamplona, Spain.
The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.

Frank B Hu (FB)

Department of Nutrition, Harvard TH Chan School of Public Health, Boston, MA, USA.
Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.

Miguel Ruiz-Canela (M)

Department of Preventive Medicine and Public Health, IdiSNA (Health Research Institute of Navarra), University of Navarra, Pamplona, Spain.
The Spanish Biomedical Research Center in Physiopathology of Obesity and Nutrition, Health Institute Carlos III, Madrid, Spain.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH