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Insulin resistance determines a differential response to changes in dietary fat modification on metabolic syndrome risk factors: the LIPGENE study.
Am J Clin Nutr 2015; 102(6):1509-17AJ

Abstract

BACKGROUND

Previous data support the benefits of reducing dietary saturated fatty acids (SFAs) on insulin resistance (IR) and other metabolic risk factors. However, whether the IR status of those suffering from metabolic syndrome (MetS) affects this response is not established.

OBJECTIVE

Our objective was to determine whether the degree of IR influences the effect of substituting high-saturated fatty acid (HSFA) diets by isoenergetic alterations in the quality and quantity of dietary fat on MetS risk factors.

DESIGN

In this single-blind, parallel, controlled, dietary intervention study, MetS subjects (n = 472) from 8 European countries classified by different IR levels according to homeostasis model assessment of insulin resistance (HOMA-IR) were randomly assigned to 4 diets: an HSFA diet; a high-monounsaturated fatty acid (HMUFA) diet; a low-fat, high-complex carbohydrate (LFHCC) diet supplemented with long-chain n-3 polyunsaturated fatty acids (1.2 g/d); or an LFHCC diet supplemented with placebo for 12 wk (control). Anthropometric, lipid, inflammatory, and IR markers were determined.

RESULTS

Insulin-resistant MetS subjects with the highest HOMA-IR improved IR, with reduced insulin and HOMA-IR concentrations after consumption of the HMUFA and LFHCC n-3 diets (P < 0.05). In contrast, subjects with lower HOMA-IR showed reduced body mass index and waist circumference after consumption of the LFHCC control and LFHCC n-3 diets and increased HDL cholesterol concentrations after consumption of the HMUFA and HSFA diets (P < 0.05). MetS subjects with a low to medium HOMA-IR exhibited reduced blood pressure, triglyceride, and LDL cholesterol levels after the LFHCC n-3 diet and increased apolipoprotein A-I concentrations after consumption of the HMUFA and HSFA diets (all P < 0.05).

CONCLUSIONS

Insulin-resistant MetS subjects with more metabolic complications responded differently to dietary fat modification, being more susceptible to a health effect from the substitution of SFAs in the HMUFA and LFHCC n-3 diets. Conversely, MetS subjects without IR may be more sensitive to the detrimental effects of HSFA intake. The metabolic phenotype of subjects clearly determines response to the quantity and quality of dietary fat on MetS risk factors, which suggests that targeted and personalized dietary therapies may be of value for its different metabolic features. This study was registered at clinicaltrials.gov as NCT00429195.

Authors+Show Affiliations

Lipids and Atherosclerosis Unit, Maimonides Institute for Biomedical Research in Cordoba, Reina Sofia University Hospital, University of Córdoba, Córdoba, Spain; CIBER Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Spain;Lipids and Atherosclerosis Unit, Maimonides Institute for Biomedical Research in Cordoba, Reina Sofia University Hospital, University of Córdoba, Córdoba, Spain; CIBER Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Spain;Nutrigenomics Research Group, University College Dublin Conway Institute, School of Public Health, University College Dublin, Dublin, Ireland;Lipids and Atherosclerosis Unit, Maimonides Institute for Biomedical Research in Cordoba, Reina Sofia University Hospital, University of Córdoba, Córdoba, Spain; CIBER Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Spain;Lipids and Atherosclerosis Unit, Maimonides Institute for Biomedical Research in Cordoba, Reina Sofia University Hospital, University of Córdoba, Córdoba, Spain; CIBER Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Spain;Lipids and Atherosclerosis Unit, Maimonides Institute for Biomedical Research in Cordoba, Reina Sofia University Hospital, University of Córdoba, Córdoba, Spain; CIBER Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Spain;Department of Cell Biology, Physiology and Immunology, University of Córdoba, Maimonides Institute for Biomedical Research in Cordoba/Reina Sofia University, CIBER Maimonides Institute for Biomedical Research in Cordoba, Córdoba, Spain;Biomedical Research Institute of Málaga, Virgen de la Victoria Hospital, University of Málaga, Málaga, Spain;Department of Nutrition, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Oslo, Norway;NRA-Joint Research Unit, UMR1260, and French National Institute of Health and Medical Research ERL1025 Lipid Nutrients and the Prevention of Metabolic Diseases, Faculty of Medicine, Marseille, France;Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Center, Maastricht, Netherlands;Department of Clinical Biochemistry, Jagiellonian University, Collegium Medicum, Kraków, Poland;Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism, Uppsala University, Uppsala, Sweden; and.Hugh Sinclair Unit of Human Nutrition and Institute for Cardiovascular and Metabolic Research, Department of Food and Nutritional Sciences, University of Reading, Reading, United Kingdom.Lipids and Atherosclerosis Unit, Maimonides Institute for Biomedical Research in Cordoba, Reina Sofia University Hospital, University of Córdoba, Córdoba, Spain; CIBER Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Spain;Nutrigenomics Research Group, University College Dublin Conway Institute, School of Public Health, University College Dublin, Dublin, Ireland;Lipids and Atherosclerosis Unit, Maimonides Institute for Biomedical Research in Cordoba, Reina Sofia University Hospital, University of Córdoba, Córdoba, Spain; CIBER Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Spain; jlopezmir@uco.es.

Pub Type(s)

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

Language

eng

PubMed ID

26561628

Citation

Yubero-Serrano, Elena M., et al. "Insulin Resistance Determines a Differential Response to Changes in Dietary Fat Modification On Metabolic Syndrome Risk Factors: the LIPGENE Study." The American Journal of Clinical Nutrition, vol. 102, no. 6, 2015, pp. 1509-17.
Yubero-Serrano EM, Delgado-Lista J, Tierney AC, et al. Insulin resistance determines a differential response to changes in dietary fat modification on metabolic syndrome risk factors: the LIPGENE study. Am J Clin Nutr. 2015;102(6):1509-17.
Yubero-Serrano, E. M., Delgado-Lista, J., Tierney, A. C., Perez-Martinez, P., Garcia-Rios, A., Alcala-Diaz, J. F., ... Lopez-Miranda, J. (2015). Insulin resistance determines a differential response to changes in dietary fat modification on metabolic syndrome risk factors: the LIPGENE study. The American Journal of Clinical Nutrition, 102(6), pp. 1509-17. doi:10.3945/ajcn.115.111286.
Yubero-Serrano EM, et al. Insulin Resistance Determines a Differential Response to Changes in Dietary Fat Modification On Metabolic Syndrome Risk Factors: the LIPGENE Study. Am J Clin Nutr. 2015;102(6):1509-17. PubMed PMID: 26561628.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Insulin resistance determines a differential response to changes in dietary fat modification on metabolic syndrome risk factors: the LIPGENE study. AU - Yubero-Serrano,Elena M, AU - Delgado-Lista,Javier, AU - Tierney,Audrey C, AU - Perez-Martinez,Pablo, AU - Garcia-Rios,Antonio, AU - Alcala-Diaz,Juan F, AU - Castaño,Justo P, AU - Tinahones,Francisco J, AU - Drevon,Christian A, AU - Defoort,Catherine, AU - Blaak,Ellen E, AU - Dembinska-Kieć,Aldona, AU - Risérus,Ulf, AU - Lovegrove,Julie A, AU - Perez-Jimenez,Francisco, AU - Roche,Helen M, AU - Lopez-Miranda,Jose, Y1 - 2015/11/11/ PY - 2015/03/15/received PY - 2015/09/15/accepted PY - 2015/11/13/entrez PY - 2015/11/13/pubmed PY - 2016/4/14/medline KW - dietary fat modification KW - insulin resistance KW - metabolic syndrome KW - monounsaturated fat KW - polyunsaturated fat SP - 1509 EP - 17 JF - The American journal of clinical nutrition JO - Am. J. Clin. Nutr. VL - 102 IS - 6 N2 - BACKGROUND: Previous data support the benefits of reducing dietary saturated fatty acids (SFAs) on insulin resistance (IR) and other metabolic risk factors. However, whether the IR status of those suffering from metabolic syndrome (MetS) affects this response is not established. OBJECTIVE: Our objective was to determine whether the degree of IR influences the effect of substituting high-saturated fatty acid (HSFA) diets by isoenergetic alterations in the quality and quantity of dietary fat on MetS risk factors. DESIGN: In this single-blind, parallel, controlled, dietary intervention study, MetS subjects (n = 472) from 8 European countries classified by different IR levels according to homeostasis model assessment of insulin resistance (HOMA-IR) were randomly assigned to 4 diets: an HSFA diet; a high-monounsaturated fatty acid (HMUFA) diet; a low-fat, high-complex carbohydrate (LFHCC) diet supplemented with long-chain n-3 polyunsaturated fatty acids (1.2 g/d); or an LFHCC diet supplemented with placebo for 12 wk (control). Anthropometric, lipid, inflammatory, and IR markers were determined. RESULTS: Insulin-resistant MetS subjects with the highest HOMA-IR improved IR, with reduced insulin and HOMA-IR concentrations after consumption of the HMUFA and LFHCC n-3 diets (P < 0.05). In contrast, subjects with lower HOMA-IR showed reduced body mass index and waist circumference after consumption of the LFHCC control and LFHCC n-3 diets and increased HDL cholesterol concentrations after consumption of the HMUFA and HSFA diets (P < 0.05). MetS subjects with a low to medium HOMA-IR exhibited reduced blood pressure, triglyceride, and LDL cholesterol levels after the LFHCC n-3 diet and increased apolipoprotein A-I concentrations after consumption of the HMUFA and HSFA diets (all P < 0.05). CONCLUSIONS: Insulin-resistant MetS subjects with more metabolic complications responded differently to dietary fat modification, being more susceptible to a health effect from the substitution of SFAs in the HMUFA and LFHCC n-3 diets. Conversely, MetS subjects without IR may be more sensitive to the detrimental effects of HSFA intake. The metabolic phenotype of subjects clearly determines response to the quantity and quality of dietary fat on MetS risk factors, which suggests that targeted and personalized dietary therapies may be of value for its different metabolic features. This study was registered at clinicaltrials.gov as NCT00429195. SN - 1938-3207 UR - https://www.unboundmedicine.com/medline/citation/26561628/Insulin_resistance_determines_a_differential_response_to_changes_in_dietary_fat_modification_on_metabolic_syndrome_risk_factors:_the_LIPGENE_study_ L2 - https://academic.oup.com/ajcn/article-lookup/doi/10.3945/ajcn.115.111286 DB - PRIME DP - Unbound Medicine ER -