Fasting Whole Blood Fatty Acid Profile and Risk of Type 2 Diabetes in Adults: A Nested Case Control Study
Fasting Whole Blood Fatty Acid Profile and Risk of Type 2 Diabetes in Adults: A Nested Case Control Study
Year: 2014
Authors: Alhazmi, A. Stojanovski, E. Garg, M.L. McEvoy, M.
Publication Name: PLoS One
Publication Details: Volume 9; Issue 5:e97001. doi: 10.1371/journal.pone.0097001. eCollection 2014.
Abstract:
Objective was to determine the association of fasting whole blood fatty acid concentrations with incidence of type 2 diabetes in adults. A nested case control study of 187 subjects from a cohort of men and women aged 55 to 85 years from the Hunter Region, New South Wales, Australia. Fasting whole blood fatty acids were measured using gas chromatography and incidence of type 2 diabetes was ascertained by self reported questionnaire at the study follow up. After adjustment for potential confounding variables, positive associations with type 2 diabetes were seen for dihomo gamma linolenic acid. Lignoceric acid (C24:0) is significantly associated with lower type 2 diabetes risk.These data suggest that higher fasting whole blood concentrations of omega 6 polyunsaturated fatty acids as well as omega 3 polyunsaturated fatty acid are associated with an increased risk of diabetes, whereas increased fasting whole blood concentrations of lignoceric acid is inversely associated with diabetes risk. (Authors abstract)
The prevalence of diabetes among the adult population worldwide is 285 million, and is expected to increase to 439 million by 2030. Since type 2 diabetes is associated with significant comorbidity and increased mortality, strategies to prevent the development of type 2 diabetes is the ideal approach to reduce the burden of this disease. Given the inconsistencies of the evidence examining the association of fatty acid intake with incident type 2 diabetes and the inaccuracy of the methods used to measure fatty acid status, the aim of this study was to use a nested case control design to determine the association of fasting whole blood fatty acid concentrations with incidence of type 2 diabetes in adults. In unadjusted analyses, increased DGLA, ARA, ALA, EPA, and DHA concentrations were all statistically significantly associated with increased risk of type 2 diabetes. After adjusting for potentially confounding variables, these fatty acids remained statistically significant independent predictors of type 2 diabetes risk. The results also suggested that Lignoceric acid may have a protective function. Direct comparisons between previous studies and the current study are complex due to the use of different biomarkers to determine fatty acid status, using survey and food frequency questionnaire method as opposed to quantitative (e.g. GC used in this study) assessment methods, and population differences in age, sex, lifestyles, and other factors may also affect the associations.
While another investigation of fatty acid biomarkers observed a lower risk of type 2 diabetes with increased plasma EPA per DHA concentration, finding of a recent meta analysis of cohort studies show no association between dietary EPA per DHA and type 2 diabetes risk. The difference in risk observed between these studies may be due to the vulnerability of dietary n3 PUFA to oxidative damage; this may adversely affect insulin resistance and increase the risk of type 2 diabetes. N3 PUFA may contribute to higher glucose concentrations through a number of mechanisms. It may increase hepatic gluconeogenesis by increasing uptake and oxidation of free fatty acids in the liver and lowering triacylglycerol, or it could lower glucose utilization and increase glucagons stimulated C peptide. Lignoceric acid is primarily originates from endogenous synthesis by successive chain elongation of shorter chain SFA. In whole blood it is mainly located in the erythrocyte membranes. Elevated levels of fasting whole blood 24:0 may be the result of its reduced degradation in the peroxisomes. Collectively, this nested case control study suggest that higher concentrations of fasting whole blood n6 PUFA (ARA and DGLA) and n3 PUFA (ALA, EPA, and DHA) [which contradicts most published research] were associated with an increased risk of diabetes, whereas increased fasting whole blood concentrations of lignoceric acid is inversely associated with diabetes risk in adults. (Editors comments)
The prevalence of diabetes among the adult population worldwide is 285 million, and is expected to increase to 439 million by 2030. Since type 2 diabetes is associated with significant comorbidity and increased mortality, strategies to prevent the development of type 2 diabetes is the ideal approach to reduce the burden of this disease. Given the inconsistencies of the evidence examining the association of fatty acid intake with incident type 2 diabetes and the inaccuracy of the methods used to measure fatty acid status, the aim of this study was to use a nested case control design to determine the association of fasting whole blood fatty acid concentrations with incidence of type 2 diabetes in adults. In unadjusted analyses, increased DGLA, ARA, ALA, EPA, and DHA concentrations were all statistically significantly associated with increased risk of type 2 diabetes. After adjusting for potentially confounding variables, these fatty acids remained statistically significant independent predictors of type 2 diabetes risk. The results also suggested that Lignoceric acid may have a protective function. Direct comparisons between previous studies and the current study are complex due to the use of different biomarkers to determine fatty acid status, using survey and food frequency questionnaire method as opposed to quantitative (e.g. GC used in this study) assessment methods, and population differences in age, sex, lifestyles, and other factors may also affect the associations.
While another investigation of fatty acid biomarkers observed a lower risk of type 2 diabetes with increased plasma EPA per DHA concentration, finding of a recent meta analysis of cohort studies show no association between dietary EPA per DHA and type 2 diabetes risk. The difference in risk observed between these studies may be due to the vulnerability of dietary n3 PUFA to oxidative damage; this may adversely affect insulin resistance and increase the risk of type 2 diabetes. N3 PUFA may contribute to higher glucose concentrations through a number of mechanisms. It may increase hepatic gluconeogenesis by increasing uptake and oxidation of free fatty acids in the liver and lowering triacylglycerol, or it could lower glucose utilization and increase glucagons stimulated C peptide. Lignoceric acid is primarily originates from endogenous synthesis by successive chain elongation of shorter chain SFA. In whole blood it is mainly located in the erythrocyte membranes. Elevated levels of fasting whole blood 24:0 may be the result of its reduced degradation in the peroxisomes. Collectively, this nested case control study suggest that higher concentrations of fasting whole blood n6 PUFA (ARA and DGLA) and n3 PUFA (ALA, EPA, and DHA) [which contradicts most published research] were associated with an increased risk of diabetes, whereas increased fasting whole blood concentrations of lignoceric acid is inversely associated with diabetes risk in adults. (Editors comments)
