Identification of Shared and Unique Serum Lipid Profiles in Diabetes Mellitus and Myocardial Infarction

Author:

Kjellqvist Sanela1,Klose Christian2,Surma Michal A.2,Hindy George3,Mollet Inês G.3,Johansson Anna1,Chavaux Patrick4,Gottfries Johan5,Simons Kai2,Melander Olle3,Fernandez Céline3

Affiliation:

1. Science for Life Laboratory, Department of Biochemistry and Biophysics, Stockholm University, Stockholm, Sweden

2. Lipotype GmbH, Dresden, Germany

3. Department of Clinical Sciences, Lund University, Malmö, Sweden

4. Department of Nutrition, Faculté de Médecine et de Pharmacie de la Timone, Aix Marseille University, Marseille, France

5. Department of Chemistry and Molecular Biology, University of Gothenburg, Sweden

Abstract

Background Diabetes mellitus ( DM ) and cardiovascular disease are associated with dyslipidemia, but the detailed lipid molecular pattern in both diseases remains unknown. Methods and Results We used shotgun mass spectrometry to determine serum levels of 255 molecular lipids in 316 controls, 171 DM , and 99 myocardial infarction ( MI ) events from a cohort derived from the Malmö Diet and Cancer study. Orthogonal projections to latent structures analyses were conducted between the lipids and clinical parameters describing DM or MI . Fatty acid desaturases ( FADS ) and elongation of very long chain fatty acid protein 5 ( ELOVL 5) activities were estimated by calculating product to precursor ratios of polyunsaturated fatty acids in complex lipids. FADS genotypes encoding these desaturases were then tested for association with lipid levels and ratios. Differences in the levels of lipids belonging to the phosphatidylcholine and triacylglyceride ( TAG ) classes contributed the most to separating DM from controls. TAG s also played a dominating role in discriminating MI from controls. Levels of C18:2 fatty acids in complex lipids were lower both in DM and MI versus controls ( DM , P =0.004; MI , P =6.0E‐06) at least due to an acceleration in the metabolic flux from C18:2 to C20:4 (eg, increased estimated ELOVL 5: DM , P =0.02; MI , P =0.04, and combined elongase‐desaturase activities: DM , P =3.0E‐06; MI , P =2.0E‐06). Minor allele carriers of FADS genotypes were associated with increased levels of C18:2 ( P ≤0.007) and lower desaturase activity ( P ≤0.002). Conclusions We demonstrate a possible relationship between decreased levels of C18:2 in complex lipids and DM or MI . We thereby highlight the importance of molecular lipids in the pathogenesis of both diseases.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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