TY  - JOUR
AB  - Purpose of review It is becoming increasingly evident that epigenetic mechanisms, particularly DNA methylation, play a role in the regulation of blood lipid levels and lipid metabolism-linked phenotypes and diseases. Recent findings Recent genome-wide methylation and candidate gene studies of blood lipids have highlighted several robustly replicated methylation markers across different ethnicities. Furthermore, many of these lipid-related CpG sites associated with blood lipids are also linked to lipid-related phenotypes and diseases. Integrating epigenome-wide association studies (EWAS) data with other layers of molecular data such as genetics or the transcriptome, accompanied by relevant statistical methods (e.g. Mendelian randomization), provides evidence for causal relationships. Recent data suggest that epigenetic changes can be consequences rather than causes of dyslipidemia. There is sparse information on many lipid classes and disorders of lipid metabolism, and also on the interplay of DNA methylation with other epigenetic layers such as histone modifications and regulatory RNAs. Summary The current review provides a literature overview of epigenetic modifications in lipid metabolism and other lipid-related phenotypes and diseases focusing on EWAS of DNA methylation from January 2016 to September 2017. Recent studies strongly support the importance of epigenetic modifications, such as DNA methylation, in lipid metabolism and related diseases for relevant biological insights, reliable biomarkers, and even future therapeutics.
AU  - Mittelstraß, K.
AU  - Waldenberger, M.
C1  - 53349
C2  - 44543
CY  - Philadelphia
SP  - 116-124
TI  - DNA methylation in human lipid metabolism and related diseases.
JO  - Curr. Opin. Lipidol.
VL  - 29
IS  - 2
PB  - Lippincott Williams & Wilkins
PY  - 2018
SN  - 0957-9672
ER  - 

TY  - JOUR
AB  - PURPOSE OF REVIEW: The delta-5 and delta-6 desaturases have long been known to be important enzymes in the endogenous formation of long-chain polyunsaturated fatty acids (LC-PUFAs). Cloning of the coding sequences and chromosomal localization of the desaturase encoding genes fatty acid desaturase 1 and 2 (FADS1 and FADS2) opened the way for analyses of genetic factors as regulators of desaturase activity and LC-PUFA homeostasis. The present review summarizes the recent association studies on FADS genotypes and LC-PUFA levels and suggests ideas how FADS genotypes can be integrated in future research. RECENT FINDINGS: An initial candidate gene study reported highly significant associations between FADS gene cluster polymorphisms and fatty acid levels in serum phospholipids with an extraordinary high genetically explained variance for arachidonic acid levels of 28.5%. Carriers of the minor alleles had enhanced levels of desaturase substrates and decreased levels of desaturase products, suggesting a decline in desaturase expression or activity because of the polymorphisms. These results were replicated in several association studies additionally showing an effect in different human tissues as well as in a recent genome-wide association study on LC-PUFA levels. SUMMARY: The validated strong association between FADS genotypes and fatty acid levels in diverse human tissues shows that FADS gene cluster polymorphisms are, in addition to nutritional regulation of fatty acid synthesis, a very important regulator of LC-PUFA synthesis.
AU  - Lattka, E.
AU  - Illig, T.
AU  - Koletzko, B.*
AU  - Heinrich, J.
C1  - 5953
C2  - 27641
SP  - 64-69
TI  - Genetic variants of the FADS1 FADS2 gene cluster as related to essential fatty acid metabolism.
JO  - Curr. Opin. Lipidol.
VL  - 21
IS  - 1
PB  - Lippincott Williams&Wilkins
PY  - 2010
SN  - 0957-9672
ER  -