Single nucleotide polymorphisms that influence lipid metabolism: interaction with dietary factors.
Cardiovascular disease (CVD) risk is the result of complex interactions between genetic and environmental factors. During the past few decades, much attention has focused on plasma lipoproteins as CVD risk factors. The current evidence supports the concept that gene-environment interactions modulate...
| Publicado en: | Annual Review of Nutrition Vol. 25; no. 1; pp. 341 - 391 |
|---|---|
| Autores principales: | , |
| Formato: | Journal Article |
| Publicado: |
Annual Reviews Inc.
2005
|
| Acceso en línea: | Ver este registro en EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=106039881&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 106039881 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 01999885 83T jtl: Annual Review of Nutrition issn: 01999885 maglogo: N pubinfo: dt: 2005 vid: 25 iid: 1 pid: 59 pub: Annual Reviews Inc. place: Palo Alto, California artinfo: ui: 106039881 2009417318 NLM16011471 106039881 ppf: 341 ppct: 50 formats: fmt: @attributes: type: P tig: atl: Single nucleotide polymorphisms that influence lipid metabolism: interaction with dietary factors. aug: au: Corella D Ordovas JM sug: ab: Cardiovascular disease (CVD) risk is the result of complex interactions between genetic and environmental factors. During the past few decades, much attention has focused on plasma lipoproteins as CVD risk factors. The current evidence supports the concept that gene-environment interactions modulate plasma lipid concentrations and potentially CVD risk. The findings from studies examining gene-diet interactions and lipid metabolism have been highly promising. Several loci (i.e., APOA1, APOA4, APOE, and LIPC) are providing proof-of-concept for the potential application of genetics in the context of personalized nutritional recommendations for CVD prevention. However, the incorporation of these findings to the clinical environment is not ready for prime time. There is a compelling need for replication using a higher level of scientific evidence. Moreover, we need to evolve from the simple scenarios examined nowadays (i.e., one single dietary component, single nucleotide polymorphism, and risk factor) to more realistic situations involving inter-actions between multiple genes, dietary components, and risk factors. In summary, there is need for both large population studies and well-standardized intervention studies. pubtype: Academic Journal doctype: Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
|---|