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Frank M. Sacks

Researcher at Harvard University

Publications -  520
Citations -  86842

Frank M. Sacks is an academic researcher from Harvard University. The author has contributed to research in topics: Cholesterol & Weight loss. The author has an hindex of 120, co-authored 490 publications receiving 80422 citations. Previous affiliations of Frank M. Sacks include Erasmus University Rotterdam & University of Texas Health Science Center at Houston.

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Dietary monounsaturated fat activates metabolic pathways for triglyceride-rich lipoproteins that involve apolipoproteins E and C-III

TL;DR: MUFA intake activates synthetic and rapid catabolic pathways for TRL metabolism that involve apo E and apo C-III and suppresses the metabolism of more slowly metabolized VLDLs and IDLs, which do not contain these apolipoproteins.
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Apolipoprotein A-II alters the proteome of human lipoproteins and enhances cholesterol efflux from ABCA1.

TL;DR: It is found that the presence of apoA-II enhanced ABCA1-mediated efflux compared with LpA-I particles, independent of the accessory protein signature suggesting that apo a-II induces a structural change in apo A-I in HDLs.
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Abdominal obesity and hyperglycemia mask the effect of a common APOC3 haplotype on the risk of myocardial infarction

TL;DR: The results support the concept that mutations in the APOC3 promoter inhibit the down-regulation of AP OC3 expression by insulin, which becomes dysfunctional in abdominal obesity and hyperglycemia.
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Lack of an effect of dietary saturated fat and cholesterol on blood pressure in normotensives.

TL;DR: In short-term nutritional studies, dietary saturated fat and cholesterol at low-to-moderate levels of intake have no significant effects on BP in normotensive adults.
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Regulation of lipoprotein metabolism by adrenergic mechanisms.

TL;DR: Studying the effects of α- and β-adrenergic blocker administration in animals and humans should provide insights into the relationship between the adrenergic nervous system and atherosclerosis and an enhanced understanding of the mechanisms by which antihypertensive agents alter serum lipids.