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Robert V. Farese

Researcher at Harvard University

Publications -  484
Citations -  54181

Robert V. Farese is an academic researcher from Harvard University. The author has contributed to research in topics: Insulin & Protein kinase C. The author has an hindex of 115, co-authored 473 publications receiving 48754 citations. Previous affiliations of Robert V. Farese include University of South Florida & University at Buffalo.

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Licorice-induced Hypermineralocorticoidism

TL;DR: Two findings argue against the claim that licorice, or glycyrrhetinic acid, does not have mineralocorticoid effects in patients with Addison's disease or adrenalectomized rats1 unless cortisone or hydrocortisone is .
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DGAT enzymes are required for triacylglycerol synthesis and lipid droplets in adipocytes

TL;DR: It is shown that DGAT1 and DGAT2 account for the vast majority of TG synthesis in mice, and DG AT function is required for LDs in adipocytes, but not in all cell types.
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DGAT1 is not essential for intestinal triacylglycerol absorption or chylomicron synthesis.

TL;DR: Interestingly, DGAT1 was not essential for quantitative dietary triacylglycerol absorption, even in mice fed a high fat diet, or for the synthesis of chylomicrons, and analysis of intestine from Dgat1 −/−mice revealed activity for two other enzymes, DGat2 and diacyl glycerol transacylase, that catalyze triACYlglycersol synthesis and apparently help to compensate for the absence of DGAT 1.
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Knockout of the mouse apolipoprotein B gene results in embryonic lethality in homozygotes and protection against diet-induced hypercholesterolemia in heterozygotes.

TL;DR: It is indicated that apolipoprotein B plays an essential role in mouse embryonic development and when fed a diet rich in fat and cholesterol, heterozygous mice were protected from diet-induced hypercholesterolemia; these mice, which constitute an animal model for hypobetalipoproteinemia, should be useful for studying the effects of decreased apoliprotein B expression on atherogenesis.
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Increased atherosclerosis in LDL receptor–null mice lacking ACAT1 in macrophages

TL;DR: It is suggested that selective inhibition of ACAT1 in lesion macrophages in the setting of hyperlipidemia can lead to the accumulation of free cholesterol in the artery wall, and that this promotes, rather than inhibits, lesion development.