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Review
. 2022 Apr 14;14(8):1643.
doi: 10.3390/nu14081643.

From Dietary Cholesterol to Blood Cholesterol, Physiological Lipid Fluxes, and Cholesterol Homeostasis

Frans Stellaard  1   2
Affiliations
Review

From Dietary Cholesterol to Blood Cholesterol, Physiological Lipid Fluxes, and Cholesterol Homeostasis

Frans Stellaard. Nutrients. .

Abstract

Dietary cholesterol (C) is a major contributor to the endogenous C pool, and it affects the serum concentration of total C, particularly the low-density lipoprotein cholesterol (LDL-C). A high serum concentration of LDL-C is associated with an increased risk for atherosclerosis and cardiovascular diseases. This concentration is dependent on hepatic C metabolism creating a balance between C input (absorption and synthesis) and C elimination (conversion to bile acids and fecal excretion). The daily C absorption rate is determined by dietary C intake, biliary C secretion, direct trans-intestinal C excretion (TICE), and the fractional C absorption rate. Hepatic C metabolism coordinates C fluxes entering the liver via chylomicron remnants (CMR), LDL, high-density lipoproteins (HDL), hepatic C synthesis, and those leaving the liver via very low-density lipoproteins (VLDL), biliary secretion, and bile acid synthesis. The knowns and the unknowns of this C homeostasis are discussed.

Keywords: absorption; bile; bile acids; cholesterol; extrahepatic; hepatic; intestine; lipoproteins; plant sterols; synthesis.

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Conflict of interest statement

The author declares no conflict of interest.

Figures

Figure 1
Figure 1
C fluxes in omnivore humans as published by Lütjohann et al. [4]. The numbers in italics are obtained by reasonable estimates based on the proportion of chylomicron remnants being extracted by the liver and the proportion of hepatic C synthesis to whole body synthesis. Chylomicron remnants not extracted by the liver are taken up by extrahepatic tissues including macrophages. CM = chylomicrons, CMR = chylomicron remnants, VLDL = very low density lipoprotein, LDL = low density lipoprotein, HDL = high density lipoprotein, FFA = free fatty acid, BA = bile acid. No numbers are available for the lipoprotein fluxes.
Figure 2
Figure 2
Fat digestion of TG and CE and micellar transport of FFAs and C to enable lipid uptake into the enterocytes. The red arrow represents TG metabolism, the green arrow C metabolism and the blue arrow BA absorption. TG = triglycerides, CE = cholesterol ester, FFA = free fatty acid, C = free cholesterol, BA = bile acid.
Figure 3
Figure 3
Uptake of FFA and C into enterocyte, CM secretion and conversion to CMR and uptake of CMR into the liver. Partial transport via HDL is also indicated. HDL= high density lipoprotein. TG = triglyceride, FFA = free fatty acid, C = free cholesterol, CE = cholesterol ester, CM = chylomicron, CMR = chylomicron remnant, ABCG= ATP-binding cassette sub-family G, NPC1L1 = Niemann–Pick C1 Like 1, ABCA1 = ATP-binding cassette transporter ABCA1, SR-B =Scavenger receptor class b type 1, LRP = LDL-receptor-related protein.
Figure 4
Figure 4
Hepatic C metabolism. TG = triglyceride, FFA = free fatty acid, C = free cholesterol, CE = cholesterol ester, CM = chylomicron, CMR = chylomicron remnant, BA = bile acid.
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