NUTRIENT HOMEOSTASIS
David M. Gibson, Robert A. Harris in Metabolic Regulation in Mammals, 2001
lipoproteins) for transport to peripheral ("extrahcpatic") tissues to support cellular membrane turnover. The secretory particle of the liver that conveys cholesterol (as the fatty асу I ester), is designated "very-low -density lipoprotein", VLDL. It is smaller than but otherwise quite similar to the chylomicron. It is loaded with triacylglyccrol synthesized in the liver and joined with B100 apoproteins in the endoplasmic reticulum. VLDL circulates through the capillaries of tissues, meets the lipoprotein lipase and is relieved of its triglyceride burden ti» supply cells w ith a second major input of fatty acids for oxidation or storage. The cholesterol ester rich remnant particles left behind, called the "intermediate density lipoproteins", IDL and the "low-density lipoproteins", LDL, proceed to many different tissues w here they are subsumed by endoevtosis and supply cells with the cholesterol needed lor membrane turnover. (Cholesterol is also the synthetic precursor of steroid hormones in the adrenal cortex ami the gonads; and of the prohormone, cholecalcifcrol or vitamin I), in the skin.) Cellular plasma mem hranes become enriched in unestcrified cholesterol w here it is pickcd up by the plasma "high-density lipoprotein", HDL, After re estcrification, cholesterol is transferred principally to I DI and returned to the liver for disposal as bile acids (Chapter 8).
Clinical studies on Shengmai San
Kam-Ming Ko in Shengmai San, 2002
Research studies have demonstrated that the lipid content of atherosclerotic plaque residing in the coronary arterial wall is mainly derived from plasma. Plasma cholesterol, triglycerides and phospholipids are incorporated with apoproteins to form lipoproteins for their dissolution and transportation in blood. The low-density lipoprotein (LDL) mainly consists of cholesterol and cholesterol esters, whereas the very low-density lipoprotein (VLDL) is mainly composed of triglycerides. The increase in plasma lipids arising from the disorder in lipid metabolism can lead to the infiltration of lipids, through the endothelial cells, into the arterial wall. The entry of lipoproteins into the middle layer of the arterial wall will cause the proliferation of smooth muscle cells and their migration towards the arterial intima. The smooth muscle cells and monocytes will then engulf a huge amount of lipids and be converted to foam cells, which, in turn, lead to the formation of a fatty streak, the earliest detectable clinical sign of atherosclerosis. The events, including proliferation of smooth muscle cells, accumulation of connective tissues, disposition of lipids and proliferation of fibrous tissue, finally culminate in the formation of atherosclerotic plaque.
Atherosclerosis
George Feuer, Felix A. de la Iglesia in Molecular Biochemistry of Human Disease, 2020
The metabolism of lipoproteins is connected with the lipids and the specific polypeptides forming the apoprotein part of these complexes.245,246,377 Chylomicrons are not present in the blood of fasting subjects. LDL and HDL are responsible for the majority of cholesterol transport. LDL carries cholesterol throughout the body and HDL mediates its transport into the liver.425 VLDL are triglyceride-rich particles. The metabolic relationship between the different lipoproteins is shown in Figure 25.561,605 The normal daily intake of fat is about 120 grams containing 0.5 to 1.0 g of cholesterol.247 Exogenous fat is transferred to chylomicrons in the mucosal cells of the gut. Apoprotein exchange occurs between chylomicrons and other circulating lipoproteins; apoC and apoE are transferred as essential steps for subsequent catabolism.
The role of the daily feeding rhythm in the regulation of the day/night rhythm in triglyceride secretion in rats
Published in Chronobiology International, 2018
Yan Su, Ewout Foppen, Frederico Sander Mansur Machado, Eric Fliers, Andries Kalsbeek
It is well known that plasma TG concentrations exhibit daily rhythmicity in both humans and laboratory rodents (Mondola et al. 1995; Pan and Hussain 2007; Rudic et al. 2004; Van Oostrom et al. 2000; Yasumoto et al. 2016). Recently, Moran-Ramos et al. (2017) showed that (part of) this rhythmicity might be caused by a day/night rhythm in TG clearance, however, until now, it remains unknown whether also a daily rhythm in TG secretion exists. Very low density lipoprotein (VLDL) is a lipoprotein mainly secreted by the liver, it transports hepatic lipids, mainly TGs, to plasma for use in peripheral tissues. As VLDL’s mostly carry TGs in plasma, the rate of VLDL secretion is a major determinant of the TG secretion rate. Lipin 1 (Chen et al. 2015), stearoyl-CoA desaturase 1(Scd1) (Lam et al. 2007), apolipoprotein B (ApoB) (Olofsson and Boren 2005; Olofsson et al. 2000), microsomal TG transfer protein (MTTP) (Jamil et al. 1995) and ADP-ribosylation factor 1 (ARF-1) (Asp et al. 2000) are other important enzymes involved in VLDL-TG assembly and secretion. A number of studies have shown that these genes exhibit a clear daily rhythm in expression (Gorne et al. 2015; Liu et al. 2013; Pan and Hussain 2007; Pan and Hussain 2009; Pan et al. 2013; Pan et al. 2010). Thus, we hypothesized that also TG secretion would show a daily rhythm.
Lipoprotein(a) in clinical practice: New perspectives from basic and translational science
Published in Critical Reviews in Clinical Laboratory Sciences, 2018
Corey A. Scipione, Marlys L. Koschinsky, Michael B. Boffa
In vitro studies have been good models to assess factors that modulate assembly rates; however, they do not address the controversy regarding which apoB-containing lipoprotein couples with apo(a) in vivo. Since triglyceride-rich very low density lipoprotein (VLDL) is the predominant apoB-containing lipoprotein produced by the liver in vivo, it can be argued that Lp(a) may be formed from VLDL. A direct comparison of Lp(a) formation from VLDL versus LDL will be required to determine conclusively if apo(a) couples to VLDL, followed by enzymatic delipidation, to produce the Lp(a) that is within the LDL density range seen in plasma. Evidence suggests that triglyceride synthesis is critical for the synthesis of apo(a) by hepatoma cells [144]. When apo(a) transgenic mice were injected with human VLDL or LDL, there was a delay in the association of apo(a) with the lipoprotein fraction of VLDL-injected, but not LDL-injected animals, suggesting that apo(a) associates with a product of VLDL metabolism [145]. Understanding the mechanistic steps allowing nascent apo(a) and apoB-containing lipoproteins to develop into mature circulating Lp(a) will be vital in the interpretation of Lp(a) in vivo kinetic models and ultimately in the development of new Lp(a)-lowering therapies.
Vitamin E for the management of major depressive disorder: possible role of the anti-inflammatory and antioxidant systems
Published in Nutritional Neuroscience, 2022
Luana M. Manosso, Anderson Camargo, Alcir L. Dafre, Ana Lúcia S. Rodrigues
Because vitamin E is fat-soluble, its intestinal absorption depends on bile salts and pancreatic secretion [15]. As a result, micelles are formed, which can be absorbed and transported through cellular membranes by passive diffusion in the enterocytes [16]. However, it has also been shown that vitamin E absorption is mediated, at least in part, by cholesterol membrane transporters including the scavenger receptor class B type I (SR-BI), CD36 molecule (CD36), NPC1-like transporter 1 (NPC1L1), and ATP-binding cassettes A1 and G1 (ABCA1 and ABCG1) [17,18]. Within the enterocytes, vitamin E is esterified and then incorporated into the chylomicrons. The chylomicrons pass through the lymphatic vessels and rapidly flow into blood vessels, and then, the enzyme lipoprotein lipase hydrolyzes triacylglycerols from the surface of the chylomicron. During this process, some vitamin E is transferred to high-density lipoproteins (HDL) and vitamin E that was not transferred remains in the chylomicron remnant [16,18]. When the chylomicron remnants reach the liver, α-tocopherol transfer protein (α-TTP) binds to α-tocopherol, separating it from the chylomicron remnant and then α-tocopherol is packaged along with apolipoproteins and triacylglycerols into very-low-density lipoprotein (VLDL). VLDL is transported through the bloodstream and broken down by lipoprotein lipases in the peripheral cell endothelium and transformed into lipoprotein particles (high-density – HDL, low-density – LDL, and very-low-density – VLDL remnants). Thus, α-tocopherol may return to the liver or is delivered to target cells [19,20].
Related Knowledge Centers
- Chylomicron
- Phospholipid
- Liver
- Lipoprotein
- Intermediate-Density Lipoprotein
- Low-Density Lipoprotein
- High-Density Lipoprotein
- Cholesterol
- Triglyceride
- Apolipoprotein