scholarly journals Regulation of Cholesterol Metabolism by Bioactive Components of Soy Proteins: Novel Translational Evidence

2020 ◽  
Vol 22 (1) ◽  
pp. 227
Author(s):  
Giusy Rita Caponio ◽  
David Q.-H. Wang ◽  
Agostino Di Ciaula ◽  
Maria De Angelis ◽  
Piero Portincasa
Keyword(s):  
Cardiovascular Disease ◽  
Clinical Medicine ◽  
Cholesterol Metabolism ◽  
Plasma Cholesterol ◽  
Dietary Cholesterol ◽  
Soy Proteins ◽  
Dietary Recommendations ◽  
Pharmacological Interventions ◽  
Cholesterol Levels ◽  
Important Amount

Hypercholesterolemia represents one key pathophysiological factor predisposing to increasing risk of developing cardiovascular disease worldwide. Controlling plasma cholesterol levels and other metabolic risk factors is of paramount importance to prevent the overall burden of disease emerging from cardiovascular-disease-related morbidity and mortality. Dietary cholesterol undergoes micellization and absorption in the small intestine, transport via blood, and uptake in the liver. An important amount of cholesterol originates from hepatic synthesis, and is secreted by the liver into bile together with bile acids (BA) and phospholipids, with all forming micelles and vesicles. In clinical medicine, dietary recommendations play a key role together with pharmacological interventions to counteract the adverse effects of chronic hypercholesterolemia. Bioactive compounds may also be part of initial dietary plans. Specifically, soybean contains proteins and peptides with biological activity on plasma cholesterol levels and this property makes soy proteins a functional food. Here, we discuss how soy proteins modulate lipid metabolism and reduce plasma cholesterol concentrations in humans, with potential outcomes in improving metabolic- and dyslipidemia-related conditions.

The role of diet during development on the regulation of adult cholesterol homeostasis

1985 ◽  
Vol 63 (5) ◽  
pp. 557-564 ◽  
Author(s):  
Sheila M. Innis
Keyword(s):  
Cholesterol Metabolism ◽  
Plasma Cholesterol ◽  
Dietary Cholesterol ◽  
Cholesterol Homeostasis ◽  
Cholesterol Levels ◽  
Effective Training ◽  
Cholesterol Intake ◽  
Lower Plasma Cholesterol ◽  
Altered Metabolism

Atherosclerosis is believed to begin early in life and to develop over several decades. Elevated plasma cholesterol is a major contributing factor. Studies in animals have shown that manipulation of cholesterol metabolism during its development in pre-and early post-natal life can permanently alter cholesterol synthesis and catabolism to favour lower plasma cholesterol levels in the adult faced with a high dietary cholesterol intake. Although the mechanisms and pathways involved are likely to be different, "metabolic training" can occur as a result of both the diet fed to the mother during gestation and lactation and from the diet fed to the animal itself in early life. The presence of cholesterol itself in the suckling diet does not appear to confer any lasting improvement to cholesterol handling in either man or animals. Although much research is still required to define the time in development for effective training of specific steps in cholesterol metabolism and the primary site and mechanism of permanently altered metabolism, significant progress has been made. These studies will form the basis of this review.

Bile Acids: The Good, the Bad, and the Ugly

Physiology ◽  
1999 ◽  
Vol 14 (1) ◽  
pp. 24-29 ◽  
Author(s):  
Alan F. Hofmann
Keyword(s):  
Bile Acids ◽  
Enterohepatic Circulation ◽  
Cholesterol Metabolism ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipid Absorption ◽  
Bile Acid Metabolism ◽  
Cholesterol Levels ◽  
Density Lipoprotein Receptor

Bile acids, amphipathic end products of cholesterol metabolism, are “good” in the infant because they enhance lipid absorption and thereby promote growth. Bile acids also induce bile flow and biliary lipid secretion. The enterohepatic circulation of bile acids is “bad” in the adult because it downregulates hepatocyte low-density lipoprotein receptor activity and thereby elevates plasma cholesterol levels. Defects in bile acid metabolism such as impaired biosynthesis or transport are “ugly” because they cause morbidity and death. New approaches for treating these defects are being developed.

Abstract 65: Flavin Monoxygenase 3 (FMO3) is a Novel Regulator of Hepatic Cholesterol Metabolism and Transintestinal Cholesterol Efflux (TICE).

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Manya Warrier ◽  
Stepahie Marshall ◽  
Allison McDaniel ◽  
Martha Wilson ◽  
Amanda Brown ◽  
...  
Keyword(s):  
Cholesteryl Ester ◽  
Plasma Levels ◽  
Cholesterol Efflux ◽  
Cholesterol Metabolism ◽  
Transcriptional Profiling ◽  
Dietary Cholesterol ◽  
High Cholesterol Diet ◽  
Hepatic Cholesterol ◽  
Hepatic Expression ◽  
Cholesterol Levels

Recent studies have revealed a novel route for cholesterol disposal through intestine known as transintestinal cholesterol efflux (TICE) that significantly contributes to fecal neutral sterol loss. This pathway is an integral part of reverse cholesterol transport (RCT), yet major mechanisms regulating TICE are not well understood. Using an unbiased transcriptional profiling approach in mouse models of augmented TICE, we found that hepatic expression of the enzyme Flavin monoxygenase 3 (FMO3) was dramatically repressed. At the same time we identified this enzyme through transcriptional profiling, it was reported that plasma levels of its product trimethylamineoxide (TMAO) are highly predictive of atheroslcerosis in humans, and TMAO is proatherogenic in mice. To further understand FMO3’s role as a regulator of cholesterol metabolism we used antisense oligonucleotides (ASO) to knockdown FMO3 expression in mouse liver in C57BL/6 mice fed either low (0.02%) or high (0.2%) levels of dietary cholesterol. As expected, FMO3 knockdown (>90% knockdown in the liver) increased the TMA/TMAO ratio in plasma more than 3-fold. Interestingly, knockdown of FMO biliary cholesterol levels were reduced by 60%, whereas fecal cholesterol loss was quite normal in FMO3 ASO treated mice fed a high cholesterol diet, which phenocopies a previously described mouse model where TICE predominates (NPC1L1-liver transgenic mice). ASO-mediated knockdown of FMO3 also unexpectedly reduced hepatic cholesteryl ester (CE) storage by 70% in mice fed 0.2% cholesterol. In parallel, knockdown of FMO3 reduces plasma VLDL cholesterol levels and the secretion rate of VLDL cholesteryl ester, but not triacylglycerol in cholesterol fed mice. FMO3 knockdown also reduced the hepatic expression of several liver X receptor (LXR) target genes, while increasing expression of genes involved in cholesterol synthesis. Collectively, these studies have identified FMO3 as a novel regulator of hepatic cholesterol metabolism and TICE. Given that plasma levels of FMO3’s product (TMAO) are strongly associated with atherosclerosis development in humans, and production of TMAO promotes atherosclerosis in mice, these studies have important implications for future cardiovascular drug discovery.

scholarly journals Genetic susceptibility, dietary cholesterol intake, and plasma cholesterol levels in a Chinese population

2020 ◽  
Vol 61 (11) ◽  
pp. 1504-1511
Author(s):  
Shaofeng Huo ◽  
Liang Sun ◽  
Geng Zong ◽  
Boyu Song ◽  
He Zheng ◽  
...  
Keyword(s):  
Genetic Susceptibility ◽  
Chinese Population ◽  
Plasma Cholesterol ◽  
Nutrition Transition ◽  
Dietary Cholesterol ◽  
Effect Sizes ◽  
Risk Scores ◽  
Asian Countries ◽  
Cholesterol Levels ◽  
Cholesterol Intake

Accompanied with nutrition transition, non-HDL-C levels of individuals in Asian countries has increased rapidly, which has caused the global epicenter of nonoptimal cholesterol to shift from Western countries to Asian countries. Thus, it is critical to underline major genetic and dietary determinants. In the current study of 2,330 Chinese individuals, genetic risk scores (GRSs) were calculated for total cholesterol (TC; GRSTC, 57 SNPs), LDL-C (GRSLDL-C, 45 SNPs), and HDL-C (GRSHDL-C, 65 SNPs) based on SNPs from the Global Lipid Genetics Consortium study. Cholesterol intake was estimated by a 74-item food-frequency questionnaire. Associations of dietary cholesterol intake with plasma TC and LDL-C strengthened across quartiles of the GRSTC (effect sizes: −0.29, 0.34, 2.45, and 6.47; Pinteraction = 0.002) and GRSLDL-C (effect sizes: −1.35, 0.17, 5.45, and 6.07; Pinteraction = 0.001), respectively. Similar interactions with non-HDL-C were observed between dietary cholesterol and GRSTC (Pinteraction = 0.001) and GRSLDL-C (Pinteraction = 0.004). The adverse effects of GRSTC on TC (effect sizes across dietary cholesterol quartiles: 0.51, 0.82, 1.21, and 1.31; Pinteraction = 0.023) and GRSLDL-C on LDL-C (effect sizes across dietary cholesterol quartiles: 0.66, 0.52, 1.12, and 1.56; Pinteraction = 0.020) were more profound in those having higher cholesterol intake compared with those with lower intake. Our findings suggest significant interactions between genetic susceptibility and dietary cholesterol intake on plasma cholesterol profiles in a Chinese population.

scholarly journals Cholesterol in pregnancy: a review of knowns and unknowns

2011 ◽  
Vol 4 (4) ◽  
pp. 147-151 ◽  
Author(s):  
Änne Bartels ◽  
Keelin O'Donoghue
Keyword(s):  
Cardiovascular Disease ◽  
Vitamin D ◽  
Fetal Development ◽  
Plasma Cholesterol ◽  
Adult Population ◽  
The Body ◽  
High Cholesterol ◽  
Cholesterol Levels ◽  
Growing Body ◽  
In Pregnancy

Cholesterol forms part of every cell in the human body, and also helps make and metabolize hormones, bile acids and vitamin D. Human plasma cholesterol levels are determined by production in the liver and by dietary intake. Lipoproteins carry cholesterol around the body, and facilitate it crossing the placenta. Cholesterol is carefully monitored in the non-pregnant adult population, where its association with atherosclerosis and cardiovascular disease is well understood. Although it is known that cholesterol rises in pregnancy, at present it is not routinely measured or treated. The effects of maternal high cholesterol on pregnancy and on fetal development are not yet fully understood. However, a growing body of evidence from animal and human studies suggests adverse consequences of high cholesterol levels in pregnancy.

scholarly journals Cholesterolaemic Effects of the Saturated Fatty Acids of Palm Oil

1994 ◽  
Vol 15 (2) ◽  
pp. 1-7 ◽  
Author(s):  
Pramod Khosla ◽  
K. C. Hayes
Keyword(s):  
Fatty Acids ◽  
Palmitic Acid ◽  
Palm Oil ◽  
Cholesterol Metabolism ◽  
Plasma Cholesterol ◽  
Saturated Fatty Acids ◽  
Dietary Cholesterol ◽  
Dietary Fatty Acids ◽  
Potential Health ◽  
Minimal Impact

Dietary saturated fats are implicated as a major risk factor in hypercholesterolaemia and cardiovascular disease. Palm oil is a major source of the world's supply of oils and fats, but because of its relatively high content of saturated fatty acids (principally palmitic acid), its consumption has come under intense scrutiny over the last decade owing to potential health implications. Based on studies carried out more than thirty years ago, the hypothesis was developed that lauric, myristic, and palmitic acid were the three principal cholesterol-raising saturated fatty acids. Since palmitic acid is the most abundant fatty acid in the diet, the cholesterol-raising effect of all saturated fatty acids was accordingly assigned to it. However, recent studies from both humans and experimental animals suggest that not all saturated fatty acids are cholesterol-raising. When all dietary fatty acids are equalized, with the exception of the two being tested, palmitic acid appears to have no impact on the plasma cholesterol in normocholesterolaemic subjects when dietary cholesterol intake is below a certain critical level (400 mg per day). Only when cholesterol consumption exceeds this level, or when hypercholesterolaemic subjects are studied, does palmitic acid appear to increase the plasma cholesterol. These differential effects of palmitic acid on plasma cholesterol are thought to reflect differences in LDL-receptor status. Collectively these data imply that, for most of the world's population, palm oil would be an inexpensive and readily metabolized source of dietary energy with minimal impact on cholesterol metabolism.

Dietary cholesterol does not normalize low plasma cholesterol levels but induces hyperbilirubinemia and hypercholanemia in Mdr2 P-glycoprotein-deficient mice

2001 ◽  
Vol 34 (2) ◽  
pp. 202-209 ◽  
Author(s):  
Peter J Voshol ◽  
Nynke R Koopen ◽  
J.Marleen L de Vree ◽  
Rick Havinga ◽  
Hans M.G Princen ◽  
...  
Keyword(s):  
Plasma Cholesterol ◽  
Dietary Cholesterol ◽  
Cholesterol Levels ◽  
P Glycoprotein ◽  
Deficient Mice
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