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Only about 20% of the cholesterol in your blood comes from the food you eat. Your body does the rest.
- 1 Describe The Function Of Cholesterol Molecules In The Plasma Membrane
- 2 Cholesterol Interaction Motifs In G Protein‐coupled Receptors: Slippery Hot Spots?
Describe The Function Of Cholesterol Molecules In The Plasma Membrane
Cholesterol has a bad reputation, thanks to its known role in promoting heart disease. Excess cholesterol in the blood is a key factor contributing to clogged arteries, which can build up and set the stage for a heart attack. However, the role of cholesterol in the body is not entirely negative.
Plasma Membrane Structure
To fully explain cholesterol, you need to understand that it is also vital to you and your well-being. Even though we measure cholesterol production in the blood, it is found in every cell of the body. The Harvard special report Managing Cholesterol explains cholesterol as a waxy, yellow-whitish fat and a critical building block in cell membranes. Cholesterol is also needed to make vitamin D, hormones (including testosterone and estrogen), and bile acids that break down fat. In fact, cholesterol production is so important that the liver and intestines produce about 80 percent of the cholesterol needed to stay healthy. Only about 20% comes from the foods you eat (see illustration).
If you eat only 200 to 300 milligrams (mg) of cholesterol per day (one egg yolk contains about 200 mg), your liver will produce an additional 800 milligrams per day from raw materials such as fats, sugars, and proteins.
Because cholesterol is a fat, it cannot travel through the bloodstream on its own. It would end up as useless pellets (imagine bacon grease floating in a pan of water). To get around this problem, the body packages cholesterol and other lipids into tiny protein-coated particles that mix easily with the blood. These tiny particles, called lipoproteins (lipids plus proteins), move cholesterol and other fats throughout the body.
Cholesterol and other lipids circulate in the bloodstream in different forms. Of these, the one that attracts the most attention is low-density lipoprotein, better known as LDL, or “bad” cholesterol. But lipoproteins come in different shapes and sizes, and each type has its own tasks. They also transform from one form to another. These are the five main types:
Cholesterol Stabilized Membrane Active Nanopores With Anticancer Activities
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What Is Vldl Cholesterol And Can It Be Harmful?
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Get helpful tips and guidance on everything from fighting inflammation to finding the best diets for weight loss… from exercises to build a stronger core to advice on treating cataracts. PLUS, the latest news on medical advances and discoveries from the experts at Harvard Medical School. Cholesterol is a lipid molecule that plays an essential role in numerous biological processes, both physiological and pathological. It is an essential structural constituent of cell membranes and is critical for the biosynthesis, integrity, and functions of biological membranes, including membrane trafficking and signaling. Furthermore, cholesterol is the main lipid component of lipid rafts, a kind of lipid-based structures that regulate the assembly and functioning of numerous cellular signaling pathways, including those related to cancer, such as tumor cell growth, adhesion, migration, invasion and apoptosis. Considering the importance of cholesterol metabolism, its homeostasis is strictly regulated at each stage: import, synthesis, export, metabolism and storage. Alterations in this homeostatic balance are known to be associated with cardiovascular disease and atherosclerosis, but growing evidence also links these behaviors to increased cancer risk. Although there is conflicting evidence regarding the role of cholesterol in the development of cancer, most studies consistently suggest that a dysregulation of cholesterol homeostasis could lead to the development of cancer. This review aims to discuss the current understanding of cholesterol homeostasis in normal and cancer cells, summarizing key findings from recent preclinical and clinical studies that have investigated the role of key players in cholesterol regulation and lipid raft organization , which could represent promising therapeutic targets.
Cholesterol is a primary lipid molecule that plays an essential role in numerous biological processes, both at a physiological and pathological level (Maxfield and Tabas, 2005).
Cholesterol Interaction Motifs In G Protein‐coupled Receptors: Slippery Hot Spots?
Cholesterol, in addition to being an important constituent of cell membranes, is fundamental for their biogenesis and is essential for maintaining the integrity and functions of biological membranes, including endocytosis, membrane trafficking and signaling (Maxfield and Tabas, 2005; Yamauchi and Rogers, 2018). Inside the cell, cholesterol, distributed heterogeneously among the organelles, modulates the immune system and represents a precursor of hormones such as sex hormones and vitamin D (Mollinedo and Gajate, 2020; Figure 1).
Recently, cholesterol has played a key role in cancer research due to its potential therapeutic implications in both prevention and treatment. However, the role of cholesterol in oncogenesis is still debated (DuBroff and de Lorgeril, 2015). Literature data have reported a contradictory role of cholesterol depending on the type of tumor (Ding et al., 2019). Excess cholesterol is linked to breast, colon, rectal, prostate and testicular cancer (Llaverias et al., 2011; Pelton et al., 2012; Murai, 2015; Radisauskas et al., 2016), while some prospective cohort studies have shown an inverse association in gastric and prostate cancers (Asano et al., 2008; Heir et al., 2016). This review aims to discuss the current knowledge on cholesterol homeostasis by critically analyzing the most recent preclinical and clinical studies investigating the role of the main players of the cholesterol biosynthetic pathway and lipid rafts of the cholesterol-based membrane structure in the field of cancer.
Cholesterol is produced through a cascade of enzymatic reactions, called the mevalonate pathway, which requires the participation of several enzymes located on the membranes of the endoplasmic reticulum (ER). In short, the combination of three molecules of acetyl-CoA leads to the formation of one molecule of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA). The latter, through the action of HMG-CoA reductase (HMGCR), is converted into mevalonate, which in turn is transformed into squalene (SQL), and finally into cholesterol through a series of reactions (Figure 2). Food can also be a source of cholesterol. In fact, the Niemann-Pick type C1-like 1 protein (NPC1L1), present on the membrane of intestinal enterocytes, is responsible for the absorption of cholesterol, which is released in the form of chylomicrons, lipid particles rich in triglycerides, and is taken up by the liver. (Altmann et al., 2004; Luo et al., 2020).
Figure 2. Cholesterol biosynthesis pathway and main inhibitors. Starting from three molecules of acetyl coenzyme A (CoA), cholesterol is synthesized in more than 20 enzymatic steps. 3-hydroxy-3-methylglutaryl-coareductase (HMGCR) and squalene epoxidase (SQLE) act as rate-limiting enzymes. The main inhibitors of cholesterol biosynthesis are statins that inhibit HMGCR, sterol-regulating binding protein (SREBP) inhibitors that inactivate the transcription of cholesterol biosynthesis genes; and bisphosphonates which act downstream of statins and inhibitfarnesyl pyrophosphate synthase resulting in a decrease infarnesyl pyrophosphate and geranylgeranyl pyrophosphate. This step of cholesterol biosynthesis is also targeted by Farnesyl Transferase inhibitors.
Cholesterol Biosynthesis Pathway And Its Feedback Mechanism….
Cholesterol is synthesized primarily in the liver and released into the bloodstream in the form of very low-density lipoprotein (VLDL). In the bloodstream, VLDL is processed to produce low-density lipoproteins (LDL), transported to peripheral cells by the bloodstream (Ikonen, 2008; Goldstein and Brown, 2009). LDL enters cells via receptor-mediated endocytosis (LDLR) and is transported to lysosomes where it is hydrolyzed into free cholesterol molecules, which are transported to cell membranes to perform its multiple functions (Brown and Goldstein, 1986; Ikonen, 2008; Maxfield and van Meer, 2010; Kuzu et al., 2016).
The mevalonate pathway is tightly regulated by transcriptional and translational mechanisms capable of responding to physiological signals. Cholesterol biosynthesis is regulated by four main players: (1) sterol regulatory element-binding protein 2 (SREBP2), which acts through a negative feedback mechanism (Sato, 2010), (2) liver X receptors (LXRs) , (3) HMGCR, and (4) squalene epoxidase (SQLE). HMGCR and SQLE are rate-limiting enzymes, which can regulate cholesterol biosynthesis, the reactions they catalyze are energetically expensive. When intracellular ATP levels are low, adenosine monophosphate-activated protein kinase (AMPK) phosphorylates HMGCR, inhibiting its function ( Loh et al., 2019 ). Furthermore, HMGCR is affected by the presence of LDL in the medium; in fact, in case of LDL deficiency, HMGCR activity
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