| Introduction |
The word "lipid" is used to designate a variety of chemically distinct compounds that have minimal functional overlap but share the feature of being soluble in organic solvents and almost insoluble in water. In the hydrophilic milieu of the circulatory system, hydrophobic lipids can be carried by macromolecular protein complexes called lipoproteins.
Lipids are necessary for health, but high levels of cholesterol and triglycerides in the blood, whether brought on by hereditary defects of lipoprotein metabolism or factors related to lifestyle, play a significant role in the development of atherosclerosis and cardiovascular disease. Although additional lipids and their roles are briefly covered, these circumstances are the main topic of this chapter.
High concentrations of different lipids are the cause of a blood lipid problem. Various types of lipids exist. Triglycerides and total cholesterol are the most prevalent. Numerous additional kinds of cholesterol are also counted. Your blood should have low levels of triglycerides, total cholesterol, and LDL ("bad") cholesterol. The HDL cholesterol level should be high. You have a higher chance of contracting a variety of cardiovascular diseases if you don't.
Your lipid levels might be affected by a healthy diet and/or drugs. When paired with exercise, they are very helpful. Together, they can aid in weight loss and body fat reduction. These lessen your chances of having low good lipids and high bad lipids.Pick workouts that will help you lose weight because lowering body weight and fat is associated with increasing your lipid levels. The greatest approach to shed pounds and keep them off is through a combination of regular exercise and a nutritious diet. Exercise aids in calorie burning and fat loss. Additionally, it lowers your risk of stroke, high blood pressure, type 2 diabetes, and heart disease. Regular exercise will enhance your health regardless of your weight or rate of weight reduction.
The word "lipid" is used to designate a variety of chemically distinct compounds that have minimal functional overlap but share the feature of being soluble in organic solvents and almost insoluble in water. In the hydrophilic milieu of the circulatory system, hydrophobic lipids can be carried by macromolecular protein complexes called lipoproteins. Lipids are necessary for health, but high levels of cholesterol and triglycerides in the blood, whether brought on by hereditary defects of lipoprotein metabolism or factors related to lifestyle, play a significant role in the development of atherosclerosis and cardiovascular disease. Although additional lipids and their roles are briefly covered, these circumstances are the main topic of this chapter.To start burning calories, do aerobic activity. Focus more on aerobic exercise as there is little evidence linking weight training to lowering blood lipids. But you should also incorporate strength training afterwards. Combining the two forms of exercise will aid in weight loss. They'll also help you become more physically and mentally fit.
Chylomicrons, which create dietary fat in the plasma, and the liver's generation of very low-density lipoproteins (VLDL) are the sources of lipoprotein formation. Nelson, (2013). (2013). Triglycerides and cholesteryl esters make up the inside of chylomicrons, whereas apoproteins B48, CI, CII, CIII, and E make up the outside. Chylomicrons' triglycerides are broken down by the lipoprotein lipase present in capillary endothelial cells when they come into contact with them. On the chylomicron surface, apo CII promotes this lipase activity. The liver then engages in endocytosis of the chylomicron remains. The apoproteins apo B48 and apo E on the residual surface are known for endocytosis. The liver is where the chylomicron residual lipoproteins are broken down.
Triglycerides are the most common lipids in very low-density lipoproteins (VLDL), which are produced and released as the first step in the liver's lipoprotein manufacturing process. VLDL's surface protein apo CII encourages capillary lipoprotein lipase to break down triglycerides. The elimination of triglycerides and apoproteins, with the exception of apo B100, transforms the remaining lipoprotein, intermediate-density lipoprotein (IDL), into low-density lipoprotein (LDL). In the liver and other organs, LDL binds to LDL receptors Pieper-Furst and Lammert (2013). Cholesterol, which is the primary lipid in LDL, is converted to bile in the liver. Cholesterol is moved from peripheral tissues to the liver via high-density lipoprotein (HDL), which is produced by the liver and gut.
| Lipid Disorders in Children and Adolescents |
Defects in the generation, transportation, and/or breakdown of lipoproteins can cause lipid abnormalities in children and adolescents. An overview of the structure, function, and metabolism of lipoproteins is given so that the many reasons of lipoprotein abnormalities may be understood. The component lipids and apolipoproteins associated with each particle, as well as the sources of each subclass of lipoprotein, are listed in Table 20-1.Food post-ingestion is digested to fatty acids, 2-monoglycerides, unesterified cholesterol, lysophospholipids, and unesterified plant sterols, whereas phospholipids, cholesterol esters, and triglycerides are converted to lysophospholipids. A microsomal triglyceride transfer protein causes these lipid-soluble products to permeate past the apical surface of the enteric membrane and reaggregate into lipoproteins (MTP). A mature chylomicron is produced when MTP (and maybe another transfer protein) conjugate triglycerides with cholesterol ester (a phospholipid monolayer) and apolipoprotein B-48 (apoB-48).
Two ATP-binding cassette (ABC) half-transporters are responsible for excreting the majority of ingested plant sterols and around half of the absorbed cholesterol back into the lumen of the intestinal cell. This limits the absorption of these sterols. Chylomicrons are too big once they have developed to pass through the capillary membrane. As a result, they are released into the lymphatic system and pass through the thoracic lymph duct to the venous plasma compartment. Several apolipoproteins, such as apoC-II and apoE, are preferentially transported to the chylomicrons from other lipoproteins when the nascent particles are discharged into the plasma (e.g., high-density lipoproteins, HDL).
Dietary triglycerides and cholesterol are transported by chylomicrons to locations for storage or metabolism. They are quickly removed from the bloodstream thanks to lipoprotein lipase (LPL). A triglyceride hydrolase called LPL is present on the capillary endothelium of many different tissues, with the concentration being greatest in adipose and muscular tissues. On the chylomicron, apo-CII activates LPL. The particle gets smaller when the triglyceride inside the chylomicron is hydrolyzed. apoC-II separates from the surface of the original triglyceride after around 80% of it has been eliminated. The liver absorbs the triglyceride-depleted chylomicrons, which are now known as chylomicron remnants, via a receptor that detects apoE on the surface of the particle. The endocytosis process, which is mediated by the low-density lipoprotein receptor-like protein (LRP), may also be used to absorb a lesser portion of the remains.
Similar to chylomicrons, very-low-density lipoproteins (VLDLs) are triglyceride-rich particles that are produced by the liver. However, unlike the chylomicrons that are sourced from the intestine, the fatty acids found in VLDL triglycerides are created from scratch using either dietary carbohydrates, leftovers from lipoproteins, or circulating fatty acids that the liver absorbs from plasma. 4 Triglyceride and cholesterol ester are assembled within the hepatocyte by an MTP and encircled by a phospholipid membrane connected to apoB-100. Other apolipoproteins, such as apoC-II and apoE, adhere to the mature VLDL surface after being discharged from the lymph and eventually into the arterial space.
| Treatment of Lipid Disorders |
With growing understanding, it has been determined that these anomalies are caused by mutations in enzymes, apolipoproteins, and receptors. However, many deficiencies are still unknown, and frequently, their expression is influenced by both genetic and environmental variables. Numerous lipid abnormalities are complications of other illnesses. For instance, insulin upregulates the LPL, and diabetic individuals with insufficient insulin production frequently have hypertriacylglycerolemia as a result of their diabetes and relative LPL deficit. An increased LDL cholesterol level can be brought on by other medical diseases, such as hypothyroidism, in which case the underlying ailment must be treated first. Medications from certain classes may also cause lipid abnormalities; in this case, the drugs can be stopped if it is medically possible.High HDL cholesterol levels are often protective against ASCVD, but elevated LDL cholesterol levels are closely linked with the development of ASCVD. In addition to a number of risk factors, the National Cholesterol Educational Program (NCEP) employs measures of LDL-cholesterol as guidelines for treatment with diet and medication.
A diet low in total fat, saturated fat, and cholesterol is the initial step in treating a fundamental disease of lipid and lipoprotein metabolism (NCEP step I and step II diets). In particular, patients with hypertriacylglycerolemia, low HDL cholesterol, glucose intolerance, and insulin resistance should focus on losing weight. Typically, drug therapy is based on the increased lipoprotein in question, starting with atherogenic LDL. The NCEP III recommendations' positive and negative risk indicators for each individual assess if the objective of treatment with diet, exercise, and pharmacological therapy has been attained. Additionally, guidelines have been put forward for low HDL cholesterol and hypertriacylglycemia.
The HMG CoA reductase inhibitors, sometimes referred to as "statins," are the preferred medications for treating excessive LDL cholesterol levels. This enzyme's inhibition lowers the amount of hepatic cholesterol in the blood, which activates LDL receptors and lowers blood levels of LDL cholesterol. Mevinolin, also known as mevastatin, is a fungus metabolite that inhibits HMG CoA reductase. It was discovered in 1976. Most of the current cholesterol-lowering medications that work by inhibiting these enzymes are either chemically altered fungal metabolites or entirely synthetic analogs of this substance. They consist of the following: simvastatin, fluvastatin, lovastatin, pravastatin, and atorvastatin. These medications, when administered in sufficiently large dosages, can also cause a substantial decrease in triacylglycerols, most likely by reducing hepatic VLDL synthesis and eliminating the IDL molecules.
The bile acid sequestrants or resins (cholestyramine or colestipol) and niacin are additional medications that are used when the LDL cholesterol level is increased. Bile acids are bound by bile acid sequestrants in the colon, facilitating their excretion in the stool. This prevents the bile acids from being reabsorbed, which increases the amount of cholesterol that the liver converts to bile acids. LDL receptors are triggered and the level of hepatic cholesterol decreases, which lowers the level of LDL cholesterol in the blood.