Journal of Translational Research

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Opinion Article - Journal of Translational Research (2023) Volume 7, Issue 2

Lipoprotein Translation: The Key to Understanding Cholesterol Metabolism.

Robert Rosenson*

Department of Vascular Medicine, Utrecht University, The Netherlands

*Corresponding Author:
Robert Rosenson
Department of Vascular Medicine
Utrecht University, The Netherlands

Received: 28-Feb-2023, Manuscript No. AATR-23-91278; Editor assigned: 04-Mar-2023, Pre QC No. AATR-23-91278 (PQ); Reviewed: 18-Mar-2023, QC No. AATR-23-91278; Revised: 23-Mar-2023, Manuscript No. AATR-23-91278 (R); Published: 29-Mar-2023, DOI:10.35841/aatr-7.2.140

Citation: Rosenson R. Lipoprotein translation: The key to understanding cholesterol metabolism. Am J Transl Res. 2023;7(2):140

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Lipoprotein translation is a crucial process that plays a significant role in the regulation of cholesterol metabolism in humans. Lipoproteins are complexes of lipids and proteins that transport cholesterol and other lipids throughout the body. They are synthesized in the liver and intestines and are classified based on their density, including high-density lipoproteins (HDL), low-density lipoproteins (LDL), and very-low-density lipoproteins (VLDL). The translation of lipoproteins occurs in several stages, starting with the synthesis of apolipoproteins, which are proteins that bind to lipids and form lipoprotein particles. The apolipoproteins are translated on ribosomes and modified by post-translational modifications such as glycosylation and phosphorylation. The lipids are then added to the apolipoproteins to form lipoprotein particles [1].

The different types of lipoproteins have distinct functions in cholesterol metabolism. HDL, also known as "good cholesterol," transports excess cholesterol from peripheral tissues to the liver for disposal. LDL, on the other hand, is known as "bad cholesterol" because it can accumulate in the walls of arteries and lead to atherosclerosis, a condition that increases the risk of heart disease. The regulation of lipoprotein translation is complex and involves various genetic and environmental factors. For example, certain genetic mutations can affect the synthesis and function of lipoproteins, leading to conditions such as familial hypercholesterolemia, a genetic disorder characterized by high levels of LDL cholesterol.

Environmental factors such as diet, exercise, and medication can also affect lipoprotein metabolism. A diet high in saturated and trans fats can increase LDL cholesterol levels, while regular exercise and certain medications such as statins can lower LDL cholesterol levels and increase HDL cholesterol levels. Lipoprotein translation is a critical process in cholesterol metabolism that determines the levels of LDL and HDL cholesterol in the body. Understanding the regulation of lipoprotein translation can help in the development of new treatments for conditions such as hypercholesterolemia and atherosclerosis [2].

Apolipoprotein synthesis begins with the translation of the apolipoprotein mRNA on ribosomes. The nascent polypeptide chain undergoes several post-translational modifications, including signal peptide cleavage, N-terminal acetylation, and glycosylation. The modified apolipoprotein is then targeted to the endoplasmic reticulum (ER), where lipidation occurs. Lipidation is the process by which lipids are added to apolipoproteins to form lipoprotein particles. In the ER, apolipoproteins are co-translationally lipidated with phospholipids and triglycerides to form pre-β-HDL particles. These particles are then secreted into the circulation, where they mature into spherical HDL particles through the acquisition of additional lipids [3].

In contrast, the apoB-containing lipoproteins, including LDL and VLDL, are synthesized differently. ApoB is a large, single-chain protein that is synthesized as a precursor protein, apoB100, in the ER. ApoB100 is post-translationally edited by an enzyme called the apolipoprotein B mRNA editing enzyme, catalytic polypeptide 1 (APOBEC1), which converts a cytosine residue to uridine at a specific site, leading to a premature stop codon. This results in the production of a shorter protein, apoB48, which is only present in the intestines, and apoB100, which is synthesized in the liver.

ApoB100-containing lipoproteins, including LDL and VLDL, are lipidated in the ER and Golgi apparatus through the addition of triglycerides and cholesterol esters. VLDL is secreted into the circulation and is rapidly converted into LDL by the action of lipoprotein lipase and hepatic lipase [4].

The regulation of lipoprotein translation is complex and involves multiple factors, including genetics, diet, and lifestyle. Genetic factors that influence lipoprotein metabolism include polymorphisms in genes that encode for apolipoproteins and enzymes involved in lipid metabolism. Diet and lifestyle factors, such as a diet high in saturated and trans fats and sedentary behaviour, can lead to dyslipidemia and increase the risk of cardiovascular disease [5].


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