scholarly journals Hepatic Lipase: a Comprehensive View of its Role on Plasma Lipid and Lipoprotein Metabolism

2015 ◽  
Vol 22 (10) ◽  
pp. 1001-1011 ◽  
Author(s):  
Junji Kobayashi ◽  
Kazuya Miyashita ◽  
Katsuyuki Nakajima ◽  
Hiroshi Mabuchi
Keyword(s):  
Hepatic Lipase ◽  
Plasma Lipid ◽  
Lipoprotein Metabolism ◽  
Comprehensive View ◽  
Lipase A

scholarly journals Lack of Association between Polymorphisms of Hepatic Lipase with Lipid Profile in Young Jordanian Adults

2014 ◽  
Vol 7 ◽  
pp. LPI.S14798
Author(s):  
Omar F. Khabour ◽  
Mahmoud A. Alomari ◽  
Karem H. Alzoubi ◽  
Mohammad Y. Gharaibeh ◽  
Farah H. Alhashimi
Keyword(s):  
Lipid Profile ◽  
Hepatic Lipase ◽  
Plasma Lipid ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Restriction Enzymes ◽  
Plasma Total Cholesterol ◽  
Chain Reaction ◽  
Males And Females ◽  
Polymerase Chain

The human hepatic lipase ( LIPC) gene encodes hepatic lipase, an enzyme involved in lipoprotein metabolism and regulation. Therefore, variants in LIPC gene may influence plasma lipoprotein levels. In this study, the association of LIPC C-514T and G-250A polymorphisms with plasma lipid profiles in 348 young Jordanians was investigated. Genotyping of C-514T and G-250A was performed by polymerase chain reaction and subsequent digestion with DraI and NiaIII restriction enzymes, respectively, while Roche analyzer was used to determine plasma total cholesterol, triglycerides, low-and high-density lipoprotein. The G-250 and C-514 alleles were most abundant in Jordanians with 79 and 80% frequencies, respectively. Additionally, no difference was found in the lipid–lipoprotein profile between the different genotype groups of C-514T or G-250A polymorphisms, even when males and females were examined separately ( P ≫ 0.05). In young Jordanian adults, the examined LIPC polymorphisms seem to play a limited role in determining the lipid profile.

Dyslipidemia of chronic renal failure: the nature, mechanisms, and potential consequences

2006 ◽  
Vol 290 (2) ◽  
pp. F262-F272 ◽  
Author(s):  
N. D. Vaziri
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Hepatic Lipase ◽  
Low Density Lipoprotein ◽  
Plasma Concentrations ◽  
Cholesterol Acyltransferase ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Triglyceride Rich Lipoprotein ◽  
Density Lipoprotein Receptor

Chronic renal failure (CRF) results in profound lipid disorders, which stem largely from dysregulation of high-density lipoprotein (HDL) and triglyceride-rich lipoprotein metabolism. Specifically, maturation of HDL is impaired and its composition is altered in CRF. In addition, clearance of triglyceride-rich lipoproteins and their atherogenic remnants is impaired, their composition is altered, and their plasma concentrations are elevated in CRF. Impaired maturation of HDL in CRF is primarily due to downregulation of lecithin-cholesterol acyltransferase (LCAT) and, to a lesser extent, increased plasma cholesteryl ester transfer protein (CETP). Triglyceride enrichment of HDL in CRF is primarily due to hepatic lipase deficiency and elevated CETP activity. The CRF-induced hypertriglyceridemia, abnormal composition, and impaired clearance of triglyceride-rich lipoproteins and their remnants are primarily due to downregulation of lipoprotein lipase, hepatic lipase, and the very-low-density lipoprotein receptor, as well as, upregulation of hepatic acyl-CoA cholesterol acyltransferase (ACAT). In addition, impaired HDL metabolism contributes to the disturbances of triglyceride-rich lipoprotein metabolism. These abnormalities are compounded by downregulation of apolipoproteins apoA-I, apoA-II, and apoC-II in CRF. Together, these abnormalities may contribute to the risk of arteriosclerotic cardiovascular disease and may adversely affect progression of renal disease and energy metabolism in CRF.

Genetic variation in the hepatic lipase gene is associated with combined hyperlipidemia, plasma lipid concentrations, and lipid-lowering drug response

2005 ◽  
Vol 150 (6) ◽  
pp. 1154-1162 ◽  
Author(s):  
Ana Cenarro ◽  
Marta Artieda ◽  
Carmen Gonzalvo ◽  
Erardo Meriño-Ibarra ◽  
Rosa Arístegui ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Drug Response ◽  
Hepatic Lipase ◽  
Plasma Lipid ◽  
Lipid Lowering ◽  
Lipase Gene ◽  
Lipid Lowering Drug ◽  
Lowering Drug ◽  
Hepatic Lipase Gene

Transcriptomic therapy for dyslipidemias utilizing nucleic acids targeted at ANGPTL3

2021 ◽  
Author(s):  
Gerald F Watts ◽  
Frederick J Raal ◽  
Dick C Chan
Keyword(s):  
Clinical Trials ◽  
Plasma Lipid ◽  
Lipoprotein Metabolism ◽  
New Approach ◽  
Cholesterol Levels ◽  
Ldl Particles ◽  
Severe Hypertriglyceridemia ◽  
Triglyceride Rich Lipoprotein ◽  
Mixed Hyperlipidemia

Angiopoietin-like protein 3 (ANGPTL3) is a key physiological regulator of plasma lipid and lipoprotein metabolism that involves the control of enzymes, lipoprotein and endothelial lipases. Inhibition of ANGPTL3 offers a new approach for correcting the health risks of dyslipidemia, including familial hypercholesterolemia, mixed hyperlipidemia, metabolic syndrome and/or severe hypertriglyceridemia. ANGPTL3 inhibition with nucleic acid-based antisense oligonucleotide and siRNA can correct dyslipidemia chiefly by reducing production and increasing catabolism of triglyceride-rich lipoprotein and LDL particles. Early clinical trials have demonstrated that these agents can safely and effectively lower plasma triglyceride and LDL-cholesterol levels by up to 70 and 50%, respectively. However, the long-term safety and cost–effectiveness of these agents await to be confirmed in an ongoing and future clinical trials.

Diagnosis of Dyslipidemia

2020 ◽  
Author(s):  
John D. Brunzell ◽  
R Alan Failor
Keyword(s):  
United States ◽  
Physical Inactivity ◽  
Hepatic Lipase ◽  
Lipoprotein Metabolism ◽  
Developed Countries ◽  
The United States ◽  
Atherosclerotic Cardiovascular Disease ◽  
High Fat Diets ◽  
Artery Disease ◽  
Fat Diets

Disorders of lipoprotein metabolism, in conjunction with the prevalence of high-fat diets, obesity, and physical inactivity, have resulted in an epidemic of atherosclerotic disease in the United States and other developed countries. The interaction of common genetic and acquired disorders of lipo­proteins with these adverse environmental factors leads to the premature development of atherosclerosis. In the United States, mortality from coronary artery disease (CAD), particularly in persons younger than 60 years, has been declining since 1970; however, atherosclerotic cardiovascular disease remains the most common cause of death among both men and women. This review contains 6 figures, 12 tables, and 47 references. Keywords: dyslipoproteinemias, hepatic lipase,  hyper­lipoproteinemia, hypoalphalipoproteinemia, lipoprotein, 

scholarly journals ILRUN , a Human Plasma Lipid GWAS Locus, Regulates Lipoprotein Metabolism in Mice

2020 ◽  
Vol 127 (11) ◽  
pp. 1347-1361 ◽  
Author(s):  
Xin Bi ◽  
Takashi Kuwano ◽  
Paul C. Lee ◽  
John S. Millar ◽  
Li Li ◽  
...  
Keyword(s):  
Plasma Lipids ◽  
Plasma Cholesterol ◽  
Plasma Lipid ◽  
Lipoprotein Metabolism ◽  
Peroxisome Proliferator ◽  
Nucleotide Polymorphisms ◽  
Genetic Associations ◽  
Peroxisome Proliferator Activated Receptor ◽  
Liver Transcriptome ◽  
Artery Disease

Rationale: Single-nucleotide polymorphisms near the ILRUN (inflammation and lipid regulator with ubiquitin-associated–like and NBR1 [next to BRCA1 gene 1 protein]-like domains) gene are genome-wide significantly associated with plasma lipid traits and coronary artery disease (CAD), but the biological basis of this association is unknown. Objective: To investigate the role of ILRUN in plasma lipid and lipoprotein metabolism. Methods and Results: ILRUN encodes a protein that contains a ubiquitin-associated–like domain, suggesting that it may interact with ubiquitinylated proteins. We generated mice globally deficient for Ilrun and found they had significantly lower plasma cholesterol levels resulting from reduced liver lipoprotein production. Liver transcriptome analysis uncovered altered transcription of genes downstream of lipid-related transcription factors, particularly PPARα (peroxisome proliferator-activated receptor alpha), and livers from Ilrun -deficient mice had increased PPARα protein. Human ILRUN was shown to bind to ubiquitinylated proteins including PPARα, and the ubiquitin-associated–like domain of ILRUN was found to be required for its interaction with PPARα. Conclusions: These findings establish ILRUN as a novel regulator of lipid metabolism that promotes hepatic lipoprotein production. Our results also provide functional evidence that ILRUN may be the casual gene underlying the observed genetic associations with plasma lipids at 6p21 in human.

Postprandial decrease in HDL cholesterol and HDL apo A-I in normal subjects in relation to triglyceride metabolism

1991 ◽  
Vol 260 (3) ◽  
pp. E492-E498 ◽  
Author(s):  
T. W. De Bruin ◽  
C. B. Brouwer ◽  
J. A. Gimpel ◽  
D. W. Erkelens
Keyword(s):  
Hepatic Lipase ◽  
Lipoprotein Metabolism ◽  
Hdl Cholesterol ◽  
Normal Subjects ◽  
Tolerance Test ◽  
Retinyl Palmitate ◽  
Cholesterol Concentration ◽  
High Density Lipoproteins ◽  
Postprandial Lipoprotein ◽  
Chylomicron Remnants

The postprandial lipoprotein metabolism is important since it determines the circulation of potentially atherogenic particles and influences the metabolism of high-density lipoproteins (HDL) in a complex manner that is at present not completely understood. Therefore, the short-term (24-h) changes in postprandial lipoprotein metabolism, including retinyl palmitate (RP), apolipoprotein A-I (apo A-I), and apolipoprotein B, were studied in relation to postheparin lipolytic activities in six healthy normolipidemic men after an oral RP fat tolerance test. The fat load (98 g) was cleared in 7 h, because the triglyceride (TG) concentrations had returned to initial values (0.72 +/- 0.31 mmol/l) at that time. RP showed a peak in plasma at 4 and 5 h but remained present in chylomicron (remnants) in low concentrations after 8 and 24 h. After the fat load, HDL cholesterol and HDL-associated apo A-I showed a significant decrease in concentration of 35 and 29%, respectively. The decrease coincided with the increase in chylomicron remnants and the transient appearance of TG-enriched HDL. Hepatic lipase was correlated to both the initial HDL cholesterol concentration as well as the peak concentration of TG in chylomicron remnants, suggesting that it could be one of the regulating common physiological pathways in postprandial HDL and TG metabolism. In the subjects studied, the atherogenic potential of plasma increased in response to an oral fat load, characterized by a decrease in HDL cholesterol and HDL-associated apo A-I.

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