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

Kobayashi, Junji; Miyashita, Kazuya; Nakajima, Katsuyuki; Mabuchi, Hiroshi

doi:10.5551/jat.31617

Cited by 71 publications

(38 citation statements)

References 85 publications

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“…To further explore the in-depth molecular mechanisms of CTS and COS regulating the process above, we examined the mRNA expressions of two important regulating factors in the liver: peroxisome proliferator-activated receptor-α (PPARα), a ligand-activated transcription factor involved in the regulation of various aspects of liver lipid metabolisms ( 13 , 14 ), and its target regulatory proteins, hepatic lipase (HL), which can catalyze TG hydrolysis in chylomicrons (CM) and VLDL-C for tissue use in the form of free fatty acid (FFA) and monoacylglycerol, and provide high-density lipoprotein (HDL) with apolipoproteins and phospholipids for the reverse cholesterol transport (RCT) process ( 15 , 16 ). Therefore, we speculated about the regulating function of CTS and its derivatives for lipid metabolism via up-regulating the expressions of liver PPARα and HL mRNA levels, which further contributes to the RCT process.…”

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confidence: 99%

Hypolipidemic effects of chitosan and its derivatives in hyperlipidemic rats induced by a high-fat diet

Pan

Yang

Huang

et al. 2016

Food & Nutrition Research

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BackgroundHyperlipidemia (HLP) is the primary risk factor of cardiovascular disease (CVD). Various factors, including genetics, physical inactivity, and daily nutritional habits, affect the prevalence of HLP. Recently, it was revealed that dietary fibers, such as pectin, psyllium, and especially chitosan (CTS), may play important roles in hypolipidemic management. Thus, this study aims to determine the hypolipidemic effect and mechanism of CTS and its water-soluble derivatives, chitosan oligosaccharides (MN≤1,000 Da (COSI) and MN≤3,000 Da (COSIII)), in male hyperlipidemic rats induced by a high-fat diet (HFD).DesignAfter the model creation, 120 Sprague-Dawley (SD) rats were equally assigned to 12 groups fed various diets as follows: the normal group with basic diet, an HFD group, an HFD group supplemented with three doses of CTS, COSI and COSIII groups, and an HFD group treated with simvastatin (7 mg/kg·d). After 6 weeks, body weight, fat/body ratio, and the relevant biomarkers of serum, liver, and feces were measured. Additionally, the histological analysis of liver and adipose tissue was performed, and the mRNA expressions of liver peroxisome proliferator-activated receptor-α (PPARα) and hepatic lipase (HL) were examined.ResultsCompared with HFD group, rats fed CTS, COSI, and COSIII showed a better ability to regulate their body weight, liver and cardiac indices, fat/body ratio, as well as serum, liver, and fecal lipids, and simultaneously to maintain the appropriate activity of liver and serum superoxide dismutase (SOD), alanine aminotransferase (ALT), aspartate aminotransferase (AST), as well as liver and fecal total bile acids (TBA). Simultaneously, there had been a higher mRNA expression of PPARα and HL in the treatment groups.ConclusionThe obtained results suggested that these three function foods can effectively improve liver lipid metabolism by normalizing the expressions of PPARα and HL, and protect liver from the oxidized trauma by enhancing hepatic function, which could be potentially used to remedy hyperlipidemia.

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confidence: 99%

Hypolipidemic effects of chitosan and its derivatives in hyperlipidemic rats induced by a high-fat diet

Pan

Yang

Huang

et al. 2016

Food & Nutrition Research

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“…LDL particles are generated in circulation as downstream metabolic products from the TG-enriched lipoproteins (liver-derived VLDL particles and their post-lipolytic remnants) by the action of two lipases, lipoprotein lipase and hepatic lipase. 31,32 Thus, a proportion of the core lipids—especially cholesterol esters—and the particle surface phospholipids are retained within the generated LDL particles. The actions of the cholesteryl ester transfer protein and phospholipid transfer protein further modulate the constituents of TG-rich and LDL particles 33 .…”

Section: Discussionmentioning

confidence: 99%

Coronary artery disease risk and lipidomic profiles are similar in familial and population-ascertained hyperlipidemias

Ripatti

Tabassum

et al. 2018

Preprint

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Abstract-20 at 5% false discovery rate) and 51 species in the population 36 samples (p-value range 0.017-6.8*10 -21 ). Hypertriglyceridemia was associated with altered levels of 37 117 lipid species in families (p-value range 0.035-1.8*10-49 ) and 119 species in the population sample 38 (p-value range 0.038-2.3*10 -56 ). The lipidomics profiles of hyperlipidemias were highly similar in 39 families and population samples. 40 Conclusion:We identified distinct lipidomic profiles associated with high LDL-C and triacylglyceride 41 levels. CAD risk, lipidomic profiles and genetic profiles are highly similar between familial and 42 population-ascertained hyperlipidemias, providing evidence of similar and overlapping underlying 43 mechanisms. Our results do not support different screening and treatment for such hyperlipidemias. 44

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“…47 The region surrounding the top variant also includes the genes LIPC and AQP9. LIPC encodes hepatic lipase, which has well-known associations with lipids 48 and coronary artery disease. 49,50 LIPC has also been linked to BP and hypertension in some studies.…”

Section: Discussionmentioning

confidence: 99%

Genetic Variants Associated With Uncontrolled Blood Pressure on Thiazide Diuretic/β‐Blocker Combination Therapy in the PEAR (Pharmacogenomic Evaluation of Antihypertensive Responses) and INVEST (International Verapamil‐SR Trandolapril Study) Trials

Magvanjav

Gong

McDonough

et al. 2017

JAHA

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BackgroundThe majority of hypertensive individuals require combination antihypertensive therapy to achieve adequate blood pressure (BP) control. This study aimed to identify genetic variants associated with uncontrolled BP on combination therapy with a thiazide diuretic and a β‐blocker.Methods and ResultsA genome‐wide association study of uncontrolled BP on combination therapy was conducted among 314 white participants of the PEAR (Pharmacogenomic Evaluation of Antihypertensive Responses) trial. Multivariable logistic regression analysis was used. Genetic variants meeting a suggestive level of significance (P<1.0E‐05) were tested for replication in an external cohort, INVEST (International Verapamil‐SR Trandolapril study). We also examined genome‐wide variant associations with systolic and diastolic BP response on combination therapy and tested for replication. We discovered a single nucleotide polymorphism, the rs261316 major allele, at chromosome 15 in the gene ALDH1A2 associated with an increased odds of having uncontrolled BP on combination therapy (odds ratio: 2.56, 95% confidence interval, 1.69–3.88, P=8.64E‐06). This single nucleotide polymorphism replicated (odds ratio: 1.86, 95% confidence interval, 1.35–2.57, P=0.001) and approached genome‐wide significance in the meta‐analysis between discovery and replication cohorts (odds ratio: 2.16, 95% confidence interval, 1.63–2.86, P=8.60E‐08). Other genes in the region surrounding rs261316 (ALDH1A2) include AQP9 and LIPC.ConclusionsA single nucleotide polymorphism in the gene ALDH1A2 may be associated with uncontrolled BP following treatment with a thiazide diuretic/β‐blocker combination.Clinical Trial RegistrationURL: https://www.clinicaltrials.gov. Unique identifier: NCT00246519.

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

Cited by 71 publications

References 85 publications

Hypolipidemic effects of chitosan and its derivatives in hyperlipidemic rats induced by a high-fat diet

Hypolipidemic effects of chitosan and its derivatives in hyperlipidemic rats induced by a high-fat diet

Coronary artery disease risk and lipidomic profiles are similar in familial and population-ascertained hyperlipidemias

Genetic Variants Associated With Uncontrolled Blood Pressure on Thiazide Diuretic/β‐Blocker Combination Therapy in the PEAR (Pharmacogenomic Evaluation of Antihypertensive Responses) and INVEST (International Verapamil‐SR Trandolapril Study) Trials

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