ArticleProceedings of the National Academy of Sciences of the United States of America1999
Induced mutant mouse lines that express lipoprotein lipase in cardiac muscle, but not in skeletal muscle and adipose tissue, have normal plasma triglyceride and high-density lipoprotein-cholesterol levels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 88 citations in OpenAlex.
- Cardiac Lipid Metabolism: Cells, Metabolites, and Rhythms.Circulation research · 2026Review
- Global knockout of VEGFB improves lipoprotein lipase activity leading to an improved lipid profile during diabetes.Frontiers in pharmacology · 2026Article
- Cardiac lipid metabolism, mitochondrial function, and heart failure.Cardiovascular research · 2023Review
- Integrated Control of Fatty Acid Metabolism in Heart Failure.Metabolites · 2023Review
- Hypertriglyceridemia and Atherosclerosis: Using Human Research to Guide Mechanistic Studies in Animal Models.Frontiers in endocrinology · 2020Review
- CRISPR/Cas9-mediatedJournal of lipid research · 2018Article
- Lipoprotein lipase regulates hematopoietic stem progenitor cell maintenance through DHA supply.Nature communications · 2018Article
- 2017 George Lyman Duff Memorial Lecture: Fat in the Blood, Fat in the Artery, Fat in the Heart: Triglyceride in Physiology and Disease.Arteriosclerosis, thrombosis, and vascular biology · 2018Review
- Krüppel-like factors: Crippling and un-crippling metabolic pathways.JACC. Basic to translational science · 2018Article
- Lipid Use and Misuse by the Heart.Circulation research · 2016Review
- Apoc2 loss-of-function zebrafish mutant as a genetic model of hyperlipidemia.Disease models & mechanisms · 2015Article
- The tissue distribution of lipoprotein lipase determines where chylomicrons bind.Journal of lipid research · 2015Article
- Embryonic viability, lipase deficiency, hypertriglyceridemia and neonatal lethality in a novel LMF1-deficient mouse model.Nutrition & metabolism · 2014Article
- Cardiac lipotoxicity: molecular pathways and therapeutic implications.Current heart failure reports · 2013Review
- Triglycerides and heart disease: still a hypothesis?Arteriosclerosis, thrombosis, and vascular biology · 2011Review
- Comparative studies of vertebrate lipoprotein lipase: a key enzyme of very low density lipoprotein metabolism.Comparative biochemistry and physiology. Part D, Genomics & proteomics · 2011Article
- Amelioration of hypertriglyceridemia with hypo-alpha-cholesterolemia in LPL deficient mice by hematopoietic cell-derived LPL.PloS one · 2011Article
- Diets Enriched in Fish-Oil or Seal-Oil have Distinct Effects on Lipid Levels and Peroxidation in BioF1B Hamsters.Nutrition and metabolic insights · 2011Article
- Very-low-density lipoprotein: complex particles in cardiac energy metabolism.Journal of lipids · 2011Article
- Adipose triglyceride lipase plays a key role in the supply of the working muscle with fatty acids.Journal of lipid research · 2010Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tissue-specific expression of lipoprotein lipase (LPL) in adipose tissue (AT), skeletal muscle (SM), and cardiac muscle (CM) is rate-limiting for the uptake of triglyceride (TG)-derived free fatty acids and decisive in the regulation of energy balance and lipoprotein metabolism. To investigate the tissue-specific metabolic effects of LPL, three independent transgenic mouse lines were established that expressed a human LPL (hLPL) minigene predominantly in CM. Through cross-breeding with heterozygous LPL knockout mice, animals were generated that produced hLPL mRNA and enzyme activity in CM but lacked the enzyme in SM and AT because of the absence of the endogenous mouse LPL gene (L0-hLPL). LPL activity in CM and postheparin plasma of L0-hLPL mice was reduced by 34% and 60%, respectively, compared with control mice. This reduced LPL expression was sufficient to rescue LPL knockout mice from neonatal death. L0-hLPL animals developed normally with regard to body weight and body-mass composition. Plasma TG levels in L0-hLPL animals were increased up to 10-fold during the suckling period but normalized after weaning and decreased in adult animals. L0-hLPL mice had normal plasma high-density lipoprotein (HDL)-cholesterol levels, indicating that LPL expression in CM alone was sufficient to allow for normal HDL production. The absence of LPL in SM and AT did not cause detectable morphological or histopathological changes in these tissues. However, the lipid composition in AT and SM exhibited a marked decrease in polyunsaturated fatty acids. From this genetic model of LPL deficiency in SM and AT, it can be concluded that CM-specific LPL expression is a major determinant in the regulation of plasma TG and HDL-cholesterol levels.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.