ArticleNutrition & metabolism2014
Embryonic viability, lipase deficiency, hypertriglyceridemia and neonatal lethality in a novel LMF1-deficient mouse model.
Article in Nutrition & metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Advancing Gene Therapy for Pancreatitis: From Genetic Insights to Clinical Translation.Research (Washington, D.C.) · 2026Review
- Pleiotropic Genes Affecting Milk Production, Fertility, and Health in Thai-Holstein Crossbred Dairy Cattle: A GWAS Approach.Animals : an open access journal from MDPI · 2025Article
- Population Genetics and Signatures of Selection in Early Neolithic European Farmers.Molecular biology and evolution · 2022Article
- Positively selected genes in the hoary bat (PeerJ · 2022Article
- Lipoprotein Lipase and Its Regulators: An Unfolding Story.Trends in endocrinology and metabolism: TEM · 2021Review
- Association of Maternal DNA Methylation and Offspring Birthweight.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Endoplasmic reticulum quality control in lipoprotein metabolism.Molecular and cellular endocrinology · 2019Review
- Identification and functional analysis of novel homozygous LMF1 variants in severe hypertriglyceridemia.Journal of clinical lipidologyArticle
- Characterization of two novel pathogenic variants at compound heterozygous status in lipase maturation factor 1 gene causing severe hypertriglyceridemia.Journal of clinical lipidologyArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLipase Maturation Factor 1 (LMF1) is an ER-chaperone involved in the post-translational maturation and catalytic activation of vascular lipases including lipoprotein lipase (LPL), hepatic lipase (HL) and endothelial lipase (EL). Mutations in LMF1 are associated with lipase deficiency and severe hypertriglyceridemia indicating the critical role of LMF1 in plasma lipid homeostasis. The currently available mouse model of LMF1 deficiency is based on a naturally occurring truncating mutation, combined lipase deficiency (cld), which may represent a hypomorphic allele. Thus, development of LMF1-null mice is needed to explore the phenotypic consequences of complete LMF1 deficiency.
findingsIn situ hybridization and qPCR analysis in the normal mouse embryo revealed ubiquitous and high-level LMF1 expression. To investigate if LMF1 was required for embryonic viability, a novel mouse model based on a null-allele of LMF1 was generated and characterized. LMF1-/- progeny were born at Mendelian ratios and exhibited combined lipase deficiency, hypertriglyceridemia and neonatal lethality.
conclusionOur results raise the possibility of a previously unrecognized role for LMF1 in embryonic development, but indicate that LMF1 is dispensable for the viability of mouse embryo. The novel mouse model developed in this study will be useful to investigate the full phenotypic spectrum of LMF1 deficiency.
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