In order to study the structural, functional and molecular evolutional relationship of fish liportein lipase (LPL) and hepatic lipase (HL) genes, seven liver LPL and HL cDNA partial sequences were isolated from Acipenser sinensis, Hypophthalmichthys molitrix, Aristichthys nobilis, Ctenopharyngodon idellus, Cirrhinus molitorella, Oreochromis niloticus, Channa maculate by RT-PCR. Three full-length cDNA sequences of LPL, HL of Acipenser sinensis and LPL of Hypophthalmichthys molitrix were obtained by RACEs. From the sequence analysis and homologous results, the amino acid sequences of LPL and HL are relatively conserved in mammals, birds and fishes. Taken together with these obtained amino acid sequences and sequences of all known LPL, HL, EL and PL from other vertebrates, a phylogenetic tree was constructed by neighbor-joining method. The result supports that all of them belong to lipase family.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.3724/SP.J.1141.2010.03239 | DOI Listing |
BMC Microbiol
December 2024
Departments of Geriatrics, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, P. R. China.
Background: Evidence has revealed that oestrogen deprivation-induced osteolysis is microbiota-dependent and can be treated by probiotics. However, the underlying mechanism require further investigation. This study aims to provide additional evidence supporting the use of probiotics as an adjuvant treatment and to explore the pathophysiology of oestrogen-deprived osteolysis.
View Article and Find Full Text PDFCell Mol Biol Lett
December 2024
Department of Hematology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Add: No.324, Jingwu Road, Jinan, 250021, Shandong, China.
Background: Disorders of lipid metabolism are critical factors in the progression of chronic lymphocytic leukemia (CLL). However, the characteristics of lipid metabolism and related regulatory mechanisms of CLL remain unclear.
Methods: Hence, we identified altered metabolites and aberrant lipid metabolism pathways in patients with CLL by ultra-high-performance liquid chromatography-mass spectrometry-based non-targeted lipidomics.
Arch Dermatol Res
December 2024
Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shannxi, China.
Lipid metabolism disorders are frequently noted in atopic dermatitis (AD) patients, prompting the long-term use of lipid-lowering drugs. However, the causal effects of circulating lipids and different lipid-lowering drugs on the risk of AD are not thoroughly understood. Using publicly available genome-wide association studies (GWAS) summary data from two different cohorts, a series of Mendelian randomization (MR) analyses were conducted to explore the causal effects of genetically proxied circulating lipids and lipid-lowering drugs on the risk of AD.
View Article and Find Full Text PDFClin Investig Arterioscler
December 2024
Unidad de Lípidos y Riesgo Cardiovascular, Servicio de Medicina Interna, Complejo Hospitalario Universitario de A Coruña, A Coruña, España. Electronic address:
The development of massive sequencing techniques and guidelines for assessing the pathogenicity of variants are allowing us the identification of new cases of familial chylomicronemia syndrome (FCS) mostly in the LPL gene, less frequently in GPIHBP1 and APOA5, and with even fewer cases in LMF1 and APOC2. From the included studies, it can be deduced that, in cases with multifactorial chylomicronemia syndrome (MCS), both loss-of-function variants and common variants in canonical genes for FCH contribute to the manifestation of this other form of chylomicronemia. Other common and rare variants in other triglyceride metabolism genes have been identified in MCS patients, although their real impact on the development of severe hypertriglyceridemia is unknown.
View Article and Find Full Text PDFCirc J
December 2024
Institute of Epidemiology and Preventive Medicine, National Taiwan University.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!