Редактирование: LPL

Lipoprotein lipase precursor (EC 3.1.1.34) (LPL) (Phospholipase A1) (EC 3.1.1.32) [LIPD]

==Publications==

{{medline-entry
|title=Survival analyses in Holstein cows considering direct disease diagnoses and specific SNP marker effects.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32684467
|abstract=The aim of the present study was to infer influences of health disorders and of specific SNP markers on longevity in Holstein cows via survival analyses. Longevity was defined as the length of productive life ([[LPL]]), reflecting the interval from first calving until the culling or censoring date. In this regard, we considered longevity records from 129,386 Holstein cows from 57 large-scale herds, with calving dates in first parity between January 2004 and December 2017 (30.27% censored records). We selected specific diseases from the overall categories claw disorders, udder diseases, metabolic disorders, and female fertility disorders within 3 stages of parities 1, 2, and 3. Lactation stage 1 was the period from calving to days in milk (DIM) 59, lactation stage 2 from DIM 60 to DIM 299, and lactation stage 3 from DIM 300 to the next calving date. The effects of the diseases on culling risk ratios were estimated via Weibull proportional hazards models. In this regard, we used 3 different modeling strategies. In modeling strategy M1S, binary diseases from different parities and lactation stages for the same diagnosis were modeled as explanatory variables in separate runs. Modeling strategy M3S included diseases for the same diagnosis from stage 1, 2, and 3 in the same parity simultaneously. Modeling strategy M9S implied consideration of diseases for the same diagnosis from different lactation stages and from all 3 parities simultaneously. The effect of the same diseases on culling risks from M1S and M3S were similar, with increasing detrimental effect of diseases recorded in later lactation stages and parities. The strongest disease effect on [[LPL]] was detected for clinical and subclinical mastitis recorded in the middle of the third lactation, with culling risks of 2.59 and 2.40, respectively, and for claw disorders from the last stage in third lactation (culling risks in the range from 1.85 to 2.29). The effective (ignoring the proportion of censoring; h ) and equivalent (considering proportion of censoring; h ) heritabilities for [[LPL]] when considering diseases from specific stages in parities 1 and 3 were quite low ( h  0.02 - 0.17; h  0.01 - 0.12). Simultaneous consideration of same disease diagnoses across stages (M3S) and across lactations (M9S) contributed to a [[LPL]] heritability increase. Ignoring diseases as explanatory variables in survival analyses was generally associated with a decline of genetic [[LPL]] variances and [[LPL]] heritabilities. A genome-wide association study for [[LPL]] was based on estimated de-regressed proofs from 17,362 genotyped cows. Six SNP located on Bos taurus autosomes 1, 4, 10, 13, and 28 were significantly associated with [[LPL]] (using a 5% false discovery rate). Gene annotations via Ensembl identified the 4 potential candidate genes [[ETV1]], [[ONECUT1]], [[MACROD2]], and [[SIRT1]], which directly (via disease resistance mechanisms) or indirectly (via milk productivity) influence dairy cow longevity. Genotypes of the 6 significantly associated SNP were considered as fixed effects in Weibull hazards models, but their effects on culling risks were nonsignificant. Heritabilities for [[LPL]] from all SNP-based survival models considering the single SNP separately or the 6 SNP simultaneously were 0.05 (h ) and 0.12 (h ). The small number of significantly associated SNP in genome-wide associations and the minor effect of specific SNP on [[LPL]] in survival analyses underline the polygenetic nature of longevity.

|keywords=* SNP effect
* Weibull hazards model
* genetic parameter
* health disorder
* longevity
|full-text-url=https://sci-hub.do/10.3168/jds.2020-18174
}}
{{medline-entry
|title=Influence of common health disorders on the length of productive life and stayability in German Holstein cows.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31677834
|abstract=The aim of this study was to infer phenotypic and genetic effects of health disorders on longevity traits, considering Holstein dairy cow records from large-scale co-operator herds. In this regard, we focused on 13 different disease traits and on 2 longevity definitions: length of productive life ([[LPL]]) and stayability (STAY). The [[LPL]] was defined as the interval in days from first calving to culling. For [[LPL]], we considered 90,215 cows with known culling dates. For binary STAY, we defined 3 survival stages in the first 3 lactations: from calving to DIM 59, from DIM 60 to DIM 299, and from DIM 300 to the next calving date. Due to the earlier trait recording possibilities, 129,386 cows were considered for the STAY analysis. Accordingly, the presence or absence of diseases in lactation stages were defined as binary traits. A further data set for the 90,215 cows with a culling date included the subjective culling reasons defined by farmers. Comparison of culling reasons, as defined by farmers, with diagnoses from the disease data set indicated some disagreements. For example, only 18.71% of the cows with the farmer culling reason "metabolic diseases" were diagnosed with a metabolic disorder. Better agreements were identified for mastitis (84.09%). Phenotypically, in most cases, occurrence of diseases at different lactation stages had negative influence on [[LPL]] and STAY. In this regard, we identified strong detrimental effects of clinical mastitis and of metabolic disorders from early lactation stages on longevity traits. For example, the presence of clinical mastitis in the first stage of first lactation was associated with [[LPL]] decrease of 95.35 d. Using generalized linear mixed models for binary health disorders, heritabilities ranged from <0.01 (±0.079 standard error) for ruminal acidosis early in first, second, and third lactation to 0.24 (±0.039) for interdigital hyperplasia from the last stage in third lactation. Heritabilities from single-trait and bivariate animal models ranged from 0.03 (±0.003) to 0.10 (±0.007) for [[LPL]], and from 0.01 (±0.002) to 0.06 (±0.007) for STAY. Genetic correlations between longevity traits and health disorders were mostly negative (i.e., favorable in a breeding sense). For improvements to longevity genetic evaluations for young bulls with a limited number of daughter culling dates, we suggest consideration of health traits from a well-organized co-operator herd monitoring system as early longevity predictors, especially for censored data. Genetic correlations between mastitis from different lactation stages with [[LPL]] and STAY ranged from -0.28 (±0.07) to -0.69 (±0.05), and from -0.26 (±0.08) to -0.77 (±0.08), respectively. Interestingly, only diagnoses for dermatitis digitalis showed opposite results phenotypically and genetically. Strong genetic associations between ruminal acidosis and STAY were observed (genetic correlations: -0.48 ± 0.18 to -0.98 ± 0.31), supporting the inferred phenotypic associations. Genetic correlations between longevity traits [[LPL]] and STAY were quite large, between 0.77 (±0.11) and 0.94 (±0.02) for the different lactation stages, suggesting utility of early STAY information when attempting genetic improvements for longevity.
|mesh-terms=* Animals
* Breeding
* Cattle
* Cattle Diseases
* Dairying
* Farmers
* Female
* Lactation
* Longevity
* Phenotype
|keywords=* genetic parameter
* health disorder
* longevity
* subjective culling reason
|full-text-url=https://sci-hub.do/10.3168/jds.2019-16985
}}
{{medline-entry
|title=GH prevents adipogenic differentiation of mesenchymal stromal stem cells derived from human trabecular bone via canonical Wnt signaling.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29694926
|abstract=The imbalance between osteogenesis and adipogenesis, which naturally accompanies bone marrow senescence, may contribute to the development of bone-associated diseases, like osteoporosis. In the present study, using primary human mesenchymal stromal cells (h[[MSC]]s) isolated from trabecular bone, we assessed the possible effect of GH on h[[MSC]] differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in h[[MSC]]s cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase ([[LPL]]) and acethylCoA carboxylase ([[ACACA]]). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced h[[MSC]], both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes [[LPL]] and [[ACACA]], were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the [[MSC]] pool is reduced due to a decrease in Wnt signaling.
|mesh-terms=* Adipogenesis
* Cancellous Bone
* Gene Expression Regulation
* Gene Silencing
* Growth Hormone
* Humans
* Lipid Droplets
* Mesenchymal Stem Cells
* Osteogenesis
* Wnt Signaling Pathway
* beta Catenin
|keywords=* Aging
* Cell signaling
* Growth hormone
* Human mesenchymal stromal cells
* Silencing
* β-catenin
|full-text-url=https://sci-hub.do/10.1016/j.bone.2018.04.014
}}
{{medline-entry
|title=Genetic correlation and genome-wide association study (GWAS) of the length of productive life, days open, and 305-days milk yield in crossbred Holstein dairy cattle.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28671246
|abstract=In this study, we estimated the genetic parameters and identified the putative quantitative trait loci (QTL) associated with the length of productive life ([[LPL]]), days open (DO), and 305-day milk yield for the first lactation (FM305) of crossbred Holstein dairy cattle. Data comprising 4,739 records collected between 1986 and 2004 were used to estimate the variance-covariance components using the multiple-trait animal linear mixed models based on the average information restricted maximum likelihood (AI-REML) algorithm. Thirty-six animals were genotyped using the Illumina BovineSNP50 Bead Chip [>50,000 single nucleotide polymorphisms (SNPs)] to identify the putative QTL in a genome-wide association study. The heritability of the production trait FM305 was 0.25 and that of the functional traits, [[LPL]] and DO, was low (0.10 and 0.06, respectively). The genetic correlation estimates demonstrated favorable negative correlations between [[LPL]] and DO (-0.02). However, we observed a favorable positive correlation between FM305 and [[LPL]] (0.43) and an unfavorable positive correlation between FM305 and DO (0.1). The GWAS results indicated that 23 QTLs on bovine chromosomes 1, 4, 5, 8, 15, 26, and X were associated with the traits of interest, and the putative QTL regions were identified within seven genes (SYT1, [[DOCK11]], [[KLHL13]], [[IL13RA1]], [[PRKG1]], [[GNA14]], and LRRC4C). In conclusion, the heritability estimates of the [[LPL]] and DO were low. Therefore, the approach of multiple-trait selection indexes should be applied, and the QTL identified here should be considered for use in marker-assisted selection in the future.
|mesh-terms=* Animals
* Cattle
* Female
* Genome-Wide Association Study
* Genotype
* Lactation
* Longevity
* Milk
* Quantitative Trait Loci
* Quantitative Trait, Heritable
* Reproduction
* Selective Breeding

|full-text-url=https://sci-hub.do/10.4238/gmr16029091
}}
{{medline-entry
|title=Association of Metabolic Syndrome with Serum Adipokines in Community-Living Elderly Japanese Women: Independent Association with Plasminogen Activator-Inhibitor-1.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26451494
|abstract=Associations between metabolic syndrome (MetS) with serum adipokines and basal lipoprotein lipase mass (serum [[LPL]]) have not been extensively studied in elderly Asians, who in general have lower body mass index than European populations. A cross-sectional analysis was conducted including 159 community-living elderly Japanese women whose age averaged 77 years. MetS was defined by the modified National Cholesterol Education Program Adult Treatment Panel III criteria, but using a body mass index ≥25 kg/m(2) instead of waist circumference. Serum [[LPL]], leptin, adiponectin, plasminogen activator inhibitor 1 (PAI-1), interleukin-6, tumor necrosis factor-alpha, and high-sensitivity C-reactive protein were measured. Both the presence of MetS and the number of MetS components were associated with higher homeostasis assessment of insulin resistance, serum levels of leptin, PAI-1, and tumor necrosis factor-alpha and with lower serum levels of [[LPL]] and adiponectin (all P < 0.05), but not with high-sensitivity C-reactive protein and interleukin-6. Among six biomarkers of MetS, PAI-1 remained associated with MetS independent of fat mass index and insulin resistance. Although proinflammatory, prothrombotic, and anti-inflammatory states were associated with MetS, higher PAI-1 was associated with MetS independent of fat mass index and insulin resistance in elderly Japanese women, in whom obesity is rare.
|mesh-terms=* Adipokines
* Adiposity
* Age Factors
* Aged
* Aged, 80 and over
* Aging
* Asian Continental Ancestry Group
* Biomarkers
* Cross-Sectional Studies
* Female
* Humans
* Independent Living
* Inflammation Mediators
* Insulin Resistance
* Japan
* Metabolic Syndrome
* Plasminogen Activator Inhibitor 1
* Risk Factors
* Sex Factors

|full-text-url=https://sci-hub.do/10.1089/met.2015.0014
}}
{{medline-entry
|title=Moderate Exercise Mitigates the Detrimental Effects of Aging on Tendon Stem Cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26086850
|abstract=Aging is known to cause tendon degeneration whereas moderate exercise imparts beneficial effects on tendons. Since stem cells play a vital role in maintaining tissue integrity, in this study we aimed to define the effects of aging and moderate exercise on tendon stem/progenitor cells (TSCs) using in vitro and in vivo models. TSCs derived from aging mice (9 and 24 months) proliferated significantly slower than TSCs obtained from young mice (2.5 and 5 months). In addition, expression of the stem cell markers Oct-4, nucleostemin (NS), Sca-1 and SSEA-1 in TSCs decreased in an age-dependent manner. Interestingly, moderate mechanical stretching (4%) of aging TSCs in vitro significantly increased the expression of the stem cell marker, NS, but 8% stretching decreased NS expression. Similarly, 4% mechanical stretching increased the expression of Nanog, another stem cell marker, and the tenocyte-related genes, collagen I and tenomodulin. However, 8% stretching increased expression of the non-tenocyte-related genes, [[LPL]], Sox-9 and Runx-2, while 4% stretching had minimal effects on the expression of these genes. In the in vivo study, moderate treadmill running (MTR) of aging mice (9 months) resulted in the increased proliferation rate of aging TSCs in culture, decreased lipid deposition, proteoglycan accumulation and calcification, and increased the expression of NS in the patellar tendons. These findings indicate that while aging impairs the proliferative ability of TSCs and reduces their stemness, moderate exercise can mitigate the deleterious effects of aging on TSCs and therefore may be responsible for decreased aging-induced tendon degeneration. 
|mesh-terms=* Aging
* Animals
* Cell Differentiation
* Cell Proliferation
* Cells, Cultured
* Gene Expression Regulation
* Mice
* Patellar Ligament
* Physical Conditioning, Animal
* Running
* Stem Cells
* Stress, Mechanical
* Weight-Bearing

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4472753
}}
{{medline-entry
|title=Association of adiponectin with serum preheparin lipoprotein lipase mass in women independent of fat mass and distribution, insulin resistance, and inflammation.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24905278
|abstract=Abstract Background: Substantially increased lipoprotein lipase ([[LPL]]) activity was reported in mice overexpressing adiponectin. Associations of serum adiponectin with serum preheparin [[LPL]] mass (serum [[LPL]]), fat mass, and fat distribution and markers of insulin resistance and inflammation were examined in 311 young and 148 middle-aged women. In young women, serum adiponectin was positively associated with high-density lipoprotein cholesterol (HDL-C) and serum [[LPL]] and inversely with body mass index (BMI), abdominal girth, trunk fat mass, trunk/lower-body fat ratio, serum leptin, and log high-sensitivity C-reactive protein. These associations were confirmed in middle-aged women. Adiponectin showed positive association with the Matsuda insulin sensitivity index and inverse associations with homeostasis model assessment of insulin resistance, serum triglycerides, leukocyte count, interleukin-6, and plasminogen activator inhibitor-1 in middle-aged women but not in young women. Multivariate analysis revealed that serum [[LPL]] and trunk/lower-body fat ratio were significant determinants of adiponectin, not only in young women but also in middle-aged women. These associations were independent of markers of inflammation and insulin sensitivity/resistance. [[LPL]] mass in preheparin serum was associated with adiponectin levels independently of fat mass and distribution, systemic inflammation, and insulin resistance in healthy women. Therefore, [[LPL]] may represent a link between low adiponectin and dyslipidemia found in metabolic syndrome and type 2 diabetes mellitus.
|mesh-terms=* Adiponectin
* Adiposity
* Adult
* Aging
* Body Fat Distribution
* Female
* Humans
* Inflammation
* Insulin Resistance
* Japan
* Lipoprotein Lipase
* Middle Aged
* Mothers
* Young Adult

|full-text-url=https://sci-hub.do/10.1089/met.2014.0023
}}
{{medline-entry
|title=[Clinical and genetic characteristics of long-livers in Moscow region].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24640693
|abstract=In Moscow region long-livers we have studied distribution of [[LPL]], [[CETP]], [[APOE]], [[F2]], [[F5]], [[F7]], F13, [[FGB]], [[ITGA2]], [[ITGB3]], PAI-1, [[MTHFR]], [[MTRR]], [[HLA-DRB1]], [[HLA-DQA1]], [[HLA-DQB1]] genes polymorphisms, associated with predisposition to age pathology. Long-livers are characterized by favorable course of cardiovascular diseases accompanied by certain genetic factors. We have established that genotype H-H- of [[LPL]], allele epsilon2 of [[APOE]], genotype CC of [[MTHFR]] (677C > T), genotype TC of [[ITGB3]], genotype GA of [[FGB]], [[HLA-DRB1]]*11 positively correlate with longevity.
|mesh-terms=* Aged
* Aged, 80 and over
* Alleles
* Cardiovascular Diseases
* Female
* Gene Frequency
* Genetic Markers
* Genetic Predisposition to Disease
* Genotype
* Humans
* Longevity
* Male
* Moscow
* Polymorphism, Genetic
* Prevalence
* Urban Population


}}