Publications by authors named "Páll I Olason"

17 Publications

  • Page 1 of 1

Germline variants at SOHLH2 influence multiple myeloma risk.

Blood Cancer J 2021 04 19;11(4):76. Epub 2021 Apr 19.

Hematology and Transfusion Medicine, Department of Laboratory Medicine, 221 84, Lund, Sweden.

Multiple myeloma (MM) is caused by the uncontrolled, clonal expansion of plasma cells. While there is epidemiological evidence for inherited susceptibility, the molecular basis remains incompletely understood. We report a genome-wide association study totalling 5,320 cases and 422,289 controls from four Nordic populations, and find a novel MM risk variant at SOHLH2 at 13q13.3 (risk allele frequency = 3.5%; odds ratio = 1.38; P = 2.2 × 10). This gene encodes a transcription factor involved in gametogenesis that is normally only weakly expressed in plasma cells. The association is represented by 14 variants in linkage disequilibrium. Among these, rs75712673 maps to a genomic region with open chromatin in plasma cells, and upregulates SOHLH2 in this cell type. Moreover, rs75712673 influences transcriptional activity in luciferase assays, and shows a chromatin looping interaction with the SOHLH2 promoter. Our work provides novel insight into MM susceptibility.
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http://dx.doi.org/10.1038/s41408-021-00468-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8055668PMC
April 2021

A meta-analysis uncovers the first sequence variant conferring risk of Bell's palsy.

Sci Rep 2021 02 18;11(1):4188. Epub 2021 Feb 18.

Rigshospitalet, Kobenhavn, Denmark.

Bell's palsy is the most common cause of unilateral facial paralysis and is defined as an idiopathic and acute inability to control movements of the facial muscles on the affected side. While the pathogenesis remains unknown, previous studies have implicated post-viral inflammation and resulting compression of the facial nerve. Reported heritability estimates of 4-14% suggest a genetic component in the etiology and an autosomal dominant inheritance has been proposed. Here, we report findings from a meta-analysis of genome-wide association studies uncovering the first unequivocal association with Bell's palsy (rs9357446-A; P = 6.79 × 10, OR = 1.23; N = 4714, N = 1,011,520). The variant also confers risk of intervertebral disc disorders (P = 2.99 × 10, OR = 1.04) suggesting a common pathogenesis in part or a true pleiotropy.
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http://dx.doi.org/10.1038/s41598-021-82736-wDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7893061PMC
February 2021

Loss-of-Function Variants in the Tumor-Suppressor Gene Confer Increased Cancer Risk.

Cancer Res 2021 04 18;81(8):1954-1964. Epub 2021 Feb 18.

deCODE Genetics/Amgen, Reykjavik, Iceland.

The success of genome-wide association studies (GWAS) in identifying common, low-penetrance variant-cancer associations for the past decade is undisputed. However, discovering additional high-penetrance cancer mutations in unknown cancer predisposing genes requires detection of variant-cancer association of ultra-rare coding variants. Consequently, large-scale next-generation sequence data with associated phenotype information are needed. Here, we used genotype data on 166,281 Icelanders, of which, 49,708 were whole-genome sequenced and 408,595 individuals from the UK Biobank, of which, 41,147 were whole-exome sequenced, to test for association between loss-of-function burden in autosomal genes and basal cell carcinoma (BCC), the most common cancer in Caucasians. A total of 25,205 BCC cases and 683,058 controls were tested. Rare germline loss-of-function variants in conferred substantial risks of BCC (OR, 8.0; = 1.9 × 10), with a quarter of carriers getting BCC before age 70 and over half in their lifetime. Furthermore, common variants at the locus were associated with BCC, suggesting as a new, high-impact BCC predisposition gene. A follow-up investigation of 24 cancers and three benign tumor types showed that loss-of-function variants are associated with high risk of cervical cancer (OR, 12.7, = 1.6 × 10) and low age at diagnosis. Our findings, using power-increasing methods with high-quality rare variant genotypes, highlight future prospects for new discoveries on carcinogenesis. SIGNIFICANCE: This study identifies the tumor-suppressor gene as a high-impact BCC predisposition gene and indicates that inactivation of by germline sequence variants may also lead to increased risk of cervical cancer.
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http://dx.doi.org/10.1158/0008-5472.CAN-20-3065DOI Listing
April 2021

Sarek: A portable workflow for whole-genome sequencing analysis of germline and somatic variants.

F1000Res 2020 29;9:63. Epub 2020 Jan 29.

Department of Cell and Molecular Biology, National Bioinformatics Infrastructure Sweden, Science for Life Laboratory, Uppsala University, Husargatan 3, Uppsala, 752 37, Sweden.

Whole-genome sequencing (WGS) is a fundamental technology for research to advance precision medicine, but the limited availability of portable and user-friendly workflows for WGS analyses poses a major challenge for many research groups and hampers scientific progress. Here we present Sarek, an open-source workflow to detect germline variants and somatic mutations based on sequencing data from WGS, whole-exome sequencing (WES), or gene panels. Sarek features (i) easy installation, (ii) robust portability across different computer environments, (iii) comprehensive documentation, (iv) transparent and easy-to-read code, and (v) extensive quality metrics reporting. Sarek is implemented in the Nextflow workflow language and supports both Docker and Singularity containers as well as Conda environments, making it ideal for easy deployment on any POSIX-compatible computers and cloud compute environments. Sarek follows the GATK best-practice recommendations for read alignment and pre-processing, and includes a wide range of software for the identification and annotation of germline and somatic single-nucleotide variants, insertion and deletion variants, structural variants, tumour sample purity, and variations in ploidy and copy number. Sarek offers easy, efficient, and reproducible WGS analyses, and can readily be used both as a production workflow at sequencing facilities and as a powerful stand-alone tool for individual research groups. The Sarek source code, documentation and installation instructions are freely available at https://github.com/nf-core/sarek and at https://nf-co.re/sarek/.
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http://dx.doi.org/10.12688/f1000research.16665.2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7111497PMC
February 2021

A whole-genome sequenced control population in northern Sweden reveals subregional genetic differences.

PLoS One 2020 11;15(9):e0237721. Epub 2020 Sep 11.

Department of Medical Biochemistry and Biophysics, Umeå University, Umeå, Sweden.

The number of national reference populations that are whole-genome sequenced are rapidly increasing. Partly driving this development is the fact that genetic disease studies benefit from knowing the genetic variation typical for the geographical area of interest. A whole-genome sequenced Swedish national reference population (n = 1000) has been recently published but with few samples from northern Sweden. In the present study we have whole-genome sequenced a control population (n = 300) (ACpop) from Västerbotten County, a sparsely populated region in northern Sweden previously shown to be genetically different from southern Sweden. The aggregated variant frequencies within ACpop are publicly available (DOI 10.17044/NBIS/G000005) to function as a basic resource in clinical genetics and for genetic studies. Our analysis of ACpop, representing approximately 0.11% of the population in Västerbotten, indicates the presence of a genetic substructure within the county. Furthermore, a demographic analysis showed that the population from which samples were drawn was to a large extent geographically stationary, a finding that was corroborated in the genetic analysis down to the level of municipalities. Including ACpop in the reference population when imputing unknown variants in a Västerbotten cohort resulted in a strong increase in the number of high-confidence imputed variants (up to 81% for variants with minor allele frequency < 5%). ACpop was initially designed for cancer disease studies, but the genetic structure within the cohort will be of general interest for all genetic disease studies in northern Sweden.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0237721PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7485808PMC
October 2020

A geographically matched control population efficiently limits the number of candidate disease-causing variants in an unbiased whole-genome analysis.

PLoS One 2019 27;14(3):e0213350. Epub 2019 Mar 27.

Department of Medical Biochemistry and Biophysics, Umeå University, SE Umeå, Sweden.

Whole-genome sequencing is a promising approach for human autosomal dominant disease studies. However, the vast number of genetic variants observed by this method constitutes a challenge when trying to identify the causal variants. This is often handled by restricting disease studies to the most damaging variants, e.g. those found in coding regions, and overlooking the remaining genetic variation. Such a biased approach explains in part why the genetic causes of many families with dominantly inherited diseases, in spite of being included in whole-genome sequencing studies, are left unsolved today. Here we explore the use of a geographically matched control population to minimize the number of candidate disease-causing variants without excluding variants based on assumptions on genomic position or functional predictions. To exemplify the benefit of the geographically matched control population we apply a typical disease variant filtering strategy in a family with an autosomal dominant form of colorectal cancer. With the use of the geographically matched control population we end up with 26 candidate variants genome wide. This is in contrast to the tens of thousands of candidates left when only making use of available public variant datasets. The effect of the local control population is dual, it (1) reduces the total number of candidate variants shared between affected individuals, and more importantly (2) increases the rate by which the number of candidate variants are reduced as additional affected family members are included in the filtering strategy. We demonstrate that the application of a geographically matched control population effectively limits the number of candidate disease-causing variants and may provide the means by which variants suitable for functional studies are identified genome wide.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0213350PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6436687PMC
December 2019

Linked selection and recombination rate variation drive the evolution of the genomic landscape of differentiation across the speciation continuum of Ficedula flycatchers.

Genome Res 2015 Nov 9;25(11):1656-65. Epub 2015 Sep 9.

Department of Evolutionary Biology, Evolutionary Biology Centre, Uppsala University, 75236 Uppsala, Sweden;

Speciation is a continuous process during which genetic changes gradually accumulate in the genomes of diverging species. Recent studies have documented highly heterogeneous differentiation landscapes, with distinct regions of elevated differentiation ("differentiation islands") widespread across genomes. However, it remains unclear which processes drive the evolution of differentiation islands; how the differentiation landscape evolves as speciation advances; and ultimately, how differentiation islands are related to speciation. Here, we addressed these questions based on population genetic analyses of 200 resequenced genomes from 10 populations of four Ficedula flycatcher sister species. We show that a heterogeneous differentiation landscape starts emerging among populations within species, and differentiation islands evolve recurrently in the very same genomic regions among independent lineages. Contrary to expectations from models that interpret differentiation islands as genomic regions involved in reproductive isolation that are shielded from gene flow, patterns of sequence divergence (d(xy) and relative node depth) do not support a major role of gene flow in the evolution of the differentiation landscape in these species. Instead, as predicted by models of linked selection, genome-wide variation in diversity and differentiation can be explained by variation in recombination rate and the density of targets for selection. We thus conclude that the heterogeneous landscape of differentiation in Ficedula flycatchers evolves mainly as the result of background selection and selective sweeps in genomic regions of low recombination. Our results emphasize the necessity of incorporating linked selection as a null model to identify genome regions involved in adaptation and speciation.
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http://dx.doi.org/10.1101/gr.196485.115DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4617962PMC
November 2015

Demographic divergence history of pied flycatcher and collared flycatcher inferred from whole-genome re-sequencing data.

PLoS Genet 2013 Nov 7;9(11):e1003942. Epub 2013 Nov 7.

Department of Evolutionary Biology, Evolutionary Biology Centre, Uppsala University, Uppsala, Sweden.

Profound knowledge of demographic history is a prerequisite for the understanding and inference of processes involved in the evolution of population differentiation and speciation. Together with new coalescent-based methods, the recent availability of genome-wide data enables investigation of differentiation and divergence processes at unprecedented depth. We combined two powerful approaches, full Approximate Bayesian Computation analysis (ABC) and pairwise sequentially Markovian coalescent modeling (PSMC), to reconstruct the demographic history of the split between two avian speciation model species, the pied flycatcher and collared flycatcher. Using whole-genome re-sequencing data from 20 individuals, we investigated 15 demographic models including different levels and patterns of gene flow, and changes in effective population size over time. ABC provided high support for recent (mode 0.3 my, range <0.7 my) species divergence, declines in effective population size of both species since their initial divergence, and unidirectional recent gene flow from pied flycatcher into collared flycatcher. The estimated divergence time and population size changes, supported by PSMC results, suggest that the ancestral species persisted through one of the glacial periods of middle Pleistocene and then split into two large populations that first increased in size before going through severe bottlenecks and expanding into their current ranges. Secondary contact appears to have been established after the last glacial maximum. The severity of the bottlenecks at the last glacial maximum is indicated by the discrepancy between current effective population sizes (20,000-80,000) and census sizes (5-50 million birds) of the two species. The recent divergence time challenges the supposition that avian speciation is a relatively slow process with extended times for intrinsic postzygotic reproductive barriers to evolve. Our study emphasizes the importance of using genome-wide data to unravel tangled demographic histories. Moreover, it constitutes one of the first examples of the inference of divergence history from genome-wide data in non-model species.
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http://dx.doi.org/10.1371/journal.pgen.1003942DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3820794PMC
November 2013

Lessons learned from implementing a national infrastructure in Sweden for storage and analysis of next-generation sequencing data.

Gigascience 2013 Jun 25;2(1). Epub 2013 Jun 25.

SNIC-UPPMAX, Uppsala University, PO Box 337, SE-751 05, Uppsala, Sweden.

: Analyzing and storing data and results from next-generation sequencing (NGS) experiments is a challenging task, hampered by ever-increasing data volumes and frequent updates of analysis methods and tools. Storage and computation have grown beyond the capacity of personal computers and there is a need for suitable e-infrastructures for processing. Here we describe UPPNEX, an implementation of such an infrastructure, tailored to the needs of data storage and analysis of NGS data in Sweden serving various labs and multiple instruments from the major sequencing technology platforms. UPPNEX comprises resources for high-performance computing, large-scale and high-availability storage, an extensive bioinformatics software suite, up-to-date reference genomes and annotations, a support function with system and application experts as well as a web portal and support ticket system. UPPNEX applications are numerous and diverse, and include whole genome-, de novo- and exome sequencing, targeted resequencing, SNP discovery, RNASeq, and methylation analysis. There are over 300 projects that utilize UPPNEX and include large undertakings such as the sequencing of the flycatcher and Norwegian spruce. We describe the strategic decisions made when investing in hardware, setting up maintenance and support, allocating resources, and illustrate major challenges such as managing data growth. We conclude with summarizing our experiences and observations with UPPNEX to date, providing insights into the successful and less successful decisions made.
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http://dx.doi.org/10.1186/2047-217X-2-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3704847PMC
June 2013

The genomic landscape of species divergence in Ficedula flycatchers.

Nature 2012 Nov 24;491(7426):756-60. Epub 2012 Oct 24.

Dept of Evolutionary Biology, Evolutionary Biology Centre, Uppsala University, Norbyvägen 18D, SE-752 36 Uppsala, Sweden.

Unravelling the genomic landscape of divergence between lineages is key to understanding speciation. The naturally hybridizing collared flycatcher and pied flycatcher are important avian speciation models that show pre- as well as postzygotic isolation. We sequenced and assembled the 1.1-Gb flycatcher genome, physically mapped the assembly to chromosomes using a low-density linkage map and re-sequenced population samples of each species. Here we show that the genomic landscape of species differentiation is highly heterogeneous with approximately 50 'divergence islands' showing up to 50-fold higher sequence divergence than the genomic background. These non-randomly distributed islands, with between one and three regions of elevated divergence per chromosome irrespective of chromosome size, are characterized by reduced levels of nucleotide diversity, skewed allele-frequency spectra, elevated levels of linkage disequilibrium and reduced proportions of shared polymorphisms in both species, indicative of parallel episodes of selection. Proximity of divergence peaks to genomic regions resistant to sequence assembly, potentially including centromeres and telomeres, indicate that complex repeat structures may drive species divergence. A much higher background level of species divergence of the Z chromosome, and a lower proportion of shared polymorphisms, indicate that sex chromosomes and autosomes are at different stages of speciation. This study provides a roadmap to the emerging field of speciation genomics.
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http://dx.doi.org/10.1038/nature11584DOI Listing
November 2012

Parental origin of sequence variants associated with complex diseases.

Nature 2009 Dec;462(7275):868-74

deCODE genetics, Sturlugata 8, 101 Reykjavík, Iceland.

Effects of susceptibility variants may depend on from which parent they are inherited. Although many associations between sequence variants and human traits have been discovered through genome-wide associations, the impact of parental origin has largely been ignored. Here we show that for 38,167 Icelanders genotyped using single nucleotide polymorphism (SNP) chips, the parental origin of most alleles can be determined. For this we used a combination of genealogy and long-range phasing. We then focused on SNPs that associate with diseases and are within 500 kilobases of known imprinted genes. Seven independent SNP associations were examined. Five-one with breast cancer, one with basal-cell carcinoma and three with type 2 diabetes-have parental-origin-specific associations. These variants are located in two genomic regions, 11p15 and 7q32, each harbouring a cluster of imprinted genes. Furthermore, we observed a novel association between the SNP rs2334499 at 11p15 and type 2 diabetes. Here the allele that confers risk when paternally inherited is protective when maternally transmitted. We identified a differentially methylated CTCF-binding site at 11p15 and demonstrated correlation of rs2334499 with decreased methylation of that site.
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http://dx.doi.org/10.1038/nature08625DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3746295PMC
December 2009

Detection of sharing by descent, long-range phasing and haplotype imputation.

Nat Genet 2008 Sep;40(9):1068-75

deCODE genetics, Reykjavik, Iceland.

Uncertainty about the phase of strings of SNPs creates complications in genetic analysis, although methods have been developed for phasing population-based samples. However, these methods can only phase a small number of SNPs effectively and become unreliable when applied to SNPs spanning many linkage disequilibrium (LD) blocks. Here we show how to phase more than 1,000 SNPs simultaneously for a large fraction of the 35,528 Icelanders genotyped by Illumina chips. Moreover, haplotypes that are identical by descent (IBD) between close and distant relatives, for example, those separated by ten meioses or more, can often be reliably detected. This method is particularly powerful in studies of the inheritance of recurrent mutations and fine-scale recombinations in large sample sets. A further extension of the method allows us to impute long haplotypes for individuals who are not genotyped.
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http://dx.doi.org/10.1038/ng.216DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4540081PMC
September 2008

Disruption of the neurexin 1 gene is associated with schizophrenia.

Hum Mol Genet 2009 Mar 22;18(5):988-96. Epub 2008 Oct 22.

Division of Molecular and Clinical Neurobiology, Department of Psychiatry, Ludwig- Maximilians University, Munich, Germany.

Deletions within the neurexin 1 gene (NRXN1; 2p16.3) are associated with autism and have also been reported in two families with schizophrenia. We examined NRXN1, and the closely related NRXN2 and NRXN3 genes, for copy number variants (CNVs) in 2977 schizophrenia patients and 33 746 controls from seven European populations (Iceland, Finland, Norway, Germany, The Netherlands, Italy and UK) using microarray data. We found 66 deletions and 5 duplications in NRXN1, including a de novo deletion: 12 deletions and 2 duplications occurred in schizophrenia cases (0.47%) compared to 49 and 3 (0.15%) in controls. There was no common breakpoint and the CNVs varied from 18 to 420 kb. No CNVs were found in NRXN2 or NRXN3. We performed a Cochran-Mantel-Haenszel exact test to estimate association between all CNVs and schizophrenia (P = 0.13; OR = 1.73; 95% CI 0.81-3.50). Because the penetrance of NRXN1 CNVs may vary according to the level of functional impact on the gene, we next restricted the association analysis to CNVs that disrupt exons (0.24% of cases and 0.015% of controls). These were significantly associated with a high odds ratio (P = 0.0027; OR 8.97, 95% CI 1.8-51.9). We conclude that NRXN1 deletions affecting exons confer risk of schizophrenia.
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http://dx.doi.org/10.1093/hmg/ddn351DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695245PMC
March 2009

Integrative analysis for finding genes and networks involved in diabetes and other complex diseases.

Genome Biol 2007 ;8(11):R253

Steno Diabetes Center, Niels Steensensvej 2, DK-2820 Gentofte, Denmark.

We have developed an integrative analysis method combining genetic interactions, identified using type 1 diabetes genome scan data, and a high-confidence human protein interaction network. Resulting networks were ranked by the significance of the enrichment of proteins from interacting regions. We identified a number of new protein network modules and novel candidate genes/proteins for type 1 diabetes. We propose this type of integrative analysis as a general method for the elucidation of genes and networks involved in diabetes and other complex diseases.
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http://dx.doi.org/10.1186/gb-2007-8-11-r253DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2258178PMC
August 2008

A human phenome-interactome network of protein complexes implicated in genetic disorders.

Nat Biotechnol 2007 Mar;25(3):309-16

Center for Biological Sequence Analysis, BioCentrum-DTU, Technical University of Denmark, Building 208, DK-2800 Lyngby, Denmark.

We performed a systematic, large-scale analysis of human protein complexes comprising gene products implicated in many different categories of human disease to create a phenome-interactome network. This was done by integrating quality-controlled interactions of human proteins with a validated, computationally derived phenotype similarity score, permitting identification of previously unknown complexes likely to be associated with disease. Using a phenomic ranking of protein complexes linked to human disease, we developed a Bayesian predictor that in 298 of 669 linkage intervals correctly ranks the known disease-causing protein as the top candidate, and in 870 intervals with no identified disease-causing gene, provides novel candidates implicated in disorders such as retinitis pigmentosa, epithelial ovarian cancer, inflammatory bowel disease, amyotrophic lateral sclerosis, Alzheimer disease, type 2 diabetes and coronary heart disease. Our publicly available draft of protein complexes associated with pathology comprises 506 complexes, which reveal functional relationships between disease-promoting genes that will inform future experimentation.
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http://dx.doi.org/10.1038/nbt1295DOI Listing
March 2007

Hyperphagia modifies FA profiles of plasma phospholipids, plasma FFA, and adipose tissue TAG.

Lipids 2003 Nov;38(11):1127-32

Department of Physiology, University of Iceland, Reykjavik, Iceland.

Hyperphagia was achieved by continuous intracerebroventricular infusion of a melanocortin receptor antagonist (HS024; Neosystem, Strasbourg, France) in rats. The effects of hyperphagia on FA composition and concentration of plasma phospholipids (PL), plasma FFA, and adipose tissue TAG were studied in rats for 8 d [short-term hyperphagia (STH); n = 8], or 28 d [long-term hyperphagia (LTH); n = 9]. The control rats were treated with artificial cerebrospinal fluid for 8 d (n = 8) or 28 d (n = 10). The rats were fed the same regular diet. In STH rats the plasma PL and fasting plasma FFA contained higher concentrations of saturated FA (SFA) and monounsaturated FA (MUFA), and plasma FFA contained lower n-6 PUFA than in the control rats. In LTH rats the plasma PL contained higher concentrations of SFA, MUFA, and n-3 PUFA and higher proportions of 16:1n-7 and 18:1n-9 at the expense of 18:2n-6 than in the control rats. In LTH rats the abundant dietary intake of 18:2n-6 did not enrich 18:2n-6 of the plasma PL or adipose tissue TAG. In LTH rats the fasting plasma FFA contained more than twofold higher concentrations of SFA and MUFA, and higher proportions of 16:1n-7 and 18:1n-9 at the expense of 18:2n-6 than in the control rats. This animal obesity model shows that LTH affects the FA composition and concentration of plasma PL, plasma FFA, and adipose tissue TAG, a result consistent with changes associated with increased risk of various diseases in humans. These results also demonstrate that LTH alters the FA composition of plasma PL and adipose tissue TAG in a way that does not reflect the FA composition of dietary fat.
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http://dx.doi.org/10.1007/s11745-003-1170-1DOI Listing
November 2003
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