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https://www.readbyqxmd.com/read/29341865/evidence-of-genetic-predisposition-for-metabolically-healthy-obesity-and-metabolically-obese-normal-weight
#1
Lam Opal Huang, Ruth Loos, Tuomas Oskari Kilpeläinen
Obesity has evolved into a global pandemic, which constitutes a major threat to public health. The majority of obesity-related health care costs are due to cardiometabolic complications, such as insulin resistance, dyslipidemia, and hypertension, which are risk factors for type 2 diabetes and cardiovascular disease. However, many obese individuals, often called metabolically healthy obese (MHO), seem to be protected from these cardiometabolic complications. Conversely, there is a group of individuals who suffer from cardiometabolic complications despite being of normal weight; a condition termed metabolically obese normal weight (MONW)...
December 20, 2017: Physiological Genomics
https://www.readbyqxmd.com/read/29341863/distinct-gene-signatures-predict-insulin-resistance-in-young-mice-with-high-fat-diet-induced-obesity
#2
Katherine Chen, Alice Jih, Olivia Osborn, Sarah T Kavaler, Wenxian Fu, Roman Sasik, Rintaro Saito, Jane J Kim
Highly inbred C57BL/6 mice show wide variation in their degree of insulin resistance in response to diet-induced obesity even though they are almost genetically identical. Here we employed transcriptional profiling by RNA sequencing (RNA-Seq) of visceral adipose tissue (VAT) and liver in young mice to determine how gene expression patterns correlate with the later development of high-fat diet (HFD)-induced insulin resistance in adulthood. To accomplish this goal, we partially removed and banked tissues from pubertal mice...
January 8, 2018: Physiological Genomics
https://www.readbyqxmd.com/read/29341130/mitochondrial-function-and-autophagy-integrating-proteotoxic-redox-and-metabolic-stress-in-parkinson-s-disease
#3
REVIEW
Jianhua Zhang, M Lillian Culp, Jason G Craver, Victor Darley-Usmar
Parkinson's disease (PD) is a movement disorder with widespread neurodegeneration in the brain. Significant oxidative, reductive, metabolic, and proteotoxic alterations have been observed in PD postmortem brains. The alterations of mitochondrial function resulting in decreased bioenergetic health is important and needs to be further examined to help develop biomarkers for PD severity and prognosis. It is now becoming clear that multiple hits on metabolic and signaling pathways are likely to exacerbate PD pathogenesis...
January 17, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29340279/effect-of-mthfr-a1298c-and-mtrr-a66g-genetic-mutations-on-homocysteine-levels-in-the-chinese-population-a-systematic-review-and-meta-analysis
#4
Jiancheng Wang, Nengtai Ouyang, Long Qu, Tengfei Lin, Xianglin Zhang, Yaren Yu, Chongfei Jiang, Liling Xie, Liping Wang, Zhigui Wang, Shuzhen Ren, Shizhi Chen, Jiang Huang, Fang Liu, Weiqing Huang, Xianhui Qin
Background and Objectives: The Chinese population typically has inadequate folate intake and no mandatory folic acid fortification. Methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) are the two key regulatory enzymes in the folate/homocysteine (Hcy) metabolism. Hcy has been implicated in the pathogenesis of cardiovascular disease. We conducted a meta-analysis to assess whether the MTHFR gene A1298C and the MTRR gene A66G polymorphisms affect Hcy levels in the Chinese population...
December 2017: Journal of Translational Internal Medicine
https://www.readbyqxmd.com/read/29340220/multilocus-analysis-of-genetic-susceptibility-to-myocardial-infarction-in-russians-replication-study
#5
N G Kukava, B V Titov, G J Osmak, N A Matveeva, O G Kulakova, A V Favorov, R M Shakhnovich, M Ya Ruda, O O Favorova
In search of genetic markers of myocardial infarction (MI) risk, which have prognostic significance for Russians, we performed a replication study of MI association with genetic variants of PCSK9 (rs562556), APOE (epsilon polymorphism, rs7412 and rs429358), LPL (rs320), MTHFR (rs1801133), eNOS (rs2070744), and the 9p21 region (rs1333049) in 405 patients with MI and 198 controls. Significant MI association was observed with variants of the lipid metabolism genes (PCSK9, APOE and LPL), and of eNOS. The SNPs in the MTHFR gene and the 9p21 region were not significantly associated with MI one by one but were included in several different MI-associated allelic combinations identified by multilocus analysis...
October 2017: Acta Naturae
https://www.readbyqxmd.com/read/29340042/identification-of-potential-genetic-causal-variants-for-rheumatoid-arthritis-by-whole-exome-sequencing
#6
Ying Li, Elaine Lai-Han Leung, Hudan Pan, Xiaojun Yao, Qingchun Huang, Min Wu, Ting Xu, Yuwei Wang, Jun Cai, Runze Li, Wei Liu, Liang Liu
Rheumatoid arthritis (RA) is a highly prevalent chronic autoimmune disease. However, genetic and environmental factors involved in RA pathogenesis are still remained largely unknown. To identify the genetic causal variants underlying pathogenesis and disease progression of RA patients, we undertook the first comprehensive whole-exome sequencing (WES) study in a total of 124 subjects including 58 RA cases and 66 healthy controls in Han Chinese population. We identified 378 novel genes that were enriched with deleterious variants in RA patients using a gene burden test...
December 19, 2017: Oncotarget
https://www.readbyqxmd.com/read/29340030/increased-efficacy-of-metformin-corresponds-to-differential-metabolic-effects-in-the-ovarian-tumors-from-obese-versus-lean-mice
#7
Jianjun Han, Weiya Z Wysham, Yan Zhong, Hui Guo, Lu Zhang, Kim M Malloy, Hallum K Dickens, Gene Huh, Douglas Lee, Liza Makowski, Chunxiao Zhou, Victoria L Bae-Jump
Obesity is a significant risk factor for ovarian cancer (OC) and associated with worse outcomes for this disease. We assessed the anti-tumorigenic effects of metformin in human OC cell lines and a genetically engineered mouse model of high grade serous OC under obese and lean conditions. Metformin potently inhibited growth in a dose-dependent manner in all four human OC cell lines through AMPK/mTOR pathways. Treatment with metformin resulted in G1 arrest, induction of apoptosis, reduction of invasion and decreased hTERT expression...
December 19, 2017: Oncotarget
https://www.readbyqxmd.com/read/29339836/the-role-of-metabolic-enzymes-in-mesenchymal-tumors-and-tumor-syndromes-genetics-pathology-and-molecular-mechanisms
#8
REVIEW
Inga-Marie Schaefer, Jason L Hornick, Judith V M G Bovée
The discovery of mutations in genes encoding the metabolic enzymes isocitrate dehydrogenase (IDH), succinate dehydrogenase (SDH), and fumarate hydratase (FH) has expanded our understanding not only of altered metabolic pathways but also epigenetic dysregulation in cancer. IDH1/2 mutations occur in enchondromas and chondrosarcomas in patients with the non-hereditary enchondromatosis syndromes Ollier disease and Maffucci syndrome and in sporadic tumors. IDH1/2 mutations result in excess production of the oncometabolite (D)-2-hydroxyglutarate...
January 16, 2018: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/29339782/loss-of-disease-tolerance-during-citrobacter-rodentium-infection-is-associated-with-impaired-epithelial-differentiation-and-hyperactivation-of-t-cell-responses
#9
Eugene Kang, Guangyan Zhou, Mitra Yousefi, Romain Cayrol, Jianguo Xia, Samantha Gruenheid
Citrobacter rodentium is an intestinal mouse pathogen widely used as a model to study the mucosal response to infection. Inbred mouse strains suffer one of two fates following infection: self-limiting colitis or fatal diarrheal disease. We previously reported that Rspo2 is a major genetic determinant of the outcome of C. rodentium infection; Rspo2 induction during infection of susceptible mice leads to loss of intestinal function and mortality. Rspo2 induction does not impact bacterial colonization, but rather, impedes the ability of the host to tolerate C...
January 16, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29339775/anti-apoptotic-a1-is-not-essential-for-lymphoma-development-in-e%C3%A2%C2%B5-myc-mice-but-helps-sustain-transplanted-e%C3%A2%C2%B5-myc-tumour-cells
#10
Mark Mensink, Natasha S Anstee, Mikara Robati, Robyn L Schenk, Marco J Herold, Suzanne Cory, Cassandra J Vandenberg
The transcription factor c-MYC regulates a multiplicity of genes involved in cellular growth, proliferation, metabolism and DNA damage response and its overexpression is a hallmark of many tumours. Since MYC promotes apoptosis under conditions of stress, such as limited availability of nutrients or cytokines, MYC-driven cells are very much dependent on signals that inhibit cell death. Stress signals trigger apoptosis via the pathway regulated by opposing fractions of the BCL-2 protein family and previous genetic studies have shown that the development of B lymphoid tumours in Eµ-Myc mice is critically dependent on expression of pro-survival BCL-2 relatives MCL-1, BCL-W and, to a lesser extent, BCL-XL, but not BCL-2 itself, and that sustained growth of these lymphomas is dependent on MCL-1...
January 16, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29339647/proceedings-of-the-11th-congress-of-the-international-society-of-nutrigenetics-and-nutrigenomics-isnn-2017
#11
William T Barrington, Anna C Salvador, Jaana A Hartiala, Raffaele De Caterina, Martin Kohlmeier, J Alfredo Martinez, Carin B Kreutzer, David Heber, Aldons J Lusis, Zhaoping Li, Hooman Allayee
The International Society of Nutrigenetics and Nutrigenomics (ISNN) held its 11th annual Congress in Los Angeles, California, between September 16 and 19, 2017. In addition to 2 keynote lectures, 4 plenary sessions included presentations by internationally renowned speakers on cutting-edge areas of research and new discoveries in genetics/genomics, the microbiome, and nutrition. Scientific topics included multi-omics approaches; diet and the microbiome; cancer, longevity, and metabolism; moving the field forward; and translational/educational aspects and the future of medicine...
January 17, 2018: Journal of Nutrigenetics and Nutrigenomics
https://www.readbyqxmd.com/read/29339473/identification-of-thioredoxin-interacting-protein-txnip-as-a-downstream-target-for-igf1-action
#12
Karthik Nagaraj, Lena Lapkina-Gendler, Rive Sarfstein, David Gurwitz, Metsada Pasmanik-Chor, Zvi Laron, Shoshana Yakar, Haim Werner
Laron syndrome (LS), or primary growth hormone (GH) insensitivity, is the best-characterized entity among the congenital insulin-like growth factor 1 (IGF1) deficiencies. Life-long exposure to minute endogenous IGF1 levels is linked to low stature as well as a number of endocrine and metabolic abnormalities. While elevated IGF1 is correlated with increased cancer incidence, epidemiological studies revealed that patients with LS do not develop tumors. The mechanisms associated with cancer protection in LS are yet to be discovered...
January 16, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29339339/proteomics-and-genetic-analyses-reveal-the-effects-of-arsenite-oxidation-on-metabolic-pathways-and-the-roles-of-aior-in-agrobacterium-tumefaciens-gw4
#13
Kaixiang Shi, Qian Wang, Xia Fan, Gejiao Wang
A heterotrophic arsenite [As(III)]-oxidizing bacterium Agrobacterium tumefaciens GW4 isolated from As(III)-rich groundwater sediment showed high As(III) resistance and could oxidize As(III) to As(V). The As(III) oxidation could generate energy and enhance growth, and AioR was the regulator for As(III) oxidase. To determine the related metabolic pathways mediated by As(III) oxidation and whether AioR regulated other cellular responses to As(III), isobaric tags for relative and absolute quantitation (iTRAQ) was performed in four treatments, GW4 (+AsIII)/GW4 (-AsIII), GW4-ΔaioR (+AsIII)/GW4-ΔaioR (-AsIII), GW4-ΔaioR (-AsIII)/GW4 (-AsIII) and GW4-ΔaioR (+AsIII)/GW4 (+AsIII)...
January 12, 2018: Environmental Pollution
https://www.readbyqxmd.com/read/29338102/circulating-serum-25-hydroxyvitamin-d-levels-and-bone-mineral-density-mendelian-randomization-study
#14
Susanna C Larsson, Håkan Melhus, Karl Michaëlsson
There is considerable discussion of the importance for increased serum 25-hydroxyvitamin D (S-25OHD) concentration associated with adequacy for bone health. Accordingly, whether long-term high S-25OHD concentration in general positively affects bone mineral density (BMD) is uncertain. We used a Mendelian randomization design to determine the association between genetically increased S-25OHD concentrations and BMD. Five single-nucleotide polymorphisms (SNPs) in or near genes encoding enzymes and carrier proteins involved in vitamin D synthesis or metabolism were used as instrumental variables to genetically predict one standard deviation increase in S-25OHD concentration...
January 16, 2018: Journal of Bone and Mineral Research: the Official Journal of the American Society for Bone and Mineral Research
https://www.readbyqxmd.com/read/29338053/selenium-regulation-of-selenoprotein-enzyme-activity-and-transcripts-in-a-pilot-study-with-founder-strains-from-the-collaborative-cross
#15
Roger A Sunde
Rodents and humans have 24-25 selenoproteins, and these proteins contain the 21st amino acid, selenocysteine, incorporated co-translationally into the peptide backbone in a series of reactions dependent on at least 6 unique gene products. In selenium (Se) deficiency, there is differential regulation of selenoprotein expression, whereby levels of some selenoproteins and their transcripts decrease dramatically in Se deficiency, but other selenoprotein transcripts are spared this decrease; the underlying mechanism, however, is not fully understood...
2018: PloS One
https://www.readbyqxmd.com/read/29337073/neofunctionalization-of-duplicated-p450-genes-drives-the-evolution-of-insecticide-resistance-in-the-brown-planthopper
#16
Christoph T Zimmer, William T Garrood, Kumar Saurabh Singh, Emma Randall, Bettina Lueke, Oliver Gutbrod, Svend Matthiesen, Maxie Kohler, Ralf Nauen, T G Emyr Davies, Chris Bass
Gene duplication is a major source of genetic variation that has been shown to underpin the evolution of a wide range of adaptive traits [1, 2]. For example, duplication or amplification of genes encoding detoxification enzymes has been shown to play an important role in the evolution of insecticide resistance [3-5]. In this context, gene duplication performs an adaptive function as a result of its effects on gene dosage and not as a source of functional novelty [3, 6-8]. Here, we show that duplication and neofunctionalization of a cytochrome P450, CYP6ER1, led to the evolution of insecticide resistance in the brown planthopper...
January 4, 2018: Current Biology: CB
https://www.readbyqxmd.com/read/29336249/mutations-of-nuclear-and-mitochondrial-genomes-as-potential-targets-for-the-treatment-of-metabolic-syndrome
#17
Elena V Galitsyn, Andrey V Zhelankin, Igor A Sobenin, Alexander N Orekhov
In addition to external factors, such as exercise, food and the environment, genetic predisposition makes great contribution to the development of metabolic disorders and cardiovascular disease. This review is aimed to examine the genetic basis of complex metabolic disorders conventionally described as "metabolic syndrome" (MetS), with the special focus on currently known mutations in the nuclear and mitochondrial genomes, which are associated both with the individual components of MetS and combinations thereof, and also on the studies of the relationship of MetS phenotype as a binary trait...
January 15, 2018: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/29335600/alteration-in-fluidity-of-cell-plasma-membrane-in-huntington-disease-revealed-by-spectral-phasor-analysis
#18
Sara Sameni, Leonel Malacrida, Zhiqun Tan, Michelle A Digman
Huntington disease (HD) is a late-onset genetic neurodegenerative disorder caused by expansion of cytosine-adenine-guanine (CAG) trinucleotide in the exon 1 of the gene encoding the polyglutamine (polyQ). It has been shown that protein degradation and lipid metabolism is altered in HD. In many neurodegenerative disorders, impaired lipid homeostasis is one of the early events in the disease onset. Yet, little is known about how mutant huntingtin may affect phospholipids membrane fluidity. Here, we investigated how membrane fluidity in the living cells (differentiated PC12 and HEK293 cell lines) are affected using a hyperspectral imaging of widely used probes, LAURDAN...
January 15, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29335581/role-of-hypoxia-in-diffuse-large-b-cell-lymphoma-metabolic-repression-and-selective-translation-of-hk2-facilitates-development-of-dlbcl
#19
Kavita Bhalla, Sausan Jaber, Nanaji Nahid M, Karen Underwood, Afshin Beheshti, Ari Landon, Binny Bhandary, Paul Bastain, Andrew M Evens, John Haley, Brian Polster, Ronald B Gartenhaus
Published molecular profiling studies in patients with lymphoma suggested the influence of hypoxia inducible factor-1 alpha (HIF1α) targets in prognosis of DLBCL. Yet, the role of hypoxia in hematological malignancies remains unclear. We observed that activation of HIF1α resulted in global translation repression during hypoxic stress in DLBCL. Protein translation efficiency as measured using 35S-labeled methionine incorporation revealed a ≥50% reduction in translation upon activation of HIF1α. Importantly, translation was not completely inhibited and expression of clinically correlated hypoxia targets such as GLUT1, HK2, and CYT-C was found to be refractory to translational repression under hypoxia in DLBCL cells...
January 15, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29335542/compartmentalized-activities-of-the-pyruvate-dehydrogenase-complex-sustain-lipogenesis-in-prostate-cancer
#20
Jingjing Chen, Ilaria Guccini, Diletta Di Mitri, Daniela Brina, Ajinkya Revandkar, Manuela Sarti, Emiliano Pasquini, Abdullah Alajati, Sandra Pinton, Marco Losa, Gianluca Civenni, Carlo V Catapano, Jacopo Sgrignani, Andrea Cavalli, Rocco D'Antuono, John M Asara, Andrea Morandi, Paola Chiarugi, Sara Crotti, Marco Agostini, Monica Montopoli, Ionica Masgras, Andrea Rasola, Ramon Garcia-Escudero, Nicolas Delaleu, Andrea Rinaldi, Francesco Bertoni, Johann de Bono, Arkaitz Carracedo, Andrea Alimonti
The mechanisms by which mitochondrial metabolism supports cancer anabolism remain unclear. Here, we found that genetic and pharmacological inactivation of pyruvate dehydrogenase A1 (PDHA1), a subunit of the pyruvate dehydrogenase complex (PDC), inhibits prostate cancer development in mouse and human xenograft tumor models by affecting lipid biosynthesis. Mechanistically, we show that in prostate cancer, PDC localizes in both the mitochondria and the nucleus. Whereas nuclear PDC controls the expression of sterol regulatory element-binding transcription factor (SREBF)-target genes by mediating histone acetylation, mitochondrial PDC provides cytosolic citrate for lipid synthesis in a coordinated manner, thereby sustaining anabolism...
January 15, 2018: Nature Genetics
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