Database : MEDLINE
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[PMID]: 29524416
[Au] Autor:Fuller M; Futerman AH
[Ad] Address:Genetics and Molecular Pathology, SA Pathology at Women's and Children's Hospital, 72 King William Road, North Adelaide and School of Medicine, University of Adelaide, Adelaide, South Australia, 5005, Australia. Electronic address: maria.fuller@adelaide.edu.au.
[Ti] Title:The brain lipidome in neurodegenerative lysosomal storage disorders.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cholesterol, sphingolipids and glycerophospholipids are critical constituents of the brain, subserving neuronal membrane architecture and providing a platform for biochemical processes essential for proper neurodevelopment and function. When lysosomal defects arise in a lipid metabolic pathway, it is therefore easy to imagine that neurological decline will transpire, however for deficits in non-lipid pathways, this becomes harder to envisage. Here we suggest the working hypothesis that neurodegenerative lysosomal storage disorders might manifest as primary and/or secondary disorders of lipid metabolism. Evidence suggests that the mere process of lysosomal substrate accumulation, ubiquitous in all lysosomal storage disorders, impairs lysosome integrity resulting in secondary lipid accumulation. Impaired lysosomal degradation of a specific lipid defines a primary disorder of lipid metabolism and as these lysosomal storage disorders additionally show secondary lipid alterations, all primary disorders can also be considered secondary disorders of lipid metabolism. The outcome is a generalized cellular lipid dyshomeostasis and consequently, the physiological architecture of the lipid-enriched plasma membrane is perturbed, including the lipid composition of specialized membrane microdomains, often termed lipid rafts. Neurotoxicity results from the complex interplay of malfunctioning signaling and vesicular trafficking important for neuronal communication and synaptic plasticity-induced by the imbalance in physiological membrane lipid composition - together with compensatory mechanisms aimed at restoring lipid homeostasis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 10158 MEDLINE  
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[PMID]: 29514073
[Au] Autor:Rhoads TW; Burhans MS; Chen VB; Hutchins PD; Rush MJP; Clark JP; Stark JL; McIlwain SJ; Eghbalnia HR; Pavelec DM; Ong IM; Denu JM; Markley JL; Coon JJ; Colman RJ; Anderson RM
[Ad] Address:Department of Medicine, University of Wisconsin-Madison, Madison, WI 53705, USA.
[Ti] Title:Caloric Restriction Engages Hepatic RNA Processing Mechanisms in Rhesus Monkeys.
[So] Source:Cell Metab;27(3):677-688.e5, 2018 Mar 06.
[Is] ISSN:1932-7420
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Caloric restriction (CR) extends lifespan and delays the onset of age-related disorders in diverse species. Metabolic regulatory pathways have been implicated in the mechanisms of CR, but the molecular details have not been elucidated. Here, we show that CR engages RNA processing of genes associated with a highly integrated reprogramming of hepatic metabolism. We conducted molecular profiling of liver biopsies collected from adult male rhesus monkeys (Macaca mulatta) at baseline and after 2 years on control or CR (30% restricted) diet. Quantitation of over 20,000 molecules from the hepatic transcriptome, proteome, and metabolome indicated that metabolism and RNA processing are major features of the response to CR. Predictive models identified lipid, branched-chain amino acid, and short-chain carbon metabolic pathways, with alternate transcript use for over half of the genes in the CR network. We conclude that RNA-based mechanisms are central to the CR response and integral in metabolic reprogramming.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  3 / 10158 MEDLINE  
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[PMID]: 29523870
[Au] Autor:Chouinard VA; Henderson DC; Dalla Man C; Valeri L; Gray BE; Ryan KP; Cypess AM; Cobelli C; Cohen BM; Öngür D
[Ad] Address:Psychotic Disorders Division, McLean Hospital, Belmont, MA, USA. vchouinard@mclean.harvard.edu.
[Ti] Title:Impaired insulin signaling in unaffected siblings and patients with first-episode psychosis.
[So] Source:Mol Psychiatry;, 2018 Mar 09.
[Is] ISSN:1476-5578
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Patients with psychotic disorders are at high risk for type 2 diabetes mellitus, and there is increasing evidence that patients display glucose metabolism abnormalities before significant antipsychotic medication exposure. In the present study, we examined insulin action by quantifying insulin sensitivity in first-episode psychosis (FEP) patients and unaffected siblings, compared to healthy individuals, using a physiological-based model and comprehensive assessment battery. Twenty-two unaffected siblings, 18 FEP patients, and 15 healthy unrelated controls were evaluated using a 2-h oral glucose tolerance test (OGTT), with 7 samples of plasma glucose and serum insulin concentration measurements. Insulin sensitivity was quantified using the oral minimal model method. Lipid, leptin, free fatty acids, and inflammatory marker levels were also measured. Anthropometric, nutrient, and activity assessments were conducted; total body composition and fat distribution were determined using whole-body dual-energy X-ray absorptiometry. Insulin sensitivity significantly differed among groups (F = 6.01 and 0.004), with patients and siblings showing lower insulin sensitivity, compared to controls (P = 0.006 and 0.002, respectively). Body mass index, visceral adipose tissue area (cm ), lipids, leptin, free fatty acids, inflammatory markers, and activity ratings were not significantly different among groups. There was a significant difference in nutrient intake with lower total kilocalories/kilogram body weight in patients, compared to siblings and controls. Overall, the findings suggest that familial abnormal glucose metabolism or a primary insulin signaling pathway abnormality is related to risk for psychosis, independent of disease expression and treatment effects. Future studies should examine underlying biological mechanisms of insulin signaling abnormalities in psychotic disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1038/s41380-018-0045-1

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[PMID]: 29501626
[Au] Autor:Qi G; Guo R; Tian H; Li L; Liu H; Mi Y; Liu X
[Ad] Address:Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science and Engineering, Northwest A&F University, Yangling, Shaanxi 712100, China.
[Ti] Title:Nobiletin protects against insulin resistance and disorders of lipid metabolism by reprogramming of circadian clock in hepatocytes.
[So] Source:Biochim Biophys Acta;1863(6):549-562, 2018 Mar 06.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:SCOPE: Circadian clock plays a principal role in orchestrating our daily physiology and metabolism, and their perturbation can evoke metabolic diseases such as fatty liver and insulin resistance. Nobiletin (NOB) has been demonstrated to possess antitumor and neuroprotective activities. The objective of the current study is to determine potential effects of NOB on modulating the core clock gene Bmal1 regarding ameliorating glucolipid metabolic disorders. RESULTS: Our results revealed that NOB partially reverse the relatively shallow daily oscillations of circadian clock genes and reset phase-shifting circadian rhythms in primary hepatocytes under metabolic disorders conditions. Importantly, NOB was found to be effective at amplifying glucose uptake via stimulating IRS-1/AKT signaling pathway, as well as blunting palmitate-induced lipogenesis in HepG2 cells via modulating AMPK-Sirt1 signaling pathway and key enzymes of de novo lipogenesis in a Bmal1-dependent manner. NOB attenuated palmitate-stimulated excessive secretions of ROS, restored the depletions of mitochondrial membrane potential, which is similar to the recovery in expressions of mitochondrial respiration complex I-IV. CONCLUSION: This study is the first to provide compelling evidences that NOB prevent cellular glucolipid metabolic imbalance and mitochondrial function in a Bmal1-dependent manner. Overall, NOB may serve as a nutritional preventive strategy in recovering metabolic disorders relevant to circadian clock.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  5 / 10158 MEDLINE  
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[PMID]: 29476879
[Au] Autor:Ren T; Yang WS; Lin Y; Liu JF; Li Y; Yang LC; Zeng KY; Peng L; Liu YJ; Ye ZH; Luo XM; Ke YJ; Diao Y; Jin X
[Ad] Address:School of Biomedical Science, Institute of Molecular Medicine, Huaqiao University, Quanzhou 612021, China.
[Ti] Title:A novel PPARα/γ agonist, propane-2-sulfonic acid octadec-9-enyl-amide, ameliorates insulin resistance and gluconeogenesis in vivo and vitro.
[So] Source:Eur J Pharmacol;826:1-8, 2018 Feb 22.
[Is] ISSN:1879-0712
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Peroxisome proliferator-activated receptor alpha/gamma (PPARα/γ) agonists have emerged as important pharmacological agents for improving insulin action. Propane-2-sulfonic acid octadec-9-enyl-amide (N15) is a novel PPARα/γ dual agonist synthesized in our laboratory. The present study investigates the efficacy and safety of N15 on insulin resistance regulation in high fat diet (HFD)-and streptozotocin (STZ)-induced diabetic mice and in palmitic acid (PA)-induced HepG2 cells. Our results showed that N15 remarkably ameliorated insulin resistance and dyslipidemia in vivo, as well as rectified the glucose consumption and gluconeogenesis in vitro. Moreover, the glucose-lowering effect of N15 was associated with PPARγ mediated up-regulation of hepatic glucose consumption and down-regulation of gluconeogenesis. Meanwhile, N15 exerted advantageous effects on glucose and lipid metabolism without triggering weight gain and hepatotoxicity in mice. In conclusion, our data demonstrated that by alleviating glucose and lipid abnormalities, N15 could be used as a potential prophylactic and therapeutic agent against type 2 diabetes and related metabolic disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  6 / 10158 MEDLINE  
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[PMID]: 29431320
[Au] Autor:Kudaeva IV; Dyakovich OA; Masnavieva LB; Popkova OV; Abramatets EA
[Ti] Title:[Features of the lipid exchange in workers employed in aluminium productions].
[So] Source:Gig Sanit;95(9):857-60, 2016.
[Is] ISSN:0016-9900
[Cp] Country of publication:Russia (Federation)
[La] Language:rus
[Ab] Abstract:Aluminum production can be referred to the category of industries of the increased health hazard for the workers. During technological process of receiving aluminum the air of a working zone is polluted by a large number of harmful substances. Workers are exposed to the complex of toxicants possessing a polytropic impact on the body. The most significant consequences are violations of different types of metabolism in the organism, including lipid metabolism. The purpose of the study is the investigation of the state of lipid metabolism in persons working in the production of aluminum. The object of research was 108 male workers of aluminum production suffering from occupational pathology of airways. The group of comparison was consisted of 103 men, apparently healthy, not exposed to toxicants. There was determined the content of the total cholesterol (TC), high and low density lipoprotein cholesterol (HDLC and LDLC), triglycerides (TG), phospholipids (PL), atherogenic index (AI). Statistical processing was performed with the use of software «Statistica 6.0¼. There were established statistically significant differences of indices of lipid exchange in the persons occupied in aluminum production when related to the group of comparison. IA values in persons from the study group proved to be higher than in the comparison group, due to elevated levels of TC and LDLC. The TG and PL level was also higher. The values of IA, TC and TG in workers of aluminum production in more than 50% cases exceeded the reference values. The average concentration of HDL cholesterol in both groups did not differ, and was above the lower reference boundary. Established features of lipid metabolism in workers of aluminum allow us to suggest the distinction in mechanisms of developing proatherogenic disorders from previously established ones for workers exposed to other chemicals. One of the causes of the shaping of these disorders can be oxidative stress, which in turn serves as a response to the exposure of complex of toxic substances to workers.
[Mh] MeSH terms primary: Aluminum
Atherosclerosis
Lipid Metabolism/drug effects
Occupational Diseases
Occupational Exposure
Workplace/standards
[Mh] MeSH terms secundary: Adult
Aluminum/adverse effects
Aluminum/analysis
Atherosclerosis/epidemiology
Atherosclerosis/etiology
Atherosclerosis/prevention & control
Humans
Male
Manufacturing Industry/methods
Manufacturing Industry/standards
Occupational Diseases/epidemiology
Occupational Diseases/etiology
Occupational Diseases/prevention & control
Occupational Exposure/adverse effects
Occupational Exposure/analysis
Occupational Exposure/prevention & control
Occupational Health/standards
Outcome Assessment (Health Care)
Russia/epidemiology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:CPD4NFA903 (Aluminum)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180213
[St] Status:MEDLINE

  7 / 10158 MEDLINE  
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[PMID]: 29031613
[Au] Autor:Majd H; King MS; Smith AC; Kunji ERS
[Ad] Address:Medical Research Council Mitochondrial Biology Unit, University of Cambridge, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
[Ti] Title:Pathogenic mutations of the human mitochondrial citrate carrier SLC25A1 lead to impaired citrate export required for lipid, dolichol, ubiquinone and sterol synthesis.
[So] Source:Biochim Biophys Acta;1859(1):1-7, 2018 01.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Missense mutations of the human mitochondrial citrate carrier, encoded by the SLC25A1 gene, lead to an autosomal recessive neurometabolic disorder characterised by neonatal-onset encephalopathy with severe muscular weakness, intractable seizures, respiratory distress, and lack of psychomotor development, often resulting in early death. Here, we have measured the effect of all twelve known pathogenic mutations on the transport activity. The results show that nine mutations abolish transport of citrate completely, whereas the other three reduce the transport rate by >70%, indicating that impaired citrate transport is the most likely primary cause of the disease. Some mutations may be detrimental to the structure of the carrier, whereas others may impair key functional elements, such as the substrate binding site and the salt bridge network on the matrix side of the carrier. To understand the consequences of impaired citrate transport on metabolism, the substrate specificity was also determined, showing that the human citrate carrier predominantly transports citrate, isocitrate, cis-aconitate, phosphoenolpyruvate and malate. Although D-2- and L-2 hydroxyglutaric aciduria is a metabolic hallmark of the disease, it is unlikely that the citrate carrier plays a significant role in the removal of hydroxyglutarate from the cytosol for oxidation to oxoglutarate in the mitochondrial matrix. In contrast, computer simulations of central metabolism predict that the export of citrate from the mitochondrion cannot be fully compensated by other pathways, restricting the cytosolic production of acetyl-CoA that is required for the synthesis of lipids, sterols, dolichols and ubiquinone, which in turn explains the severe disease phenotypes.
[Mh] MeSH terms primary: Anion Transport Proteins
Citric Acid/metabolism
Computer Simulation
Dolichol
Mitochondrial Proteins
Models, Biological
Mutation, Missense
Sterols
Ubiquinone
[Mh] MeSH terms secundary: Anion Transport Proteins/chemistry
Anion Transport Proteins/genetics
Anion Transport Proteins/metabolism
Biological Transport, Active/genetics
Brain Diseases, Metabolic, Inborn/enzymology
Brain Diseases, Metabolic, Inborn/genetics
Catalytic Domain
Dolichol/biosynthesis
Dolichol/chemistry
Dolichol/genetics
Humans
Mitochondrial Proteins/chemistry
Mitochondrial Proteins/genetics
Mitochondrial Proteins/metabolism
Sterols/biosynthesis
Sterols/chemistry
Sterols/metabolism
Ubiquinone/biosynthesis
Ubiquinone/chemistry
Ubiquinone/genetics
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Anion Transport Proteins); 0 (Mitochondrial Proteins); 0 (Slc25a1 protein, human); 0 (Sterols); 1339-63-5 (Ubiquinone); 2067-66-5 (Dolichol); 2968PHW8QP (Citric Acid)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:171017
[St] Status:MEDLINE

  8 / 10158 MEDLINE  
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[PMID]: 29519318
[Au] Autor:Ding T; Wang S; Zhang X; Zai W; Fan J; Chen W; Bian Q; Luan J; Shen Y; Zhang Y; Ju D; Mei X
[Ad] Address:Department of Nephrology, Changhai Hospital, Second Military Medical University, Shanghai 200433, PR China.
[Ti] Title:Kidney protection effects of dihydroquercetin on diabetic nephropathy through suppressing ROS and NLRP3 inflammasome.
[So] Source:Phytomedicine;41:45-53, 2018 Mar 01.
[Is] ISSN:1618-095X
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:BACKGROUND: Diabetic nephropathy (DN), the leading cause of end-stage renal disease, is acknowledged as an independent risk factor for cardiovascular disease, which underlines the urgent need for new medications to DN. Dihydroquercetin (DHQ), an important natural dihydroflavone, exerts significant antioxidant, anti-inflammatory, and antifibrotic properties, but its effects on DN have not been investigated yet. PURPOSE: We aimed to explore the kidney protection effects of DHQ on DN rats induced by high-fat diet/streptozotocin in vivo and the underlying mechanisms of DHQ on renal cells including HBZY-1 and HK2 exposed to high glucose in vitro. METHODS: Major biochemical indexes were measured including urine microalbumin, fasting serum glucose, serum levels of creatinine, total cholesterol and low density lipoprotein cholesterol. Renal histologic sections were stained with hematoxylin-eosin, periodic acid-Schiff and Masson. The cell proliferation was assessed by MTT assay. Reactive oxygen species (ROS) generation was detected by DCFH-DA assay and laser scanning confocal microscope. Expression of all proteins was examined by western-blot. RESULTS: In high-fat diet/streptozotocin-induced DN rats, DHQ at the dose of 100 mg/kg/day significantly attenuated the increasing urine microalbumin excretion, hyperglycemia and lipid metabolism disorders, and mitigated renal histopathological lesions. In in vitro studies, DHQ significantly suppressed cell proliferation and the excessive ROS generation, and alleviated the activation of nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome and the expression of renal fibrosis-associated proteins in renal cells exposed to high glucose. CONCLUSION: The results revealed that DHQ possesses kidney protection effects including attenuating urine microalbumin excretion, hyperglycemia and lipid metabolism disorders, and mitigating renal histopathological lesions on DN, and one of the possible renal-protective mechanisms is suppressing ROS and NLRP3 inflammasome.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process

  9 / 10158 MEDLINE  
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[PMID]: 29518061
[Au] Autor:Sato F; Kohsaka A; Bhawal UK; Muragaki Y
[Ad] Address:Department of Pathology, Wakayama Medical University School of Medicine, 811-1 Kimiidera, Wakayama 641-8509, Japan. fsatoDEC1DEC2@yahoo.co.jp.
[Ti] Title:Potential Roles of Dec and Bmal1 Genes in Interconnecting Circadian Clock and Energy Metabolism.
[So] Source:Int J Mol Sci;19(3), 2018 Mar 08.
[Is] ISSN:1422-0067
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:The daily rhythm of mammalian energy metabolism is subject to the circadian clock system, which is made up of the molecular clock machinery residing in nearly all cells throughout the body. The clock genes have been revealed not only to form the molecular clock but also to function as a mediator that regulates both circadian and metabolic functions. While the circadian signals generated by clock genes produce metabolic rhythms, clock gene function is tightly coupled to fundamental metabolic processes such as glucose and lipid metabolism. Therefore, defects in the clock genes not only result in the dysregulation of physiological rhythms but also induce metabolic disorders including diabetes and obesity. Among the clock genes, ( / / ), ( / ), and ( / ) have been shown to be particularly relevant to the regulation of energy metabolism at the cellular, tissue, and organismal levels. This paper reviews our current knowledge of the roles of , , and in coordinating the circadian and metabolic pathways.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Process

  10 / 10158 MEDLINE  
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[PMID]: 29517982
[Au] Autor:Mittelstraß K; Waldenberger M
[Ti] Title:DNA methylation in human lipid metabolism and related diseases.
[So] Source:Curr Opin Lipidol;29(2):116-124, 2018 Apr.
[Is] ISSN:1473-6535
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:PURPOSE OF REVIEW: It is becoming increasingly evident that epigenetic mechanisms, particularly DNA methylation, play a role in the regulation of blood lipid levels and lipid metabolism-linked phenotypes and diseases. RECENT FINDINGS: Recent genome-wide methylation and candidate gene studies of blood lipids have highlighted several robustly replicated methylation markers across different ethnicities. Furthermore, many of these lipid-related CpG sites associated with blood lipids are also linked to lipid-related phenotypes and diseases. Integrating epigenome-wide association studies (EWAS) data with other layers of molecular data such as genetics or the transcriptome, accompanied by relevant statistical methods (e.g. Mendelian randomization), provides evidence for causal relationships. Recent data suggest that epigenetic changes can be consequences rather than causes of dyslipidemia. There is sparse information on many lipid classes and disorders of lipid metabolism, and also on the interplay of DNA methylation with other epigenetic layers such as histone modifications and regulatory RNAs. SUMMARY: The current review provides a literature overview of epigenetic modifications in lipid metabolism and other lipid-related phenotypes and diseases focusing on EWAS of DNA methylation from January 2016 to September 2017. Recent studies strongly support the importance of epigenetic modifications, such as DNA methylation, in lipid metabolism and related diseases for relevant biological insights, reliable biomarkers, and even future therapeutics.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1097/MOL.0000000000000491


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