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Molecular metabolism 8건

  1. [해외논문]   Editorial Board, cover figure description and credits  


    Molecular metabolism v.5 no.5 ,pp. IFC , 2016 ,

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  2. [해외논문]   Editorial Board, cover figure description and credits   SCIE SCOPUS


    Molecular metabolism v.5 no.5 ,pp. IFC - IFC , 2016 ,

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  3. [해외논문]   A healthy gastrointestinal microbiome is dependent on dietary diversity   SCIE

    Heiman, Mark L. (MicroBiome Therapeutics, 1316 Jefferson Avenue, New Orleans, LA 70115, USA ) , Greenway, Frank L. (Pennington Biomedical Research Center, Louisiana State University System, 6400 Perkins Road, Baton Rouge, LA 70808, USA)
    Molecular metabolism v.5 no.5 ,pp. 317 - 320 , 2016 ,

    초록

    Background Like all healthy ecosystems, richness of microbiota species characterizes the GI microbiome in healthy individuals. Conversely, a loss in species diversity is a common finding in several disease states. This biome is flooded with energy in the form of undigested and partially digested foods, and in some cases drugs and dietary supplements. Each microbiotic species in the biome transforms that energy into new molecules, which may signal messages to physiological systems of the host. Scope of review Dietary choices select substrates for species, providing a competitive advantage over other GI microbiota. The more diverse the diet, the more diverse the microbiome and the more adaptable it will be to perturbations. Unfortunately, dietary diversity has been lost during the past 50 years and dietary choices that exclude food products from animals or plants will narrow the GI microbiome further. Major conclusion Additional research into expanding gut microbial richness by dietary diversity is likely to expand concepts in healthy nutrition, stimulate discovery of new diagnostics, and open up novel therapeutic possibilities.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  4. [해외논문]   High density lipoprotein and metabolic disease: Potential benefits of restoring its functional properties   SCIE

    Klancic, Teja (Institute for Diabetes and Regeneration Research, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Neuherberg, Germany ) , Woodward, Lavinia (University of Oxford, Oxford, United Kingdom ) , Hofmann, Susanna M. (Institute for Diabetes and Regeneration Research, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Neuherberg, Germany ) , Fisher, Edward A. (Department of Medicine and Division of Cardiology, New York University School of Medicine, New York, NY 10016, USA)
    Molecular metabolism v.5 no.5 ,pp. 321 - 327 , 2016 ,

    초록

    Background High density lipoproteins (HDLs) are thought to be atheroprotective and to reduce the risk of cardiovascular disease (CVD). Besides their antioxidant, antithrombotic, anti-inflammatory, anti-apoptotic properties in the vasculature, HDLs also improve glucose metabolism in skeletal muscle. Scope of the review Herein, we review the functional role of HDLs to improve metabolic disorders, especially those involving insulin resistance and to induce regression of CVD with a particular focus on current pharmacological treatment options as well as lifestyle interventions, particularly exercise. Major conclusions Functional properties of HDLs continue to be considered important mediators to reverse metabolic dysfunction and to regress atherosclerotic cardiovascular disease. Lifestyle changes are often recommended to reduce the risk of CVD, with exercise being one of the most important of these. Understanding how exercise improves HDL function will likely lead to new approaches to battle the expanding burden of obesity and the metabolic syndrome.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  5. [해외논문]   Obesogenic memory can confer long-term increases in adipose tissue but not liver inflammation and insulin resistance after weight loss  

    Schmitz, J. (Max Planck Institute for Metabolism Research, Cologne, Germany ) , Evers, N. (Max Planck Institute for Metabolism Research, Cologne, Germany ) , Awazawa, M. (Max Planck Institute for Metabolism Research, Cologne, Germany ) , Nicholls, H.T. (Max Planck Institute for Metabolism Research, Cologne, Germany ) , Brö (Max Planck Institute for Metabolism Research, Cologne, Germany ) , nneke, H.S. (Department of Surgery, University of Leipzig, Leipzig, Germany ) , Dietrich, A. (Max Planck Institute for Metabolism Research, Cologne, Germany ) , Mauer, J. (Department of Medicine, University of Leipzig, Leipzig, Germany ) , Blü (Max Planck Institute for Metabolism Research, Cologne, Germany) , her, M. , Brü , ning, J.C.
    Molecular metabolism v.5 no.5 ,pp. 328 - 339 , 2016 ,

    초록

    Objective Obesity represents a major risk factor for the development of type 2 diabetes mellitus, atherosclerosis and certain cancer entities. Treatment of obesity is hindered by the long-term maintenance of initially reduced body weight, and it remains unclear whether all pathologies associated with obesity are fully reversible even upon successfully maintained weight loss. Methods We compared high fat diet-fed, weight reduced and lean mice in terms of body weight development, adipose tissue and liver insulin sensitivity as well as inflammatory gene expression. Moreover, we assessed similar parameters in a human cohort before and after bariatric surgery. Results Compared to lean animals, mice that demonstrated successful weight reduction showed increased weight gain following exposure to ad libitum control diet. However, pair-feeding weight-reduced mice with lean controls efficiently stabilized body weight, indicating that hyperphagia was the predominant cause for the observed weight regain. Additionally, whereas glucose tolerance improved rapidly after weight loss, systemic insulin resistance was retained and ameliorated only upon prolonged pair-feeding. Weight loss enhanced insulin action and resolved pro-inflammatory gene expression exclusively in the liver, whereas visceral adipose tissue displayed no significant improvement of metabolic and inflammatory parameters compared to obese mice. Similarly, bariatric surgery in humans (n = 55) resulted in massive weight reduction, improved hepatic inflammation and systemic glucose homeostasis, while adipose tissue inflammation remained unaffected and adipocyte-autonomous insulin action only exhibit minor improvements in a subgroup of patients (42%). Conclusions These results demonstrate that although sustained weight loss improves systemic glucose homeostasis, primarily through improved inflammation and insulin action in liver, a remarkable obesogenic memory can confer long-term increases in adipose tissue inflammation and insulin resistance in mice as well as in a significant subpopulation of obese patients. Highlights • Upon weight loss in mice liver insulin sensitivity rapidly improves. • Upon weight loss in mice fat retains metabolic inflammation and insulin resistance. • Weight gain upon successful weight reduction in mice is driven by increased food intake. • A proportion of human subjects undergoing bariatric surgery retain AT-inflammation.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  6. [해외논문]   Thioesterase superfamily member 1 suppresses cold thermogenesis by limiting the oxidation of lipid droplet-derived fatty acids in brown adipose tissue   SCIE

    Okada, Kosuke (Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA ) , LeClair, Katherine B. (Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA ) , Zhang, Yongzhao (Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA ) , Li, Yingxia (Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA ) , Ozdemir, Cafer (Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA ) , Krisko, Tibor I. (Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA ) , Hagen, Susan J. (Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA ) , Betensky, Rebecca A. (Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, USA ) , Banks, Alexander S. (Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA ) , Cohen, David E. (Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA)
    Molecular metabolism v.5 no.5 ,pp. 340 - 351 , 2016 ,

    초록

    Objective Non-shivering thermogenesis in brown adipose tissue (BAT) plays a central role in energy homeostasis. Thioesterase superfamily member 1 (Them1), a BAT-enriched long chain fatty acyl-CoA thioesterase, is upregulated by cold and downregulated by warm ambient temperatures. Them1 −/− mice exhibit increased energy expenditure and resistance to diet-induced obesity and diabetes, but the mechanistic contribution of Them1 to the regulation of cold thermogenesis remains unknown. Methods Them1 −/− and Them1 +/+ mice were subjected to continuous metabolic monitoring to quantify the effects of ambient temperatures ranging from thermoneutrality (30 °C) to cold (4 °C) on energy expenditure, core body temperature, physical activity and food intake. The effects of Them1 expression on O 2 consumption rates, thermogenic gene expression and lipolytic protein activation were determined ex vivo in BAT and in primary brown adipocytes. Results Them1 suppressed thermogenesis in mice even in the setting of ongoing cold exposure. Without affecting thermogenic gene transcription, Them1 reduced O 2 consumption rates in both isolated BAT and primary brown adipocytes. This was attributable to decreased mitochondrial oxidation of endogenous but not exogenous fatty acids. Conclusions These results show that Them1 may act as a break on uncontrolled heat production and limit the extent of energy expenditure. Pharmacologic inhibition of Them1 could provide a targeted strategy for the management of metabolic disorders via activation of brown fat. Highlights • Them1 is a fatty acyl-CoA thioesterase that is highly expressed in brown adipose tissue. • Them1 expression is strongly upregulated by cold ambient temperatures. • Mice lacking Them1 exhibit increased cold thermogenesis. • Them1 limits the mitochondrial oxidation of lipid-droplet derived fatty acids.

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  7. [해외논문]   White-to-brite conversion in human adipocytes promotes metabolic reprogramming towards fatty acid anabolic and catabolic pathways   SCIE

    Barquissau, V. (INSERM, UMR 1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France ) , Beuzelin, D. (INSERM, UMR 1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France ) , Pisani, D.F. (University of Nice Sophia Antipolis, Nice, France ) , Beranger, G.E. (University of Nice Sophia Antipolis, Nice, France ) , Mairal, A. (INSERM, UMR 1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France ) , Montagner, A. (University of Toulouse, Paul Sabatier University, France ) , Roussel, B. (INSERM, UMR 1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France ) , Tavernier, G. (INSERM, UMR 1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France ) , Marques, M.-A. (INSERM, UMR 1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France ) , Moro, C. (INSERM, UMR 1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France ) , Guillou, H. (University of Toulouse, Paul Sabatier University, France ) , Amri, E.-Z. (University of Nice Sophia Antipolis, Nice, France ) , Langin, D. (INSERM, UMR 1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France)
    Molecular metabolism v.5 no.5 ,pp. 352 - 365 , 2016 ,

    초록

    Objective Fat depots with thermogenic activity have been identified in humans. In mice, the appearance of thermogenic adipocytes within white adipose depots (so-called brown-in-white i.e. , brite or beige adipocytes) protects from obesity and insulin resistance. Brite adipocytes may originate from direct conversion of white adipocytes. The purpose of this work was to characterize the metabolism of human brite adipocytes. Methods Human multipotent adipose-derived stem cells were differentiated into white adipocytes and then treated with peroxisome proliferator-activated receptor (PPAR)γ or PPARα agonists between day 14 and day 18. Gene expression profiling was determined using DNA microarrays and RT-qPCR. Variations of mRNA levels were confirmed in differentiated human preadipocytes from primary cultures. Fatty acid and glucose metabolism was investigated using radiolabelled tracers, Western blot analyses and assessment of oxygen consumption. Pyruvate dehydrogenase kinase 4 (PDK4) knockdown was achieved using siRNA. In vivo , wild type and PPARα-null mice were treated with a β 3 -adrenergic receptor agonist (CL316,243) to induce appearance of brite adipocytes in white fat depot. Determination of mRNA and protein levels was performed on inguinal white adipose tissue. Results PPAR agonists promote a conversion of white adipocytes into cells displaying a brite molecular pattern. This conversion is associated with transcriptional changes leading to major metabolic adaptations. Fatty acid anabolism i.e., fatty acid esterification into triglycerides, and catabolism i.e. , lipolysis and fatty acid oxidation, are increased. Glucose utilization is redirected from oxidation towards glycerol-3-phophate production for triglyceride synthesis. This metabolic shift is dependent on the activation of PDK4 through inactivation of the pyruvate dehydrogenase complex. In vivo , PDK4 expression is markedly induced in wild-type mice in response to CL316,243, while this increase is blunted in PPARα-null mice displaying an impaired britening response. Conclusions Conversion of human white fat cells into brite adipocytes results in a major metabolic reprogramming inducing fatty acid anabolic and catabolic pathways. PDK4 redirects glucose from oxidation towards triglyceride synthesis and favors the use of fatty acids as energy source for uncoupling mitochondria. Highlights • PPARγ and α agonists induce conversion of human white into brite adipocytes. • Fatty acid anabolism and catabolism are activated in human brite adipocytes. • Glucose use in brite adipocytes is redirected from oxidation to glyceroneogenesis. • PDK4 induction is responsible for the shift from glucose to fatty acid oxidation.

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  8. [해외논문]   Inter-domain tagging implicates caveolin-1 in insulin receptor trafficking and Erk signaling bias in pancreatic beta-cells   SCIE SCOPUS

    Boothe, Tobias (Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, BC, Canada ) , Lim, Gareth E. (Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, BC, Canada ) , Cen, Haoning (Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, BC, Canada ) , Skovsø, Søs (Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, BC, Canada ) , Piske, Micah (Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, BC, Canada ) , Li, Shu Nan (Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, BC, Canada ) , Nabi, Ivan R. (Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, BC, Canada ) , Gilon, Patrick (Pôle d'endocrinologie, diabète et nutrition, Institut de recherche expérimentale et clinique, Université) , Johnson, James D. (catholique de Louvain, Brussels, Belgium )
    Molecular metabolism v.5 no.5 ,pp. 366 - 378 , 2016 ,

    초록

    Abstract Objective The role and mechanisms of insulin receptor internalization remain incompletely understood. Previous trafficking studies of insulin receptors involved fluorescent protein tagging at their termini, manipulations that may be expected to result in dysfunctional receptors. Our objective was to determine the trafficking route and molecular mechanisms of functional tagged insulin receptors and endogenous insulin receptors in pancreatic beta-cells. Methods We generated functional insulin receptors tagged with pH-resistant fluorescent proteins between domains. Confocal, TIRF and STED imaging revealed a trafficking pattern of inter-domain tagged insulin receptors and endogenous insulin receptors detected with antibodies. Results Surprisingly, interdomain-tagged and endogenous insulin receptors in beta-cells bypassed classical Rab5a- or Rab7-mediated endocytic routes. Instead, we found that removal of insulin receptors from the plasma membrane involved tyrosine-phosphorylated caveolin-1, prior to trafficking within flotillin-1-positive structures to lysosomes. Multiple methods of inhibiting caveolin-1 significantly reduced Erk activation in vitro or in vivo , while leaving Akt signaling mostly intact. Conclusions We conclude that phosphorylated caveolin-1 plays a role in insulin receptor internalization towards lysosomes through flotillin-1-positive structures and that caveolin-1 helps bias physiological beta-cell insulin signaling towards Erk activation. Highlights Insulin receptors are tagged between domains to maintain the functionality and endogenous intracellular trafficking patterns. Insulin receptors have virtually no co-localization with classical endocytosis markers, but co-localize with Cav11. Insulin receptor internalization and anti-apoptotic Erk signaling are modulated by phosphorylated Cav1.

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