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Cell Metabolism

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https://www.readbyqxmd.com/read/28712655/insulin-regulation-of-proteostasis-and-clinical-implications
#1
REVIEW
Haleigh A James, Brian T O'Neill, K Sreekumaran Nair
Maintenance and modification of the cellular proteome are at the core of normal cellular physiology. Although insulin is well known for its control of glucose homeostasis, its critical role in maintaining proteome homeostasis (proteostasis) is less appreciated. Insulin signaling regulates protein synthesis and degradation as well as posttranslational modifications at the tissue level and coordinates proteostasis at the organism level. Here, we review regulation of proteostasis by insulin in postabsorptive, postprandial, and diabetic states...
July 10, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683298/metabolic-regulation-of-t-cell-longevity-and-function-in-tumor-immunotherapy
#2
REVIEW
Rigel J Kishton, Madhusudhanan Sukumar, Nicholas P Restifo
Cancer immunotherapy is an increasingly successful strategy for the treatment of patients who have advanced or conventional therapy-resistant cancers. T cells are key mediators of tumor destruction and their specificity for tumor-expressed antigens is of paramount importance, but other T cell-intrinsic qualities, such as durability, longevity, and functionality also play important roles in determining the efficacy of immunotherapy. The cellular energetic pathways that are utilized by T cells play a key role in regulating each of these qualities...
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683297/fighting-fire-with-fiber-preventing-t-cell-infiltration-in-diabetes
#3
Sydney Lavoie, Wendy S Garrett
Diet can alter the gut microbiota and shift its production of metabolites, which affect systemic immune function. In Nature Immunology, Mariño et al. (2017) explore diet-gut microbiome interactions in type 1 diabetes and identify mechanisms by which short-chain fatty acids prevent T cell destruction of pancreatic β-cells.
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683296/inflammasomes-on-the-crossroads-of-innate-immune-recognition-and-metabolic-control
#4
REVIEW
Tomasz Próchnicki, Eicke Latz
Inflammasomes are protein complexes formed upon encounter of microbial or damage-associated stimuli. The main output of inflammasome assembly is activation of caspase-1, a protease involved in both pro-inflammatory and host-protective responses. Defined bacterial or viral ligands have been identified for the inflammasome-forming receptors AIM2, NLRP1, and NLRC4. The signals activating other inflammasomes, NLRP3, NLRP6, and pyrin, are less well understood. Recent studies implicated several low-molecular-weight compounds traditionally linked to metabolism, not immunity, in modulation of inflammasome signaling...
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683295/will-gut-microbiota-help-design-the-next-generation-of-glp-1-based-therapies-for-type-2-diabetes
#5
Sandrine Paule Claus
Glucagon-like peptide one (GLP-1)-based therapies for reducing hyperglycemia in type 2 diabetic patients are efficient, though some individuals develop GLP-1 resistance. In a recent issue of Cell Metabolism, Grasset et al. (2017) demonstrated that GLP-1 sensitivity is modulated by gut bacteria through NO signaling in the enteric nervous system.
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683294/similarities-and-distinctions-of-cancer-and-immune-metabolism-in-inflammation-and-tumors
#6
REVIEW
Gabriela Andrejeva, Jeffrey C Rathmell
It has been appreciated for nearly 100 years that cancer cells are metabolically distinct from resting tissues. More recently understood is that this metabolic phenotype is not unique to cancer cells but instead reflects characteristics of proliferating cells. Similar metabolic transitions also occur in the immune system as cells transition from resting state to stimulated effectors. A key finding in immune metabolism is that the metabolic programs of different cell subsets are distinctly associated with immunological function...
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683293/a-specific-gut-microbiota-dysbiosis-of-type-2-diabetic-mice-induces-glp-1-resistance-through-an-enteric-no-dependent-and-gut-brain-axis-mechanism
#7
Estelle Grasset, Anthony Puel, Julie Charpentier, Xavier Collet, Jeffrey E Christensen, François Tercé, Rémy Burcelin
No abstract text is available yet for this article.
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683292/mice-under-caloric-restriction-self-impose-a-temporal-restriction-of-food-intake-as-revealed-by-an-automated-feeder-system
#8
Victoria A Acosta-Rodríguez, Marleen H M de Groot, Filipa Rijo-Ferreira, Carla B Green, Joseph S Takahashi
Caloric restriction (CR) extends lifespan in mammals, yet the mechanisms underlying its beneficial effects remain unknown. The manner in which CR has been implemented in longevity experiments is variable, with both timing and frequency of meals constrained by work schedules. It is commonplace to find that nocturnal rodents are fed during the daytime and meals are spaced out, introducing prolonged fasting intervals. Since implementation of feeding paradigms over the lifetime is logistically difficult, automation is critical, but existing systems are expensive and not amenable to scale...
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683291/lack-of-glycogenin-causes-glycogen-accumulation-and-muscle-function-impairment
#9
Giorgia Testoni, Jordi Duran, Mar García-Rocha, Francisco Vilaplana, Antonio L Serrano, David Sebastián, Iliana López-Soldado, Mitchell A Sullivan, Felipe Slebe, Marta Vilaseca, Pura Muñoz-Cánoves, Joan J Guinovart
Glycogenin is considered essential for glycogen synthesis, as it acts as a primer for the initiation of the polysaccharide chain. Against expectations, glycogenin-deficient mice (Gyg KO) accumulate high amounts of glycogen in striated muscle. Furthermore, this glycogen contains no covalently bound protein, thereby demonstrating that a protein primer is not strictly necessary for the synthesis of the polysaccharide in vivo. Strikingly, in spite of the higher glycogen content, Gyg KO mice showed lower resting energy expenditure and less resistance than control animals when subjected to endurance exercise...
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683290/cry1-2-selectively-repress-ppar%C3%AE-and-limit-exercise-capacity
#10
Sabine D Jordan, Anna Kriebs, Megan Vaughan, Drew Duglan, Weiwei Fan, Emma Henriksson, Anne-Laure Huber, Stephanie J Papp, Madelena Nguyen, Megan Afetian, Michael Downes, Ruth T Yu, Anastasia Kralli, Ronald M Evans, Katja A Lamia
Cellular metabolite balance and mitochondrial function are under circadian control, but the pathways connecting the molecular clock to these functions are unclear. Peroxisome proliferator-activated receptor delta (PPARδ) enables preferential utilization of lipids as fuel during exercise and is a major driver of exercise endurance. We show here that the circadian repressors CRY1 and CRY2 function as co-repressors for PPARδ. Cry1(-/-);Cry2(-/-) myotubes and muscles exhibit elevated expression of PPARδ target genes, particularly in the context of exercise...
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683289/modulation-of-autophagy-by-bdnf-underlies-synaptic-plasticity
#11
Vassiliki Nikoletopoulou, Kyriaki Sidiropoulou, Emmanouela Kallergi, Yannis Dalezios, Nektarios Tavernarakis
Autophagy is crucial for neuronal integrity. Loss of key autophagic components leads to progressive neurodegeneration and structural defects in pre- and postsynaptic morphologies. However, the molecular mechanisms regulating autophagy in the brain remain elusive. Similarly, while it is widely accepted that protein turnover is required for synaptic plasticity, the contribution of autophagy to the degradation of synaptic proteins is unknown. Here, we report that BDNF signaling via the tropomyosin receptor kinase B (TrkB) and the phosphatidylinositol-3' kinase (PI3K)/Akt pathway suppresses autophagy in vivo...
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683288/hypothalamic-ampk-er-stress-jnk1-axis-mediates-the-central-actions-of-thyroid-hormones-on-energy-balance
#12
Noelia Martínez-Sánchez, Patricia Seoane-Collazo, Cristina Contreras, Luis Varela, Joan Villarroya, Eva Rial-Pensado, Xabier Buqué, Igor Aurrekoetxea, Teresa C Delgado, Rafael Vázquez-Martínez, Ismael González-García, Juan Roa, Andrew J Whittle, Beatriz Gomez-Santos, Vidya Velagapudi, Y C Loraine Tung, Donald A Morgan, Peter J Voshol, Pablo B Martínez de Morentin, Tania López-González, Laura Liñares-Pose, Francisco Gonzalez, Krishna Chatterjee, Tomás Sobrino, Gema Medina-Gómez, Roger J Davis, Núria Casals, Matej Orešič, Anthony P Coll, Antonio Vidal-Puig, Jens Mittag, Manuel Tena-Sempere, María M Malagón, Carlos Diéguez, María Luz Martínez-Chantar, Patricia Aspichueta, Kamal Rahmouni, Rubén Nogueiras, Guadalupe Sabio, Francesc Villarroya, Miguel López
Thyroid hormones (THs) act in the brain to modulate energy balance. We show that central triiodothyronine (T3) regulates de novo lipogenesis in liver and lipid oxidation in brown adipose tissue (BAT) through the parasympathetic (PSNS) and sympathetic nervous system (SNS), respectively. Central T3 promotes hepatic lipogenesis with parallel stimulation of the thermogenic program in BAT. The action of T3 depends on AMP-activated protein kinase (AMPK)-induced regulation of two signaling pathways in the ventromedial nucleus of the hypothalamus (VMH): decreased ceramide-induced endoplasmic reticulum (ER) stress, which promotes BAT thermogenesis, and increased c-Jun N-terminal kinase (JNK) activation, which controls hepatic lipid metabolism...
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683287/the-sense-of-smell-impacts-metabolic-health-and-obesity
#13
Celine E Riera, Eva Tsaousidou, Jonathan Halloran, Patricia Follett, Oliver Hahn, Mafalda M A Pereira, Linda Engström Ruud, Jens Alber, Kevin Tharp, Courtney M Anderson, Hella Brönneke, Brigitte Hampel, Carlos Daniel de Magalhaes Filho, Andreas Stahl, Jens C Brüning, Andrew Dillin
Olfactory inputs help coordinate food appreciation and selection, but their role in systemic physiology and energy balance is poorly understood. Here we demonstrate that mice upon conditional ablation of mature olfactory sensory neurons (OSNs) are resistant to diet-induced obesity accompanied by increased thermogenesis in brown and inguinal fat depots. Acute loss of smell perception after obesity onset not only abrogated further weight gain but also improved fat mass and insulin resistance. Reduced olfactory input stimulates sympathetic nerve activity, resulting in activation of β-adrenergic receptors on white and brown adipocytes to promote lipolysis...
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683286/microglial-inflammatory-signaling-orchestrates-the-hypothalamic-immune-response-to-dietary-excess-and-mediates-obesity-susceptibility
#14
Martin Valdearcos, John D Douglass, Megan M Robblee, Mauricio D Dorfman, Daniel R Stifler, Mariko L Bennett, Irene Gerritse, Rachael Fasnacht, Ben A Barres, Joshua P Thaler, Suneil K Koliwad
Dietary excess triggers accumulation of pro-inflammatory microglia in the mediobasal hypothalamus (MBH), but the components of this microgliosis and its metabolic consequences remain uncertain. Here, we show that microglial inflammatory signaling determines the immunologic response of the MBH to dietary excess and regulates hypothalamic control of energy homeostasis in mice. Either pharmacologically depleting microglia or selectively restraining microglial NF-κB-dependent signaling sharply reduced microgliosis, an effect that includes prevention of MBH entry by bone-marrow-derived myeloid cells, and greatly limited diet-induced hyperphagia and weight gain...
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683285/il-6-stat3-dependent-induction-of-a-distinct-obesity-associated-nk-cell-subpopulation-deteriorates-energy-and-glucose-homeostasis
#15
Sebastian Theurich, Eva Tsaousidou, Ruth Hanssen, Adelheid M Lempradl, Jan Mauer, Katharina Timper, Katharina Schilbach, Kat Folz-Donahue, Christian Heilinger, Veronika Sexl, John Andrew Pospisilik, F Thomas Wunderlich, Jens C Brüning
Natural killer (NK) cells contribute to the development of obesity-associated insulin resistance. We demonstrate that in mice obesity promotes expansion of a distinct, interleukin-6 receptor (IL6R)a-expressing NK subpopulation, which also expresses a number of other myeloid lineage genes such as the colony-stimulating factor 1 receptor (Csf1r). Selective ablation of this Csf1r-expressing NK cell population prevents obesity and insulin resistance. Moreover, conditional inactivation of IL6Ra or Stat3 in NK cells limits obesity-associated formation of these myeloid signature NK cells, protecting from obesity, insulin resistance, and obesity-associated inflammation...
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683284/is-type-2-diabetes-a-glycogen-storage-disease-of-pancreatic-%C3%AE-cells
#16
REVIEW
Frances M Ashcroft, Maria Rohm, Anne Clark, Melissa F Brereton
Elevated plasma glucose leads to pancreatic β cell dysfunction and death in type 2 diabetes. Glycogen accumulation, due to impaired metabolism, contributes to this "glucotoxicity" via dysregulated biochemical pathways promoting β cell dysfunction. Here, we review emerging data, and re-examine published findings, on the role of glycogen in β cells in normoglycemia and in diabetes.
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683283/inhibition-of-ikk%C3%A9-and-tbk1-improves-glucose-control-in-a-subset-of-patients-with-type-2-diabetes
#17
Elif A Oral, Shannon M Reilly, Andrew V Gomez, Rasimcan Meral, Laura Butz, Nevin Ajluni, Thomas L Chenevert, Evgenia Korytnaya, Adam H Neidert, Rita Hench, Diana Rus, Jeffrey F Horowitz, BreAnne Poirier, Peng Zhao, Kim Lehmann, Mohit Jain, Ruth Yu, Christopher Liddle, Maryam Ahmadian, Michael Downes, Ronald M Evans, Alan R Saltiel
Numerous studies indicate an inflammatory link between obesity and type 2 diabetes. The inflammatory kinases IKKɛ and TBK1 are elevated in obesity; their inhibition in obese mice reduces weight, insulin resistance, fatty liver and inflammation. Here we studied amlexanox, an inhibitor of IKKɛ and TBK1, in a proof-of-concept randomized, double-blind, placebo-controlled study of 42 obese patients with type 2 diabetes and nonalcoholic fatty liver disease. Treatment of patients with amlexanox produced a statistically significant reduction in Hemoglobin A1c and fructosamine...
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683282/specific-and-complex-reprogramming-of-cellular-metabolism-in-myeloid-cells-during-innate-immune-responses
#18
REVIEW
Rinke Stienstra, Romana T Netea-Maier, Niels P Riksen, Leo A B Joosten, Mihai G Netea
Renewed interest in immune cell metabolism has led to the emergence of a research field aimed at studying the importance of metabolic processes for an effective immune response. In addition to the adaptive immune system, cells of the myeloid lineage have been shown to undergo robust metabolic changes upon activation. Whereas the specific metabolic requirements of myeloid cells after lipopolysaccharide/TLR4 stimulation have been extensively studied, recent evidence suggested that this model does not represent a metabolic blueprint for activated myeloid cells...
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683281/how-does-fat-transition-from-white-to-beige
#19
Marc L Reitman
Fischer et al. (2017) recently reported that interleukin-4 (IL-4) does not increase adipose thermogenesis and that activated macrophages do not synthesize catecholamines. These findings are unexpected because IL-4 activation of macrophages has been proposed to have a pivotal role in cold-induced thermogenesis by stimulating macrophage catecholamine production to recruit thermogenic beige or brite fat.
July 5, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28683280/ancillary-activity-beyond-core-metabolism-in-immune-cells
#20
REVIEW
Daniel J Puleston, Matteo Villa, Erika L Pearce
Immune cell function and fate are intimately linked to engagement of metabolic pathways. The contribution of core metabolic pathways to immune cell bioenergetics has been vigorously investigated in recent years. However, precisely how other peripheral metabolic pathways support immune cells beyond energy generation is less well understood. Here we survey the literature and highlight recent advances in our understanding of several ancillary metabolic pathways and how they support processes beyond ATP production and ultimately contribute to protective immunity...
July 5, 2017: Cell Metabolism
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