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Cell Metabolism

Giorgia Benegiamo, Ludovic S Mure, Galina Erikson, Hiep D Le, Ermanno Moriggi, Steven A Brown, Satchidananda Panda
The mechanisms by which feeding and fasting drive rhythmic gene expression for physiological adaptation to daily rhythm in nutrient availability are not well understood. Here we show that, upon feeding, the RNA-binding protein NONO accumulates within speckle-like structures in liver cell nuclei. Combining RNA-immunoprecipitation and sequencing (RIP-seq), we find that an increased number of RNAs are bound by NONO after feeding. We further show that NONO binds and regulates the rhythmicity of genes involved in nutrient metabolism post-transcriptionally...
January 17, 2018: Cell Metabolism
Shuai Jiang, Wei Yan, Shizhen Emily Wang, David Baltimore
The control of uptake and utilization of necessary extracellular nutrients-glucose and glutamine-is an important aspect of B cell activation. Let-7 is a family of microRNAs known to be involved in metabolic control. Here, we employed several engineered mouse models, including B cell-specific overexpression of Lin28a or the let-7a-1/let-7d/let-7f-1 cluster (let-7adf) and knockout of individual let-7 clusters to show that let-7adf specifically inhibits T cell-independent (TI) antigen-induced immunoglobulin (Ig)M antibody production...
January 10, 2018: Cell Metabolism
Thomas G McWilliams, Alan R Prescott, Lambert Montava-Garriga, Graeme Ball, François Singh, Erica Barini, Miratul M K Muqit, Simon P Brooks, Ian G Ganley
Dysregulated mitophagy has been linked to Parkinson's disease (PD) due to the role of PTEN-induced kinase 1 (PINK1) in mediating depolarization-induced mitophagy in vitro. Elegant mouse reporters have revealed the pervasive nature of basal mitophagy in vivo, yet the role of PINK1 and tissue metabolic context remains unknown. Using mito-QC, we investigated the contribution of PINK1 to mitophagy in metabolically active tissues. We observed a high degree of mitophagy in neural cells, including PD-relevant mesencephalic dopaminergic neurons and microglia...
January 10, 2018: Cell Metabolism
Natalya N Pavlova, Sheng Hui, Jonathan M Ghergurovich, Jing Fan, Andrew M Intlekofer, Richard M White, Joshua D Rabinowitz, Craig B Thompson, Ji Zhang
When mammalian cells are deprived of glutamine, exogenous asparagine rescues cell survival and growth. Here we report that this rescue results from use of asparagine in protein synthesis. All mammalian cell lines tested lacked cytosolic asparaginase activity and could not utilize asparagine to produce other amino acids or biosynthetic intermediates. Instead, most glutamine-deprived cell lines are capable of sufficient glutamine synthesis to maintain essential amino acid uptake and production of glutamine-dependent biosynthetic precursors, with the exception of asparagine...
January 10, 2018: Cell Metabolism
Amin Ardestani, Blaz Lupse, Yoshiaki Kido, Gil Leibowitz, Kathrin Maedler
The mechanistic target of rapamycin complex 1 (mTORC1) is a central regulator of metabolic and nutrient cues that integrates environmental inputs into downstream signaling pathways to control cellular metabolism, growth, and survival. While numerous in vitro and in vivo studies reported the positive functions of mTORC1 in the regulation of β cell survival and proliferation under physiological conditions, more recent work demonstrates the opposite in the long term; this is exemplified by the constitutive inappropriate hyper-activation of mTORC1 in diabetic islets or β cells under conditions of increased β cell stress and metabolic demands...
December 20, 2017: Cell Metabolism
John R Ussher, Jonathan E Campbell, Erin E Mulvihill, Laurie L Baggio, Holly E Bates, Brent A McLean, Keshav Gopal, Megan Capozzi, Bernardo Yusta, Xiemin Cao, Safina Ali, Minsuk Kim, M Golam Kabir, Yutaka Seino, Jinya Suzuki, Daniel J Drucker
Incretin hormones exert pleiotropic metabolic actions beyond the pancreas. Although the heart expresses both incretin receptors, the cardiac biology of GIP receptor (GIPR) action remains incompletely understood. Here we show that GIPR agonism did not impair the response to cardiac ischemia. In contrast, genetic elimination of the Gipr reduced myocardial infarction (MI)-induced ventricular injury and enhanced survival associated with reduced hormone sensitive lipase (HSL) phosphorylation; it also increased myocardial triacylglycerol (TAG) stores...
December 20, 2017: Cell Metabolism
Jun Yoshino, Joseph A Baur, Shin-Ichiro Imai
Research on the biology of NAD+has been gaining momentum, providing many critical insights into the pathogenesis of age-associated functional decline and diseases. In particular, two key NAD+intermediates, nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN), have been extensively studied over the past several years. Supplementing these NAD+intermediates has shown preventive and therapeutic effects, ameliorating age-associated pathophysiologies and disease conditions. Although the pharmacokinetics and metabolic fates of NMN and NR are still under intensive investigation, these NAD+intermediates can exhibit distinct behavior, and their fates appear to depend on the tissue distribution and expression levels of NAD+biosynthetic enzymes, nucleotidases, and presumptive transporters for each...
December 14, 2017: Cell Metabolism
Xuecai Ge, Hong Yang, Maria A Bednarek, Hadas Galon-Tilleman, Peirong Chen, Michael Chen, Joshua S Lichtman, Yan Wang, Olivier Dalmas, Yiyuan Yin, Hui Tian, Lutz Jermutus, Joseph Grimsby, Cristina M Rondinone, Anish Konkar, Daniel D Kaplan
Ghrelin, an appetite-stimulatory hormone secreted by the stomach, was discovered as a ligand for the growth hormone secretagogue receptor (GHSR). Through GHSR, ghrelin stimulates growth hormone (GH) secretion, a function that evolved to protect against starvation-induced hypoglycemia. Though the biology mediated by ghrelin has been described in great detail, regulation of ghrelin action is poorly understood. Here, we report the discovery of liver-expressed antimicrobial peptide 2 (LEAP2) as an endogenous antagonist of GHSR...
December 6, 2017: Cell Metabolism
Xia-Di He, Wei Gong, Jia-Nong Zhang, Ji Nie, Cui-Fang Yao, Fu-Shen Guo, Yan Lin, Xiao-Hui Wu, Feng Li, Jie Li, Wei-Cheng Sun, En-Duo Wang, Yan-Peng An, Hui-Ru Tang, Guo-Quan Yan, Peng-Yuan Yang, Yun Wei, Yun-Zi Mao, Peng-Cheng Lin, Jian-Yuan Zhao, Yanhui Xu, Wei Xu, Shi-Min Zhao
Amino acids are known regulators of cellular signaling and physiology, but how they are sensed intracellularly is not fully understood. Herein, we report that each aminoacyl-tRNA synthetase (ARS) senses its cognate amino acid sufficiency through catalyzing the formation of lysine aminoacylation (K-AA) on its specific substrate proteins. At physiologic levels, amino acids promote ARSs bound to their substrates and form K-AAs on the ɛ-amine of lysines in their substrates by producing reactive aminoacyl adenylates...
November 27, 2017: Cell Metabolism
Stephen O'Rahilly
With the identification of its receptor in a highly specific region of the brain, interesting issues come to light regarding the normal physiological functions of GDF15, a secreted protein long identified as a biomarker of diverse disease states.
November 27, 2017: Cell Metabolism
Ronald W Alfa, Sangbin Park, Kathleen-Rose Skelly, Gregory Poffenberger, Nimit Jain, Xueying Gu, Lutz Kockel, Jing Wang, Yinghua Liu, Alvin C Powers, Seung K Kim
No abstract text is available yet for this article.
February 6, 2018: Cell Metabolism
Nikhil R Gandasi, Peng Yin, Muhmmad Omar-Hmeadi, Emilia Ottosson Laakso, Petter Vikman, Sebastian Barg
Glucose-stimulated insulin secretion is biphasic, with a rapid first phase and a slowly developing sustained second phase; both are disturbed in type 2 diabetes (T2D). Biphasic secretion results from vastly different release probabilities of individual insulin granules, but the morphological and molecular basis for this is unclear. Here, we show that human insulin secretion and exocytosis critically depend on the availability of membrane-docked granules and that T2D is associated with a strong reduction in granule docking...
February 6, 2018: Cell Metabolism
Ismail Syed, Jennifer Lee, Pedro M Moraes-Vieira, Cynthia J Donaldson, Alexandra Sontheimer, Pratik Aryal, Kerry Wellenstein, Matthew J Kolar, Andrew T Nelson, Dionicio Siegel, Jacek Mokrosinski, I Sadaf Farooqi, Juan Juan Zhao, Mark M Yore, Odile D Peroni, Alan Saghatelian, Barbara B Kahn
Palmitic acid hydroxystearic acids (PAHSAs) are endogenous lipids with anti-diabetic and anti-inflammatory effects. PAHSA levels are reduced in serum and adipose tissue of insulin-resistant people and high-fat diet (HFD)-fed mice. Here, we investigated whether chronic PAHSA treatment enhances insulin sensitivity and which receptors mediate PAHSA effects. Chronic PAHSA administration in chow- and HFD-fed mice raises serum and tissue PAHSA levels ∼1.4- to 3-fold. This improves insulin sensitivity and glucose tolerance without altering body weight...
February 6, 2018: Cell Metabolism
Leandro Z Agudelo, Duarte M S Ferreira, Igor Cervenka, Galyna Bryzgalova, Shamim Dadvar, Paulo R Jannig, Amanda T Pettersson-Klein, Tadepally Lakshmikanth, Elahu G Sustarsic, Margareta Porsmyr-Palmertz, Jorge C Correia, Manizheh Izadi, Vicente Martínez-Redondo, Per M Ueland, Øivind Midttun, Zachary Gerhart-Hines, Petter Brodin, Teresa Pereira, Per-Olof Berggren, Jorge L Ruas
The role of tryptophan-kynurenine metabolism in psychiatric disease is well established, but remains less explored in peripheral tissues. Exercise training activates kynurenine biotransformation in skeletal muscle, which protects from neuroinflammation and leads to peripheral kynurenic acid accumulation. Here we show that kynurenic acid increases energy utilization by activating G protein-coupled receptor Gpr35, which stimulates lipid metabolism, thermogenic, and anti-inflammatory gene expression in adipose tissue...
February 6, 2018: Cell Metabolism
Cholsoon Jang, Sheng Hui, Wenyun Lu, Alexis J Cowan, Raphael J Morscher, Gina Lee, Wei Liu, Gregory J Tesz, Morris J Birnbaum, Joshua D Rabinowitz
Excessive consumption of sweets is a risk factor for metabolic syndrome. A major chemical feature of sweets is fructose. Despite strong ties between fructose and disease, the metabolic fate of fructose in mammals remains incompletely understood. Here we use isotope tracing and mass spectrometry to track the fate of glucose and fructose carbons in vivo, finding that dietary fructose is cleared by the small intestine. Clearance requires the fructose-phosphorylating enzyme ketohexokinase. Low doses of fructose are ∼90% cleared by the intestine, with only trace fructose but extensive fructose-derived glucose, lactate, and glycerate found in the portal blood...
February 6, 2018: Cell Metabolism
Xinshou Ouyang, Sheng-Na Han, Ji-Yuan Zhang, Balazs Tamas Nemeth, Pal Pacher, Dechun Feng, Ramon Bataller, Joaquin Cabezas, Peter Stärkel, Joan Caballeria, Rebecca LePine Pongratz, Shi-Ying Cai, Bernd Schnabl, Rafaz Hoque, Yonglin Chen, Wei-Hong Yang, Irma Garcia Martinez, Fu-Sheng Wang, Bin Gao, Natalie Julia Torok, Richard Glenn Kibbey, Wajahat Zafar Mehal
Sterile inflammation after tissue damage is a ubiquitous response, yet it has the highest amplitude in the liver. This has major clinical consequences, for alcoholic and non-alcoholic steatohepatitis (ASH and NASH) account for the majority of liver disease in industrialized countries and both lack therapy. Requirements for sustained sterile inflammation include increased oxidative stress and activation of the HIF-1α signaling pathway. We demonstrate the ability of digoxin, a cardiac glycoside, to protect from liver inflammation and damage in ASH and NASH...
February 6, 2018: Cell Metabolism
Jin Zhang, Jing Zhao, Perrine Dahan, Vivian Lu, Cheng Zhang, Hu Li, Michael A Teitell
Emerging and seminal studies have shown that cell metabolism influences gene expression by modifying the epigenome, which can regulate stem cell pluripotency, differentiation, and somatic cell reprogramming. Core pluripotency factors and developmental regulators reciprocally control the expression of key metabolism genes and their encoded pathways. Recent technological advances enabling sensitive detection methods during early mammalian development revealed the state-specific and context-dependent coordination of signal transduction, histone modifications, and gene expression in developing, resting, and malnourished embryos...
February 6, 2018: Cell Metabolism
Mette Trauelsen, Michael Lückmann, Thomas M Frimurer, Thue W Schwartz
It is known but generally unappreciated that the fatty acid receptor FFAR1 (GPR40) is responsible for a major part of glucose-induced insulin secretion. This puzzling fact is now explained by Tunaru et al. (2018), who demonstrate that glucose-induced 20-hydroxyeicosatetraenoic acid (20-HETE) amplifies insulin secretion through autocrine activation of FFAR1.
February 6, 2018: Cell Metabolism
Martin Giera, Filipe Branco Dos Santos, Gary Siuzdak
Metabolomics combined with systems biology can be used to identify endogenous metabolites that modulate protein expression. Recent examples include the 2-fold enhancements of pertussis toxin protein in vaccine production and myelin basic protein expression in oligodendrocyte maturation; both applied a metabolomics-systems strategy to identify active metabolites.
February 6, 2018: Cell Metabolism
Manon Torres, Achim Kramer
You are what you eat; but when you eat also seems to be important for a healthy metabolism. In this issue of Cell Metabolism, Benegiamo et al. (2018) uncover a mechanism by which the RNA-binding protein NONO promotes the time-of-day-dependent expression of key metabolic genes at a post-transcriptional level in response to nutrition.
February 6, 2018: Cell Metabolism
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