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Cell Metabolism

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https://www.readbyqxmd.com/read/29233536/leap2-is-an-endogenous-antagonist-of-the-ghrelin-receptor
#1
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
https://www.readbyqxmd.com/read/29198988/sensing-and-transmitting-intracellular-amino-acid-signals-through-reversible-lysine-aminoacylations
#2
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
https://www.readbyqxmd.com/read/29195860/gdf15-from-biomarker-to-allostatic-hormone
#3
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
https://www.readbyqxmd.com/read/29153408/ampk-sensing-glucose-as-well-as-cellular-energy-status
#4
REVIEW
Sheng-Cai Lin, D Grahame Hardie
Mammalian AMPK is known to be activated by falling cellular energy status, signaled by rising AMP/ATP and ADP/ATP ratios. We review recent information about how this occurs but also discuss new studies suggesting that AMPK is able to sense glucose availability independently of changes in adenine nucleotides. The glycolytic intermediate fructose-1,6-bisphosphate (FBP) is sensed by aldolase, which binds to the v-ATPase on the lysosomal surface. In the absence of FBP, interactions between aldolase and the v-ATPase are altered, allowing formation of an AXIN-based AMPK-activation complex containing the v-ATPase, Ragulator, AXIN, LKB1, and AMPK, causing increased Thr172 phosphorylation and AMPK activation...
November 15, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29153407/brown-fat-akt2-is-a-cold-induced-kinase-that-stimulates-chrebp-mediated-de-novo-lipogenesis-to-optimize-fuel-storage-and-thermogenesis
#5
Joan Sanchez-Gurmaches, Yuefeng Tang, Naja Zenius Jespersen, Martina Wallace, Camila Martinez Calejman, Sharvari Gujja, Huawei Li, Yvonne J K Edwards, Christian Wolfrum, Christian M Metallo, Søren Nielsen, Camilla Scheele, David A Guertin
Brown adipose tissue (BAT) is a therapeutic target for metabolic diseases; thus, understanding its metabolic circuitry is clinically important. Many studies of BAT compare rodents mildly cold to those severely cold. Here, we compared BAT remodeling between thermoneutral and mild-cold-adapted mice, conditions more relevant to humans. Although BAT is renowned for catabolic β-oxidative capacity, we find paradoxically that the anabolic de novo lipogenesis (DNL) genes encoding ACLY, ACSS2, ACC, and FASN were among the most upregulated by mild cold and that, in humans, DNL correlates with Ucp1 expression...
November 15, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29129787/cd38-nad-axis-regulates-immunotherapeutic-anti-tumor-t-cell-response
#6
Shilpak Chatterjee, Anusara Daenthanasanmak, Paramita Chakraborty, Megan W Wyatt, Payal Dhar, Shanmugam Paneer Selvam, Jianing Fu, Jinyu Zhang, Hung Nguyen, Inhong Kang, Kyle Toth, Mazen Al-Homrani, Mahvash Husain, Gyda Beeson, Lauren Ball, Kristi Helke, Shahid Husain, Elizabeth Garrett-Mayer, Gary Hardiman, Meenal Mehrotra, Michael I Nishimura, Craig C Beeson, Melanie Gubbels Bupp, Jennifer Wu, Besim Ogretmen, Chrystal M Paulos, Jeffery Rathmell, Xue-Zhong Yu, Shikhar Mehrotra
Heightened effector function and prolonged persistence, the key attributes of Th1 and Th17 cells, respectively, are key features of potent anti-tumor T cells. Here, we established ex vivo culture conditions to generate hybrid Th1/17 cells, which persisted long-term in vivo while maintaining their effector function. Using transcriptomics and metabolic profiling approaches, we showed that the enhanced anti-tumor property of Th1/17 cells was dependent on the increased NAD(+)-dependent activity of the histone deacetylase Sirt1...
November 8, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29129786/mechanisms-by-which-a-very-low-calorie-diet-reverses-hyperglycemia-in-a-rat-model-of-type-2-diabetes
#7
Rachel J Perry, Liang Peng, Gary W Cline, Yongliang Wang, Aviva Rabin-Court, Joongyu D Song, Dongyan Zhang, Xian-Man Zhang, Yuichi Nozaki, Sylvie Dufour, Kitt Falk Petersen, Gerald I Shulman
Caloric restriction rapidly reverses type 2 diabetes (T2D), but the mechanism(s) of this reversal are poorly understood. Here we show that 3 days of a very-low-calorie diet (VLCD, one-quarter their typical intake) lowered plasma glucose and insulin concentrations in a rat model of T2D without altering body weight. The lower plasma glucose was associated with a 30% reduction in hepatic glucose production resulting from suppression of both gluconeogenesis from pyruvate carboxylase (VPC), explained by a reduction in hepatic acetyl-CoA content, and net hepatic glycogenolysis...
November 8, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29129785/advances-in-hypoxia-inducible-factor-biology
#8
REVIEW
Hani Choudhry, Adrian L Harris
Hypoxia-inducible factor (HIF), a central regulator for detecting and adapting to cellular oxygen levels, transcriptionally activates genes modulating oxygen homeostasis and metabolic activation. Beyond this, HIF influences many other processes. Hypoxia, in part through HIF-dependent mechanisms, influences epigenetic factors, including DNA methylation and histone acetylation, which modulate hypoxia-responsive gene expression in cells. Hypoxia profoundly affects expression of many noncoding RNAs classes that have clinicopathological implications in cancer...
November 8, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29103923/artemether-does-not-turn-%C3%AE-cells-into-%C3%AE-cells
#9
Talitha van der Meulen, Sharon Lee, Els Noordeloos, Cynthia J Donaldson, Michael W Adams, Glyn M Noguchi, Alex M Mawla, Mark O Huising
Pancreatic α cells retain considerable plasticity and can, under the right circumstances, transdifferentiate into functionally mature β cells. In search of a targetable mechanistic basis, a recent paper suggested that the widely used anti-malaria drug artemether suppresses the α cell transcription factor Arx to promote transdifferentiation into β cells. However, key initial experiments in this paper were carried out in islet cell lines, and most subsequent validation experiments implied transdifferentiation without direct demonstration of α to β cell conversion...
November 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29103922/17%C3%AE-estradiol-directly-lowers-mitochondrial-membrane-microviscosity-and-improves-bioenergetic-function-in-skeletal-muscle
#10
Maria J Torres, Kim A Kew, Terence E Ryan, Edward Ross Pennington, Chien-Te Lin, Katherine A Buddo, Amy M Fix, Cheryl A Smith, Laura A Gilliam, Sira Karvinen, Dawn A Lowe, Espen E Spangenburg, Tonya N Zeczycki, Saame Raza Shaikh, P Darrell Neufer
Menopause results in a progressive decline in 17β-estradiol (E2) levels, increased adiposity, decreased insulin sensitivity, and a higher risk for type 2 diabetes. Estrogen therapies can help reverse these effects, but the mechanism(s) by which E2 modulates susceptibility to metabolic disease is not well understood. In young C57BL/6N mice, short-term ovariectomy decreased-whereas E2 therapy restored-mitochondrial respiratory function, cellular redox state (GSH/GSSG), and insulin sensitivity in skeletal muscle...
November 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29107504/overlapping-brain-circuits-for-homeostatic-and-hedonic-feeding
#11
REVIEW
Mark A Rossi, Garret D Stuber
Central regulation of food intake is a key mechanism contributing to energy homeostasis. Many neural circuits that are thought to orchestrate feeding behavior overlap with the brain's reward circuitry both anatomically and functionally. Manipulation of numerous neural pathways can simultaneously influence food intake and reward. Two key systems underlying these processes-those controlling homeostatic and hedonic feeding-are often treated as independent. Homeostatic feeding is necessary for basic metabolic processes and survival, while hedonic feeding is driven by sensory perception or pleasure...
October 26, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29107505/system-wide-benefits-of-intermeal-fasting-by-autophagy
#12
Nuria Martinez-Lopez, Elena Tarabra, Miriam Toledo, Marina Garcia-Macia, Srabani Sahu, Luisa Coletto, Ana Batista-Gonzalez, Nir Barzilai, Jeffrey E Pessin, Gary J Schwartz, Sander Kersten, Rajat Singh
Autophagy failure is associated with metabolic insufficiency. Although caloric restriction (CR) extends healthspan, its adherence in humans is poor. We established an isocaloric twice-a-day (ITAD) feeding model wherein ITAD-fed mice consume the same food amount as ad libitum controls but at two short windows early and late in the diurnal cycle. We hypothesized that ITAD feeding will provide two intervals of intermeal fasting per circadian period and induce autophagy. We show that ITAD feeding modifies circadian autophagy and glucose/lipid metabolism that correlate with feeding-driven changes in circulating insulin...
October 24, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29107506/dietary-restriction-and-ampk-increase-lifespan-via-mitochondrial-network-and-peroxisome-remodeling
#13
Heather J Weir, Pallas Yao, Frank K Huynh, Caroline C Escoubas, Renata L Goncalves, Kristopher Burkewitz, Raymond Laboy, Matthew D Hirschey, William B Mair
Mitochondrial network remodeling between fused and fragmented states facilitates mitophagy, interaction with other organelles, and metabolic flexibility. Aging is associated with a loss of mitochondrial network homeostasis, but cellular processes causally linking these changes to organismal senescence remain unclear. Here, we show that AMP-activated protein kinase (AMPK) and dietary restriction (DR) promote longevity in C. elegans via maintaining mitochondrial network homeostasis and functional coordination with peroxisomes to increase fatty acid oxidation (FAO)...
October 23, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29107503/abrogating-mitochondrial-dynamics-in-mouse-hearts-accelerates-mitochondrial-senescence
#14
Moshi Song, Antonietta Franco, Julie A Fleischer, Lihong Zhang, Gerald W Dorn
Mitochondrial fusion and fission are critical to heart health; genetically interrupting either is rapidly lethal. To understand whether it is loss of, or the imbalance between, fusion and fission that underlies observed cardiac phenotypes, we engineered mice in which Mfn-mediated fusion and Drp1-mediated fission could be concomitantly abolished. Compared to fusion-defective Mfn1/Mfn2 cardiac knockout or fission-defective Drp1 cardiac knockout mice, Mfn1/Mfn2/Drp1 cardiac triple-knockout mice survived longer and manifested a unique pathological form of cardiac hypertrophy...
October 21, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29056514/molecular-mechanisms-linking-exercise-to-cancer-prevention-and-treatment
#15
REVIEW
Pernille Hojman, Julie Gehl, Jesper F Christensen, Bente K Pedersen
The benefits of exercise training for cancer patients are becoming increasingly evident. Physical exercise has been shown to reduce cancer incidence and inhibit tumor growth. Here we provide the status of the current molecular understanding of the effect of exercise on cancer. We propose that exercise has a role in controlling cancer progression through a direct effect on tumor-intrinsic factors, interplay with whole-body exercise effects, alleviation of cancer-related adverse events, and improvement of anti-cancer treatment efficacy...
October 17, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29056513/metformin-alters-upper-small-intestinal-microbiota-that-impact-a-glucose-sglt1-sensing-glucoregulatory-pathway
#16
Paige V Bauer, Frank A Duca, T M Zaved Waise, Brittany A Rasmussen, Mona A Abraham, Helen J Dranse, Akshita Puri, Catherine A O'Brien, Tony K T Lam
The gut microbiota alters energy homeostasis. In parallel, metformin regulates upper small intestinal sodium glucose cotransporter-1 (SGLT1), but whether changes of the microbiota or SGLT1-dependent pathways in the upper small intestine mediate metformin action is unknown. Here we report that upper small intestinal glucose sensing triggers an SGLT1-dependent pathway to lower glucose production in rodents. High-fat diet (HFD) feeding reduces glucose sensing and SGLT1 expression in the upper small intestine. Upper small intestinal metformin treatment restores SGLT1 expression and glucose sensing while shifting the upper small intestinal microbiota partly by increasing the abundance of Lactobacillus...
October 17, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29056515/in%C3%A2-vivo-imaging-of-glutamine-metabolism-to-the-oncometabolite-2-hydroxyglutarate-in-idh1-2-mutant-tumors
#17
Lucia Salamanca-Cardona, Hardik Shah, Alex J Poot, Fabian M Correa, Valentina Di Gialleonardo, Hui Lui, Vesselin Z Miloushev, Kristin L Granlund, Sui S Tee, Justin R Cross, Craig B Thompson, Kayvan R Keshari
The oncometabolite 2-hydroxyglutarate (2-HG) is a signature biomarker in various cancers, where it accumulates as a result of mutations in isocitrate dehydrogenase (IDH). The metabolic source of 2-HG, in a wide variety of cancers, dictates both its generation and also potential therapeutic strategies, but this remains difficult to access in vivo. Here, utilizing patient-derived chondrosarcoma cells harboring endogenous mutations in IDH1 and IDH2, we report that 2-HG can be rapidly generated from glutamine in vitro...
October 16, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29056512/acetyl-coa-carboxylase-1-dependent-protein-acetylation-controls-breast-cancer-metastasis-and-recurrence
#18
Marcos Rios Garcia, Brigitte Steinbauer, Kshitij Srivastava, Mahak Singhal, Frits Mattijssen, Adriano Maida, Sven Christian, Holger Hess-Stumpp, Hellmut G Augustin, Karin Müller-Decker, Peter P Nawroth, Stephan Herzig, Mauricio Berriel Diaz
Breast tumor recurrence and metastasis represent the main causes of cancer-related death in women, and treatments are still lacking. Here, we define the lipogenic enzyme acetyl-CoA carboxylase (ACC) 1 as a key player in breast cancer metastasis. ACC1 phosphorylation was increased in invading cells both in murine and human breast cancer, serving as a point of convergence for leptin and transforming growth factor (TGF) β signaling. ACC1 phosphorylation was mediated by TGFβ-activated kinase (TAK) 1, and ACC1 inhibition was indispensable for the elevation of cellular acetyl-CoA, the subsequent increase in Smad2 transcription factor acetylation and activation, and ultimately epithelial-mesenchymal transition and metastasis induction...
October 12, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28988820/atf4-induced-metabolic-reprograming-is-a-synthetic-vulnerability-of-the-p62-deficient-tumor-stroma
#19
Juan F Linares, Thekla Cordes, Angeles Duran, Miguel Reina-Campos, Tania Valencia, Christopher S Ahn, Elias A Castilla, Jorge Moscat, Christian M Metallo, Maria T Diaz-Meco
Tumors undergo nutrient stress and need to reprogram their metabolism to survive. The stroma may play a critical role in this process by providing nutrients to support the epithelial compartment of the tumor. Here we show that p62 deficiency in stromal fibroblasts promotes resistance to glutamine deprivation by the direct control of ATF4 stability through its p62-mediated polyubiquitination. ATF4 upregulation by p62 deficiency in the stroma activates glucose carbon flux through a pyruvate carboxylase-asparagine synthase cascade that results in asparagine generation as a source of nitrogen for stroma and tumor epithelial proliferation...
September 27, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29211981/mait-cells-a-link-between-gut-integrity-and-type-1-diabetes
#20
Elke Gülden, Noah Palm, Kevan C Herold
Type 1 diabetes (T1D) is a multifactorial autoimmune disease whose etiology involves complex interactions between the immune system and the intestinal microbiota. Recent studies by Rouxel et al. (2017) suggest that innate-like mucosal-associated invariant T cells (MAIT cells) may link gut integrity, the microbiota, and T1D.
December 5, 2017: Cell Metabolism
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