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Cell Metabolism

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https://www.readbyqxmd.com/read/28089568/inhibition-of-intracellular-triglyceride-lipolysis-suppresses-cold-induced-brown-adipose-tissue-metabolism-and-increases-shivering-in-humans
#1
Denis P Blondin, Frédérique Frisch, Serge Phoenix, Brigitte Guérin, Éric E Turcotte, François Haman, Denis Richard, André C Carpentier
Indirect evidence from human studies suggests that brown adipose tissue (BAT) thermogenesis is fueled predominantly by fatty acids hydrolyzed from intracellular triglycerides (TGs). However, no direct experimental evidence to support this assumption currently exists in humans. The aim of this study was to determine the role of intracellular TG in BAT thermogenesis, in cold-exposed men. Using positron emission tomography with (11)C-acetate and (18)F-fluorodeoxyglucose, we showed that oral nicotinic acid (NiAc) administration, an inhibitor of intracellular TG lipolysis, suppressed the cold-induced increase in BAT oxidative metabolism and glucose uptake, despite no difference in BAT blood flow...
January 11, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28089567/adipose-tissue-clk2-promotes-energy-expenditure-during-high-fat-diet-intermittent-fasting
#2
Maximilian Hatting, Amy K Rines, Chi Luo, Mitsuhisa Tabata, Kfir Sharabi, Jessica A Hall, Francisco Verdeguer, Christian Trautwein, Pere Puigserver
A promising approach to treating obesity is to increase diet-induced thermogenesis in brown adipose tissue (BAT), but the regulation of this process remains unclear. Here we find that CDC-like kinase 2 (CLK2) is expressed in BAT and upregulated upon refeeding. Mice lacking CLK2 in adipose tissue exhibit exacerbated obesity and decreased energy expenditure during high-fat diet intermittent fasting. Additionally, tissue oxygen consumption and protein levels of UCP1 are reduced in CLK2-deficient BAT. Phosphorylation of CREB, a transcriptional activator of UCP1, is markedly decreased in BAT cells lacking CLK2 due to enhanced CREB dephosphorylation...
January 11, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28089569/prevention-of-dietary-fat-fueled-ketogenesis-attenuates-braf-v600e-tumor-growth
#3
Siyuan Xia, Ruiting Lin, Lingtao Jin, Liang Zhao, Hee-Bum Kang, Yaozhu Pan, Shuangping Liu, Guoqing Qian, Zhiyu Qian, Evmorfia Konstantakou, Baotong Zhang, Jin-Tang Dong, Young Rock Chung, Omar Abdel-Wahab, Taha Merghoub, Lu Zhou, Ragini R Kudchadkar, David H Lawson, Hanna J Khoury, Fadlo R Khuri, Lawrence H Boise, Sagar Lonial, Benjamin H Lee, Brian P Pollack, Jack L Arbiser, Jun Fan, Qun-Ying Lei, Jing Chen
Lifestyle factors, including diet, play an important role in the survival of cancer patients. However, the molecular mechanisms underlying pathogenic links between diet and particular oncogenic mutations in human cancers remain unclear. We recently reported that the ketone body acetoacetate selectively enhances BRAF V600E mutant-dependent MEK1 activation in human cancers. Here we show that a high-fat ketogenic diet increased serum levels of acetoacetate, leading to enhanced tumor growth potential of BRAF V600E-expressing human melanoma cells in xenograft mice...
January 9, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28065829/medullary-reticular-neurons-mediate-neuropeptide-y-induced-metabolic-inhibition-and-mastication
#4
Yoshiko Nakamura, Yuchio Yanagawa, Shaun F Morrison, Kazuhiro Nakamura
Hypothalamic neuropeptide Y (NPY) elicits hunger responses to increase the chances of surviving starvation: an inhibition of metabolism and an increase in feeding. Here we elucidate a key central circuit mechanism through which hypothalamic NPY signals drive these hunger responses. GABAergic neurons in the intermediate and parvicellular reticular nuclei (IRt/PCRt) of the medulla oblongata, which are activated by NPY-triggered neural signaling from the hypothalamus, potentially through the nucleus tractus solitarius, mediate the NPY-induced inhibition of metabolic thermogenesis in brown adipose tissue (BAT) via their innervation of BAT sympathetic premotor neurons...
January 4, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28065828/adipocyte-dynamics-and-reversible-metabolic-syndrome-in-mice-with-an-inducible-adipocyte-specific-deletion-of-the-insulin-receptor
#5
Masaji Sakaguchi, Shiho Fujisaka, Weikang Cai, Jonathon N Winnay, Masahiro Konishi, Brian T O'Neill, Mengyao Li, Rubén García-Martín, Hirokazu Takahashi, Jiang Hu, Rohit N Kulkarni, C Ronald Kahn
Insulin and IGF1 signaling are important for adipose tissue development and function; however, their role in mature adipocytes is unclear. Mice with a tamoxifen-inducible knockout of insulin and/or IGF1 receptors (IR/IGF1R) demonstrate a rapid loss of white and brown fat due to increased lipolysis and adipocyte apoptosis. This results in insulin resistance, glucose intolerance, hepatosteatosis, islet hyperplasia with hyperinsulinemia, and cold intolerance. This phenotype, however, resolves over 10-30 days due to a proliferation of preadipocytes and rapid regeneration of both brown and white adipocytes as identified by mTmG lineage tracing...
January 4, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28065827/gastric-bypass-surgery-recruits-a-gut-ppar-%C3%AE-striatal-d1r-pathway-to-reduce-fat-appetite-in-obese-rats
#6
Mohammed K Hankir, Florian Seyfried, Constantin A Hintschich, Thi-Ai Diep, Karen Kleberg, Mathias Kranz, Winnie Deuther-Conrad, Luis A Tellez, Michael Rullmann, Marianne Patt, Jens Teichert, Swen Hesse, Osama Sabri, Peter Brust, Harald S Hansen, Ivan E de Araujo, Ute Krügel, Wiebke K Fenske
Bariatric surgery remains the single most effective long-term treatment modality for morbid obesity, achieved mainly by lowering caloric intake through as yet ill-defined mechanisms. Here we show in rats that Roux-en-Y gastric bypass (RYGB)-like rerouting of ingested fat mobilizes lower small intestine production of the fat-satiety molecule oleoylethanolamide (OEA). This was associated with vagus nerve-driven increases in dorsal striatal dopamine release. We also demonstrate that RYGB upregulates striatal dopamine 1 receptor (D1R) expression specifically under high-fat diet feeding conditions...
January 2, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28089566/metformin-inhibits-hepatic-mtorc1-signaling-via-dose-dependent-mechanisms-involving-ampk-and-the-tsc-complex
#7
Jessica J Howell, Kristina Hellberg, Marc Turner, George Talbott, Matthew J Kolar, Debbie S Ross, Gerta Hoxhaj, Alan Saghatelian, Reuben J Shaw, Brendan D Manning
Metformin is the most widely prescribed drug for the treatment of type 2 diabetes. However, knowledge of the full effects of metformin on biochemical pathways and processes in its primary target tissue, the liver, is limited. One established effect of metformin is to decrease cellular energy levels. The AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) are key regulators of metabolism that are respectively activated and inhibited in acute response to cellular energy depletion...
December 30, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/28041957/human-pancreatic-%C3%AE-cell-lncrnas-control-cell-specific-regulatory-networks
#8
Ildem Akerman, Zhidong Tu, Anthony Beucher, Delphine M Y Rolando, Claire Sauty-Colace, Marion Benazra, Nikolina Nakic, Jialiang Yang, Huan Wang, Lorenzo Pasquali, Ignasi Moran, Javier Garcia-Hurtado, Natalia Castro, Roser Gonzalez-Franco, Andrew F Stewart, Caroline Bonner, Lorenzo Piemonti, Thierry Berney, Leif Groop, Julie Kerr-Conte, Francois Pattou, Carmen Argmann, Eric Schadt, Philippe Ravassard, Jorge Ferrer
Recent studies have uncovered thousands of long non-coding RNAs (lncRNAs) in human pancreatic β cells. β cell lncRNAs are often cell type specific and exhibit dynamic regulation during differentiation or upon changing glucose concentrations. Although these features hint at a role of lncRNAs in β cell gene regulation and diabetes, the function of β cell lncRNAs remains largely unknown. In this study, we investigated the function of β cell-specific lncRNAs and transcription factors using transcript knockdowns and co-expression network analysis...
December 28, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/28089565/fgf21-is-an-exocrine-pancreas-secretagogue
#9
Katie C Coate, Genaro Hernandez, Curtis A Thorne, Shengyi Sun, Thao D V Le, Kevin Vale, Steven A Kliewer, David J Mangelsdorf
The metabolic stress hormone FGF21 is highly expressed in exocrine pancreas, where its levels are increased by refeeding and chemically induced pancreatitis. However, its function in the exocrine pancreas remains unknown. Here, we show that FGF21 stimulates digestive enzyme secretion from pancreatic acinar cells through an autocrine/paracrine mechanism that requires signaling through a tyrosine kinase receptor complex composed of an FGF receptor and β-Klotho. Mice lacking FGF21 accumulate zymogen granules and are susceptible to pancreatic ER stress, an effect that is reversed by administration of recombinant FGF21...
December 27, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/28041958/srebp1-contributes-to-resolution-of-pro-inflammatory-tlr4-signaling-by-reprogramming-fatty-acid-metabolism
#10
Yumiko Oishi, Nathanael J Spann, Verena M Link, Evan D Muse, Tobias Strid, Chantle Edillor, Matthew J Kolar, Takashi Matsuzaka, Sumio Hayakawa, Jenhan Tao, Minna U Kaikkonen, Aaron F Carlin, Michael T Lam, Ichiro Manabe, Hitoshi Shimano, Alan Saghatelian, Christopher K Glass
Macrophages play pivotal roles in both the induction and resolution phases of inflammatory processes. Macrophages have been shown to synthesize anti-inflammatory fatty acids in an LXR-dependent manner, but whether the production of these species contributes to the resolution phase of inflammatory responses has not been established. Here, we identify a biphasic program of gene expression that drives production of anti-inflammatory fatty acids 12-24 hr following TLR4 activation and contributes to downregulation of mRNAs encoding pro-inflammatory mediators...
December 21, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/28041956/basal-ganglia-dysfunction-contributes-to-physical-inactivity-in-obesity
#11
Danielle M Friend, Kavya Devarakonda, Timothy J O'Neal, Miguel Skirzewski, Ioannis Papazoglou, Alanna R Kaplan, Jeih-San Liow, Juen Guo, Sushil G Rane, Marcelo Rubinstein, Veronica A Alvarez, Kevin D Hall, Alexxai V Kravitz
Obesity is associated with physical inactivity, which exacerbates the health consequences of weight gain. However, the mechanisms that mediate this association are unknown. We hypothesized that deficits in dopamine signaling contribute to physical inactivity in obesity. To investigate this, we quantified multiple aspects of dopamine signaling in lean and obese mice. We found that D2-type receptor (D2R) binding in the striatum, but not D1-type receptor binding or dopamine levels, was reduced in obese mice. Genetically removing D2Rs from striatal medium spiny neurons was sufficient to reduce motor activity in lean mice, whereas restoring Gi signaling in these neurons increased activity in obese mice...
December 20, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/27916530/enhanced-respiratory-chain-supercomplex-formation-in-response-to-exercise-in-human-skeletal-muscle
#12
Chiara Greggio, Pooja Jha, Sameer S Kulkarni, Sylviane Lagarrigue, Nicholas T Broskey, Marie Boutant, Xu Wang, Sonia Conde Alonso, Emmanuel Ofori, Johan Auwerx, Carles Cantó, Francesca Amati
Mitochondrial dysfunction is a hallmark of multiple metabolic complications. Physical activity is known to increase mitochondrial content in skeletal muscle, counteracting age-related decline in muscle function and protecting against metabolic and cardiovascular complications. Here, we investigated the effect of 4 months of exercise training on skeletal muscle mitochondria electron transport chain complexes and supercomplexes in 26 healthy, sedentary older adults. Exercise differentially modulated respiratory complexes...
November 28, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/27889389/exercise-mimetics-impact-on-health-and-performance
#13
REVIEW
Weiwei Fan, Ronald M Evans
The global epidemic of obesity and its associated chronic diseases is largely attributed to an imbalance between caloric intake and energy expenditure. While physical exercise remains the best solution, the development of muscle-targeted "exercise mimetics" may soon provide a pharmaceutical alternative to battle an increasingly sedentary lifestyle. At the same time, these advances are fueling a raging debate on their escalating use as performance-enhancing drugs in high-profile competitions such as the Olympics...
November 18, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/27916529/applications-and-limitations-of-mouse-models-for-understanding-human-atherosclerosis
#14
REVIEW
Moritz von Scheidt, Yuqi Zhao, Zeyneb Kurt, Calvin Pan, Lingyao Zeng, Xia Yang, Heribert Schunkert, Aldons J Lusis
Most of the biological understanding of mechanisms underlying coronary artery disease (CAD) derives from studies of mouse models. The identification of multiple CAD loci and strong candidate genes in large human genome-wide association studies (GWASs) presented an opportunity to examine the relevance of mouse models for the human disease. We comprehensively reviewed the mouse literature, including 827 literature-derived genes, and compared it to human data. First, we observed striking concordance of risk factors for atherosclerosis in mice and humans...
November 17, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/27839907/immunotherapy-for-type-1-diabetes-why-do-current-protocols-not-halt-the-underlying-disease-process
#15
Hubert Kolb, Matthias von Herrath
T cell-directed immunosuppression only transiently delays the loss of β cell function in recent-onset type 1 diabetes. We argue here that the underlying disease process is carried by innate immune reactivity. Inducing a non-polarized functional state of local innate immunity will support regulatory T cell development and β cell proliferation.
November 5, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/28094012/mammalian-mitochondria-and-aging-an-update
#16
REVIEW
Timo E S Kauppila, Johanna H K Kauppila, Nils-Göran Larsson
Mitochondria were first postulated to contribute to aging more than 40 years ago. During the following decades, multiple lines of evidence in model organisms and humans showed that impaired mitochondrial function can contribute to age-associated disease phenotypes and aging. However, in contrast to the original theory favoring oxidative damage as a cause for mtDNA mutations, there are now strong data arguing that most mammalian mtDNA mutations originate as replication errors made by the mtDNA polymerase. Currently, a substantial amount of mitochondrial research is focused on finding ways to either remove or counteract the effects of mtDNA mutations with the hope of extending the human health- and lifespan...
January 10, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28094011/metabolomics-and-metabolic-diseases-where-do-we-stand
#17
REVIEW
Christopher B Newgard
Metabolomics, or the comprehensive profiling of small molecule metabolites in cells, tissues, or whole organisms, has undergone a rapid technological evolution in the past two decades. These advances have led to the application of metabolomics to defining predictive biomarkers for incident cardiometabolic diseases and, increasingly, as a blueprint for understanding those diseases' pathophysiologic mechanisms. Progress in this area and challenges for the future are reviewed here.
January 10, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28076767/-s-pot-on-mitochondria-cannabinoids-disrupt-cellular-respiration-to-limit-neuronal-activity
#18
Tibor Harkany, Tamas L Horvath
Classical views posit G protein-coupled cannabinoid receptor 1s (CB1Rs) at the cell surface with cytosolic Giα-mediated signal transduction. Hebert-Chatelain et al. (2016) instead place CB1Rs at mitochondria limiting neuronal respiration by soluble adenylyl cyclase-dependent modulation of complex I activity. Thus, neuronal bioenergetics link to synaptic plasticity and, globally, learning and memory.
January 10, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28076766/are-gut-microbes-responsible-for-post-dieting-weight-rebound
#19
Julien Chilloux, Marc-Emmanuel Dumas
One of the dieting conundrums in the age of the obesity epidemic is the cycle of weight loss and regain known as the "yo-yo effect." Thaiss et al. (2016) demonstrate that the microbiome plays a key role in this phenomenon and that simple dietary supplementations can reset the weight-rebound clock.
January 10, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28076765/building-a-beautiful-beast-mammalian-respiratory-complex-i
#20
Adela M Guaras, José Antonio Enríquez
Understanding the mammalian respiratory complex I assembly has been an arduous task due to the lack of appropriate techniques and the complexity of the process. In this issue, a new tour de force based on complexome profiling provides an encyclopedic description of the process (Guerrero-Castillo et al., 2017).
January 10, 2017: Cell Metabolism
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