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Cell Metabolism

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https://www.readbyqxmd.com/read/28768182/dna-pk-promotes-the-mitochondrial-metabolic-and-physical-decline-that-occurs-during-aging
#1
Sung-Jun Park, Oksana Gavrilova, Alexandra L Brown, Jamie E Soto, Shannon Bremner, Jeonghan Kim, Xihui Xu, Shutong Yang, Jee-Hyun Um, Lauren G Koch, Steven L Britton, Richard L Lieber, Andrew Philp, Keith Baar, Steven G Kohama, E Dale Abel, Myung K Kim, Jay H Chung
No abstract text is available yet for this article.
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768181/long-term-cold-adaptation-does-not-require-fgf21-or-ucp1
#2
Susanne Keipert, Maria Kutschke, Mario Ost, Thomas Schwarzmayr, Evert M van Schothorst, Daniel Lamp, Laura Brachthäuser, Isabel Hamp, Sithandiwe E Mazibuko, Sonja Hartwig, Stefan Lehr, Elisabeth Graf, Oliver Plettenburg, Frauke Neff, Matthias H Tschöp, Martin Jastroch
Brown adipose tissue (BAT)-dependent thermogenesis and its suggested augmenting hormone, FGF21, are potential therapeutic targets in current obesity and diabetes research. Here, we studied the role of UCP1 and FGF21 for metabolic homeostasis in the cold and dissected underlying molecular mechanisms using UCP1-FGF21 double-knockout mice. We report that neither UCP1 nor FGF21, nor even compensatory increases of FGF21 serum levels in UCP1 knockout mice, are required for defense of body temperature or for maintenance of energy metabolism and body weight...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768180/increased-total-mtdna-copy-number-cures-male-infertility-despite-unaltered-mtdna-mutation-load
#3
Min Jiang, Timo Eino Sakari Kauppila, Elisa Motori, Xinping Li, Ilian Atanassov, Kat Folz-Donahue, Nina Anna Bonekamp, Sara Albarran-Gutierrez, James Bruce Stewart, Nils-Göran Larsson
Mutations of mtDNA cause mitochondrial diseases and are implicated in age-associated diseases and aging. Pathogenic mtDNA mutations are often present in a fraction of all mtDNA copies, and it has been widely debated whether the proportion of mutant genomes or the absolute number of wild-type molecules determines if oxidative phosphorylation (OXPHOS) will be impaired. Here, we have studied the male infertility phenotype of mtDNA mutator mice and demonstrate that decreasing mtDNA copy number worsens mitochondrial aberrations of spermatocytes and spermatids in testes, whereas an increase in mtDNA copy number rescues the fertility phenotype and normalizes testes morphology as well as spermatocyte proteome changes...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768179/mtorc1-regulates-mitochondrial-integrated-stress-response-and-mitochondrial-myopathy-progression
#4
Nahid A Khan, Joni Nikkanen, Shuichi Yatsuga, Christopher Jackson, Liya Wang, Swagat Pradhan, Riikka Kivelä, Alberto Pessia, Vidya Velagapudi, Anu Suomalainen
Mitochondrial dysfunction elicits various stress responses in different model systems, but how these responses relate to each other and contribute to mitochondrial disease has remained unclear. Mitochondrial myopathy (MM) is the most common manifestation of adult-onset mitochondrial disease and shows a multifaceted tissue-specific stress response: (1) transcriptional response, including metabolic cytokines FGF21 and GDF15; (2) remodeling of one-carbon metabolism; and (3) mitochondrial unfolded protein response...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768178/triglyceride-synthesis-by-dgat1-protects-adipocytes-from-lipid-induced-er-stress-during-lipolysis
#5
Chandramohan Chitraju, Niklas Mejhert, Joel T Haas, L Grisell Diaz-Ramirez, Carrie A Grueter, Jason E Imbriglio, Shirly Pinto, Suneil K Koliwad, Tobias C Walther, Robert V Farese
Triglyceride (TG) storage in adipose tissue provides the major reservoir for metabolic energy in mammals. During lipolysis, fatty acids (FAs) are hydrolyzed from adipocyte TG stores and transported to other tissues for fuel. For unclear reasons, a large portion of hydrolyzed FAs in adipocytes is re-esterified to TGs in a "futile," ATP-consuming, energy dissipating cycle. Here we show that FA re-esterification during adipocyte lipolysis is mediated by DGAT1, an ER-localized DGAT enzyme. Surprisingly, this re-esterification cycle does not preserve TG mass but instead functions to protect the ER from lipotoxic stress and related consequences, such as adipose tissue inflammation...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768177/acetyl-coa-carboxylase-inhibition-reduces-hepatic-steatosis-but-elevates-plasma-triglycerides-in-mice-and-humans-a-bedside-to-bench-investigation
#6
Chai-Wan Kim, Carol Addy, Jun Kusunoki, Norma N Anderson, Stanislaw Deja, Xiaorong Fu, Shawn C Burgess, Cai Li, Manu Chakravarthy, Steve Previs, Stuart Milstein, Kevin Fitzgerald, David E Kelley, Jay D Horton
Inhibiting lipogenesis prevents hepatic steatosis in rodents with insulin resistance. To determine if reducing lipogenesis functions similarly in humans, we developed MK-4074, a liver-specific inhibitor of acetyl-CoA carboxylase (ACC1) and (ACC2), enzymes that produce malonyl-CoA for fatty acid synthesis. MK-4074 administered to subjects with hepatic steatosis for 1 month lowered lipogenesis, increased ketones, and reduced liver triglycerides by 36%. Unexpectedly, MK-4074 increased plasma triglycerides by 200%...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768176/a-hypothalamic-phosphatase-switch-coordinates-energy-expenditure-with-feeding
#7
Garron T Dodd, Zane B Andrews, Stephanie E Simonds, Natalie J Michael, Michael DeVeer, Jens C Brüning, David Spanswick, Michael A Cowley, Tony Tiganis
Beige adipocytes can interconvert between white and brown-like states and switch between energy storage versus expenditure. Here we report that beige adipocyte plasticity is important for feeding-associated changes in energy expenditure and is coordinated by the hypothalamus and the phosphatase TCPTP. A fasting-induced and glucocorticoid-mediated induction of TCPTP, inhibited insulin signaling in AgRP/NPY neurons, repressed the browning of white fat and decreased energy expenditure. Conversely feeding reduced hypothalamic TCPTP, to increase AgRP/NPY neuronal insulin signaling, white adipose tissue browning and energy expenditure...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768175/neuronal-stimulation-triggers-neuronal-glycolysis-and-not-lactate-uptake
#8
Carlos Manlio Díaz-García, Rebecca Mongeon, Carolina Lahmann, Dorothy Koveal, Hannah Zucker, Gary Yellen
Proper brain function requires a substantial energy supply, up to 20% of whole-body energy in humans, and brain activation produces large dynamic variations in energy demand. While local increases in cerebral blood flow are well known, the cellular responses to energy demand are controversial. During brain excitation, glycolysis of glucose to lactate temporarily exceeds the rate of mitochondrial fuel oxidation; although the increased energy demand occurs mainly within neurons, some have suggested this glycolysis occurs mainly in astrocytes, which then shuttle lactate to neurons as their primary fuel...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768174/loss-of-brain-aerobic-glycolysis-in-normal-human-aging
#9
Manu S Goyal, Andrei G Vlassenko, Tyler M Blazey, Yi Su, Lars E Couture, Tony J Durbin, Randall J Bateman, Tammie L-S Benzinger, John C Morris, Marcus E Raichle
The normal aging human brain experiences global decreases in metabolism, but whether this affects the topography of brain metabolism is unknown. Here we describe PET-based measurements of brain glucose uptake, oxygen utilization, and blood flow in cognitively normal adults from 20 to 82 years of age. Age-related decreases in brain glucose uptake exceed that of oxygen use, resulting in loss of brain aerobic glycolysis (AG). Whereas the topographies of total brain glucose uptake, oxygen utilization, and blood flow remain largely stable with age, brain AG topography changes significantly...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768173/the-sustained-effects-of-a-dual-gip-glp-1-receptor-agonist-nnc0090-2746-in-patients-with-type-2-diabetes
#10
Juan Pablo Frias, Edward J Bastyr, Louis Vignati, Matthias H Tschöp, Christophe Schmitt, Klara Owen, Rune Haubo Christensen, Richard D DiMarchi
Unimolecular dual incretins derived from hybridized glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) sequences have demonstrated synergistic reduction of adiposity in animal models and reductions of hyperglycemia in short-duration human trials. Here, we extend the characterization of NNC0090-2746 (also known as RG7697), a fatty-acylated dual agonist possessing in vitro balanced GIPR and GLP-1R agonism. In this 12-week, randomized, placebo-controlled, double-blind phase 2a trial, patients with type 2 diabetes inadequately controlled with metformin received 1...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768172/sweet-sixteenth-for-chrebp-established-roles-and-future-goals
#11
REVIEW
Aya Abdul-Wahed, Sandra Guilmeau, Catherine Postic
With the identification of ChREBP in 2001, our interest in understanding the molecular control of carbohydrate sensing has surged. While ChREBP was initially studied as a master regulator of lipogenesis in liver and fat tissue, it is now clear that ChREBP functions as a central metabolic coordinator in a variety of cell types in response to environmental and hormonal signals, with wide implications in health and disease. Celebrating its sweet sixteenth birthday, we review here the current knowledge about the function and regulation of ChREBP throughout usual and less explored tissues, to recapitulate ChREBP's role as a whole-body glucose sensor...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768171/the-dawn-of-the-age-of-amino-acid-sensors-for-the-mtorc1-pathway
#12
REVIEW
Rachel L Wolfson, David M Sabatini
The mechanistic target of rapamycin complex 1 (mTORC1) is a master regulator of cell growth that responds to a diverse set of environmental inputs, including amino acids. Over the past 10 years, a number of proteins have been identified that help transmit amino acid availability to mTORC1. However, amino acid sensors for this pathway have only recently been discovered. Here, we review these recent advances and highlight the variety of unexplored questions that emerge from the identification of these sensors...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768170/causes-characteristics-and-consequences-of-metabolically-unhealthy-normal-weight-in-humans
#13
REVIEW
Norbert Stefan, Fritz Schick, Hans-Ulrich Häring
A BMI in the normal range associates with a decreased risk of cardiometabolic disease and all-cause mortality. However, not all subjects in this BMI range have this low risk. Compared to people who are of normal weight and metabolically healthy, subjects who are of normal weight but metabolically unhealthy (∼20% of the normal weight adult population) have a greater than 3-fold higher risk of all-cause mortality and/or cardiovascular events. Here we address to what extent major risk phenotypes determine metabolic health in lean compared to overweight and obese people and provide support for the existence of a lipodystrophy-like phenotype in the general population...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768169/once-blind-now-we-see-glp-1-molecular-action
#14
John P Mayer, Matthias H Tschöp, Richard D DiMarchi
The macromolecular mechanics of GLP-1 with its cell surface receptor came into focus as two landmark publications recently published in Nature collectively herald advancement in structure-based design for a receptor class of great therapeutic importance (Jazayeri et al., 2017; Zhang et al., 2017).
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768168/what-s-so-special-about-fgf19-unique-effects-reported-on-skeletal-muscle-mass-and-function
#15
David J Glass
In a recent study published in Nature Medicine, Benoit et al. (2017) reported unique effects of FGF19 on mouse skeletal muscle: FGF19 induced skeletal muscle hypertrophy and blocked muscle atrophy, acting via FGF receptors and ßKlotho, while a related FGF21 hormone was ineffective.
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768167/burning-fat-and-building-bone-by-fsh-blockade
#16
Carlos Henrique Sponton, Shingo Kajimura
The rise of follicle-stimulating hormone (FSH) is a hallmark of menopause associated with osteoporosis and visceral adiposity. In Nature, Zaidi and colleagues (Liu et al., 2017) report that blocking FSH action reduces body fat by promoting brown/beige fat thermogenesis, potentially providing a new intervention for the treatment of menopause-related metabolic diseases.
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768166/holding-onto-youth
#17
Alain Dagher, Bratislav Misic
Aerobic glycolysis (AG), the synthesis of lactate despite the presence of oxygen, has been implicated in the growth of cancer cells, synaptic development, and brain plasticity. In this issue of Cell Metabolism, Goyal et al. (2017) demonstrate that AG declines with age in the human brain, disappearing almost completely by age 60.
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768165/plasma-mannose-levels-are-associated-with-incident-type-2-diabetes-and-cardiovascular-disease
#18
LETTER
Adil Mardinoglu, Alena Stančáková, Luca A Lotta, Johanna Kuusisto, Jan Boren, Matthias Blüher, Nicholas J Wareham, Ele Ferrannini, Per Henrik Groop, Markku Laakso, Claudia Langenberg, Ulf Smith
Plasma mannose levels are elevated in subjects with insulin resistance independently of obesity. Here, we found that elevated plasma mannose levels are strong markers of future risk of several chronic diseases including T2D, CVD, and albuminuria, and that it may contribute to their development rather than just being a novel biomarker.
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28768164/chronic-sucralose-or-l-glucose-ingestion-does-not-suppress-food-intake
#19
LETTER
Qiao-Ping Wang, Stephen J Simpson, Herbert Herzog, G Gregory Neely
Despite widespread consumption of non-nutritive sweeteners (NNSs), the impact of manipulating the perceived sweetness of food is unclear. Previously we reported that chronic consumption of the NNSs sucralose or L-glucose led to increased calories consumed post-exposure; however, a recent study suggested this effect occurs because NNSs acutely suppress food intake, leading to a caloric debt. Here we show that acute ingestion of sucralose in the context of a low-carbohydrate diet causes a pronounced increase in calories consumed...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28712655/insulin-regulation-of-proteostasis-and-clinical-implications
#20
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...
August 1, 2017: Cell Metabolism
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