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Glucose metabolism and autophagy

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https://www.readbyqxmd.com/read/28736261/genetic-disruption-of-the-cardiomyocyte-circadian-clock-differentially-influences-insulin-mediated-processes-in-the-heart
#1
Graham R McGinnis, Yawen Tang, Rachel A Brewer, Manoja K Brahma, Haley L Stanley, Gobinath Shanmugam, Namakkal Soorappan Rajasekaran, Glenn C Rowe, Stuart J Frank, Adam R Wende, E Dale Abel, Heinrich Taegtmeyer, Silvio Litovsky, Victor Darley-Usmar, Jianhua Zhang, John C Chatham, Martin E Young
Cardiovascular physiology exhibits time-of-day-dependent oscillations, which are mediated by both extrinsic (e.g., environment/behavior) and intrinsic (e.g., circadian clock) factors. Disruption of circadian rhythms negatively affects multiple cardiometabolic parameters. Recent studies suggest that the cardiomyocyte circadian clock directly modulates responsiveness of the heart to metabolic stimuli (e.g., fatty acids) and stresses (e.g., ischemia/reperfusion). The aim of this study was to determine whether genetic disruption of the cardiomyocyte circadian clock impacts insulin-regulated pathways in the heart...
July 20, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28729213/physical-exercise-increases-sestrin-2-protein-levels-and-induces-autophagy-in-the-skeletal-muscle-of-old-mice
#2
Luciene Lenhare, Barbara M Crisol, Vagner R R Silva, Carlos K Katashima, André V Cordeiro, Karina D Pereira, Augusto D Luchessi, Adelino S R da Silva, Dennys E Cintra, Leandro P Moura, José R Pauli, Eduardo R Ropelle
Sestrins and autophagy deficiencies are associated with several aging-related organic dysfunctions and metabolic disorders. Here we evaluate the effects of acute exercise on Sestrin 2 (Sesn2) protein content and autophagy markers in the skeletal muscle of experimental models of aging. Twenty-four months-old C57BL/6J male mice were submitted to a single bout of swimming exercise and the gastrocnemius muscle was evaluated by Western blot. Transcriptomic and phenotypic analysis were also performed by using strains of genetically-diverse BXD mice...
July 17, 2017: Experimental Gerontology
https://www.readbyqxmd.com/read/28712893/the-glucagon-like-peptide-1-analogue-liraglutide-promotes-autophagy-through-the-modulation-of-5-amp-activated-protein-kinase-in-ins-1-%C3%AE-cells-under-high-glucose-conditions
#3
Xinyu Miao, Zhaoyan Gu, Yu Liu, Mengmeng Jin, Yanhui Lu, Yanping Gong, Lin Li, Chunlin Li
Glucagon-like peptide-1 (GLP-1) is a potent therapeutic agent for the treatment of diabetes and has been proven to protect pancreatic β-cells from glucotoxicity; however, its mechanisms of action are not entirely understood. Autophagy is a dynamic lysosomal degradation process that can protect organisms against metabolic stress. Studies have shown that autophagy plays a protective role in the survival of pancreatic β-cells under high glucose conditions. In the present study, we explored the role of autophagy in GLP-1-induced protection of pancreatic β-cells exposed to high glucose...
July 13, 2017: Peptides
https://www.readbyqxmd.com/read/28709868/protective-effect-of-p53-on-the-viability-of-intervertebral-disc-nucleus-pulposus-cells-under-low-glucose-condition
#4
Xifeng Xiong, Libing Dai, Weiguo Liang, Jinli Zhang, Shengnan Qin, Wenjuan Cao, Dongping Ye, Peihong Liang, Zhihe Liu
P53 is a famous cancer suppressor and plays key roles in metabolism. Intervertebral disc (IVD) is the largest avascular cartilaginous structure in humans and its degeneration is a common cause of spine diseases initiated from damaged nucleus pulposus (NP) cells. The potential cause of disc degeneration has been attributed to aging, genetic factors, mechanical factors and nutrition. In this study, we found that p53 decreased and leaked to the cytoplasm in NP cells as the glucose level decreases, in contrast to cancer cells in which p53 increases and concentrates to the nuclei...
July 11, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28702322/mitochondrial-transcription-factor-b2-is-essential-for-mitochondrial-and-cellular-function-in-pancreatic-%C3%AE-cells
#5
Lisa M Nicholas, Bérengère Valtat, Anya Medina, Lotta Andersson, Mia Abels, Inês G Mollet, Deepak Jain, Lena Eliasson, Nils Wierup, Malin Fex, Hindrik Mulder
OBJECTIVE: Insulin release from pancreatic β-cells is controlled by plasma glucose levels via mitochondrial fuel metabolism. Therefore, insulin secretion is critically dependent on mitochondrial DNA (mtDNA) and the genes it encodes. Mitochondrial transcription factor B2 (TFB2M) controls transcription of mitochondrial-encoded genes. However, its precise role in mitochondrial metabolism in pancreatic β-cells and, consequently, in insulin secretion remains unknown. METHODS: To elucidate the role of TFB2M in mitochondrial function and insulin secretion in vitro and in vivo, mice with a β-cell specific homozygous or heterozygous knockout of Tfb2m and rat clonal insulin-producing cells in which the gene was silenced were examined with an array of metabolic and functional assays...
July 2017: Molecular Metabolism
https://www.readbyqxmd.com/read/28698309/differential-control-of-ageing-and-lifespan-by-isoforms-and-splice-variants-across-the-mtor-network
#6
REVIEW
Patricia Razquin Navas, Kathrin Thedieck
Ageing can be defined as the gradual deterioration of physiological functions, increasing the incidence of age-related disorders and the probability of death. Therefore, the term ageing not only reflects the lifespan of an organism but also refers to progressive functional impairment and disease. The nutrient-sensing kinase mTOR (mammalian target of rapamycin) is a major determinant of ageing. mTOR promotes cell growth and controls central metabolic pathways including protein biosynthesis, autophagy and glucose and lipid homoeostasis...
July 15, 2017: Essays in Biochemistry
https://www.readbyqxmd.com/read/28676863/muscle-lipid-metabolism-role-of-lipid-droplets-and-perilipins
#7
REVIEW
Pablo Esteban Morales, Jose Luis Bucarey, Alejandra Espinosa
Skeletal muscle is one of the main regulators of carbohydrate and lipid metabolism in our organism, and therefore, it is highly susceptible to changes in glucose and fatty acid (FA) availability. Skeletal muscle is an extremely complex tissue: its metabolic capacity depends on the type of fibers it is made up of and the level of stimulation it undergoes, such as acute or chronic contraction. Obesity is often associated with increased FA levels, which leads to the accumulation of toxic lipid intermediates, oxidative stress, and autophagy in skeletal fibers...
2017: Journal of Diabetes Research
https://www.readbyqxmd.com/read/28661473/autophagy-fails-to-prevent-glucose-deprivation-glucose-reintroduction-induced-neuronal-death-due-to-calpain-mediated-lysosomal-dysfunction-in-cortical-neurons
#8
Cristian Gerónimo-Olvera, Teresa Montiel, Ruth Rincon-Heredia, Susana Castro-Obregón, Lourdes Massieu
Autophagy is triggered during nutrient and energy deprivation in a variety of cells as a homeostatic response to metabolic stress. In the CNS, deficient autophagy has been implicated in neurodegenerative diseases and ischemic brain injury. However, its role in hypoglycemic damage is poorly understood and the dynamics of autophagy during the hypoglycemic and the glucose reperfusion periods, has not been fully described. In the present study, we analyzed the changes in the content of the autophagy proteins BECN1, LC3-II and p62/SQSTM1 by western blot, and autophagosome formation was followed through time-lapse experiments, during glucose deprivation (GD) and glucose reintroduction (GR) in cortical cultures...
June 29, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28650662/glucose-restriction-combined-with-autophagy-inhibition-and-chemotherapy-in-hct-116-spheroids-decreases-cell-clonogenicity-and-viability-regulated-by-tumor-suppressor-genes
#9
Monica M Schroll, Gabriel J LaBonia, Katelyn R Ludwig, Amanda B Hummon
Drug resistance is a prevalent phenomenon that decreases the efficacy of cancer treatments and contributes to cancer progression and metastasis. Weakening drug-resistant cancer cells prior to chemotherapy is a potential strategy to combat chemoresistance. One approach to damage resistant cancer cells is modulation of nutritional intake. The combination of nutrient restriction with targeted compound treatment results in pronounced molecular changes. This study provides valuable information about augmenting existing chemotherapeutic regimes with simultaneous glucose restriction and autophagy inhibition in colorectal cancer cells...
July 3, 2017: Journal of Proteome Research
https://www.readbyqxmd.com/read/28640445/ubiquitin-ligases-and-posttranslational-regulation-of-energy-in-the-heart-the-hand-that-feeds
#10
David I Brown, Traci L Parry, Monte S Willis
Heart failure (HF) is a costly and deadly syndrome characterized by the reduced capacity of the heart to adequately provide systemic blood flow. Mounting evidence implicates pathological changes in cardiac energy metabolism as a contributing factor in the development of HF. While the main source of fuel in the healthy heart is the oxidation of fatty acids, in the failing heart the less energy efficient glucose and glycogen metabolism are upregulated. The ubiquitin proteasome system plays a key role in regulating metabolism via protein-degradation/regulation of autophagy and regulating metabolism-related transcription and cell signaling processes...
June 18, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28605878/an-oasis-in-the-desert-of-cancer-chemotherapeutic-resistance-the-enlightenment-from-reciprocal-crosstalk-between-signaling-pathways-of-upr-and-autophagy-in-cancers
#11
REVIEW
Yuhang Zhang, Xianjun Qu, Lingfan Jiang
Endoplasmic reticulum (ER), principal but complex, functions as the pleiotropic organelle for proper protein folding, Ca(2+) storage as well as lipid and carbohydrate metabolisms. Diverse microenviromental insults including, but not limited to, inflammatory reaction, glucose imbalance and hypoxia, elicit the accumulation of potentially toxic unfolded proteins in the ER lumen. Under the condition of these cellular threats, the autophagy with the well-orchestrated program containing over 30 autophagy-related genes (ATGs) might be initiated for degrading and recycling of the cumulative misfolded proteins and other related abnormal cytoplasmic components...
August 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28602638/autophagy-dependent-shuttling-of-tbc1d5-controls-plasma-membrane-translocation-of-glut1-and-glucose-uptake
#12
Srirupa Roy, Andrew M Leidal, Jordan Ye, Sabrina M Ronen, Jayanta Debnath
Autophagy traditionally sustains metabolism in stressed cells by promoting intracellular catabolism and nutrient recycling. Here, we demonstrate that in response to stresses requiring increased glycolytic demand, the core autophagy machinery also facilitates glucose uptake and glycolytic flux by promoting cell surface expression of the glucose transporter GLUT1/Slc2a1. During metabolic stress, LC3(+) autophagic compartments bind and sequester the RabGAP protein TBC1D5 away from its inhibitory interactions with the retromer complex, thereby enabling retromer recruitment to endosome membranes and GLUT1 plasma membrane translocation...
July 6, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28593174/current-evidence-for-a-role-of-neuropeptides-in-the-regulation-of-autophagy
#13
REVIEW
Elisabetta Catalani, Clara De Palma, Cristiana Perrotta, Davide Cervia
Neuropeptides drive a wide diversity of biological actions and mediate multiple regulatory functions involving all organ systems. They modulate intercellular signalling in the central and peripheral nervous systems as well as the cross talk among nervous and endocrine systems. Indeed, neuropeptides can function as peptide hormones regulating physiological homeostasis (e.g., cognition, blood pressure, feeding behaviour, water balance, glucose metabolism, pain, and response to stress), neuroprotection, and immunomodulation...
2017: BioMed Research International
https://www.readbyqxmd.com/read/28590260/ghrelin-and-autophagy
#14
Silvia Ezquerro, Gema Frühbeck, Amaia Rodríguez
PURPOSE OF REVIEW: A compromised autophagy is associated with the onset of obesity, type 2 diabetes, nonalcoholic fatty liver disease, cardiovascular and neurodegenerative diseases. Our aim is to review the potential role of ghrelin, a gut hormone involved in energy homeostasis, in the regulation of autophagy. RECENT FINDINGS: In the recent years, it has been demonstrated that autophagy constitutes an important mechanism by which ghrelin exerts a plethora of central and peripheral actions...
June 3, 2017: Current Opinion in Clinical Nutrition and Metabolic Care
https://www.readbyqxmd.com/read/28580387/impaired-glucose-tolerance-attenuates-bone-accrual-by-promoting-the-maturation-of-osteoblasts-role-of-beclin1-mediated-autophagy
#15
E Rendina-Ruedy, J L Graef, S A Lightfoot, J W Ritchey, S L Clarke, E A Lucas, B J Smith
Patients with type 2 diabetes mellitus (T2DM) experience a 1.5-3.5 fold increase in fracture risk, but the mechanisms responsible for these alterations in bone biomechanical properties remain elusive. Macroautophagy, often referred to as autophagy, is regulated by signaling downstream of the insulin receptor. Metabolic changes associated with the progression of glucose intolerance have been shown to alter autophagy in various tissues, but limited information is available in relation to bone cells. The aim of this study was to (a) investigate whether autophagy is altered in bone tissue during impaired glucose tolerance, and (b) determine how autophagy impacts osteoblast differentiation, activity, and maturation...
December 2016: Bone Reports
https://www.readbyqxmd.com/read/28575849/the-nucleocytoplasmic-translocation-and-up-regulation-of-ing5-protein-in-breast-cancer-a-potential-target-for-gene-therapy
#16
Xiao-Qing Ding, Shuang Zhao, Lei Yang, Xin Zhao, Gui-Feng Zhao, Shu-Peng Zhao, Zhi-Jie Li, Hua-Chuan Zheng
Here, we found that ING5 overexpression resulted in a lower proliferation, reduced glucose metabolism, S arrest, decreased migration and invasion, apoptotic induction, fat accumulation, autophagy, senescence and mesenchymal-epithelial-transition of breast cancer cells. It also suppressed the tumor growth of breast cancer cells by inhibiting proliferation, inducing apoptosis and autophagy. ING5-mediated chemoresistance was positively linked to Akt and NF-κB activation, MRP1 and GST-π overexpression, and FBXW7 hypoexpression...
May 17, 2017: Oncotarget
https://www.readbyqxmd.com/read/28574511/signalome-wide-rnai-screen-identifies-gba1-as-a-positive-mediator-of-autophagic-cell-death
#17
Santosh K Dasari, Shani Bialik, Smadar Levin-Zaidman, Vered Levin-Salomon, Alfred H Merrill, Anthony H Futerman, Adi Kimchi
Activating alternative cell death pathways, including autophagic cell death, is a promising direction to overcome the apoptosis resistance observed in various cancers. Yet, whether autophagy acts as a death mechanism by over consumption of intracellular components is still controversial and remains undefined at the ultrastructural and the mechanistic levels. Here we identified conditions under which resveratrol-treated A549 lung cancer cells die by a mechanism that fulfills the previous definition of autophagic cell death...
June 2, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28558013/downregulation-of-sirt1-signaling-underlies-hepatic-autophagy-impairment-in-glycogen-storage-disease-type-ia
#18
Jun-Ho Cho, Goo-Young Kim, Chi-Jiunn Pan, Javier Anduaga, Eui-Ju Choi, Brian C Mansfield, Janice Y Chou
A deficiency in glucose-6-phosphatase-α (G6Pase-α) in glycogen storage disease type Ia (GSD-Ia) leads to impaired glucose homeostasis and metabolic manifestations including hepatomegaly caused by increased glycogen and neutral fat accumulation. A recent report showed that G6Pase-α deficiency causes impairment in autophagy, a recycling process important for cellular metabolism. However, the molecular mechanism underlying defective autophagy is unclear. Here we show that in mice, liver-specific knockout of G6Pase-α (L-G6pc-/-) leads to downregulation of sirtuin 1 (SIRT1) signaling that activates autophagy via deacetylation of autophagy-related (ATG) proteins and forkhead box O (FoxO) family of transcriptional factors which transactivate autophagy genes...
May 2017: PLoS Genetics
https://www.readbyqxmd.com/read/28552719/regulation-of-longevity-by-fgf21-interaction-between-energy-metabolism-and-stress-responses
#19
REVIEW
Antero Salminen, Kai Kaarniranta, Anu Kauppinen
Fibroblast growth factor 21 (FGF21) is a hormone-like member of FGF family which controls metabolic multiorgan crosstalk enhancing energy expenditure through glucose and lipid metabolism. In addition, FGF21 acts as a stress hormone induced by endoplasmic reticulum stress and dysfunctions of mitochondria and autophagy in several tissues. FGF21 also controls stress responses and metabolism by modulating the functions of somatotropic axis and hypothalamic-pituitary-adrenal (HPA) pathway. FGF21 is a potent longevity factor coordinating interactions between energy metabolism and stress responses...
August 2017: Ageing Research Reviews
https://www.readbyqxmd.com/read/28552616/nucleus-translocated-acss2-promotes-gene-transcription-for-lysosomal-biogenesis-and-autophagy
#20
Xinjian Li, Willie Yu, Xu Qian, Yan Xia, Yanhua Zheng, Jong-Ho Lee, Wei Li, Jianxin Lyu, Ganesh Rao, Xiaochun Zhang, Chao-Nan Qian, Steven G Rozen, Tao Jiang, Zhimin Lu
Overcoming metabolic stress is a critical step in tumor growth. Acetyl coenzyme A (acetyl-CoA) generated from glucose and acetate uptake is important for histone acetylation and gene expression. However, how acetyl-CoA is produced under nutritional stress is unclear. We demonstrate here that glucose deprivation results in AMP-activated protein kinase (AMPK)-mediated acetyl-CoA synthetase 2 (ACSS2) phosphorylation at S659, which exposed the nuclear localization signal of ACSS2 for importin α5 binding and nuclear translocation...
June 1, 2017: Molecular Cell
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