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Glucose metabolism and autophagy

Richard T Jaspers, M Carola Zillikens, Edith C H Friesema, Giuseppe Delli Paoli, Wilhelm Bloch, André G Uitterlinden, Fernando Goglia, Antonia Lanni, Pieter de Lange
Obesity and type 2 diabetes are associated disorders that involve a multiplicity of tissues. Both fasting and physical exercise are known to counteract dyslipidemia/hyperglycemia. Skeletal muscle plays a key role in the control of blood glucose levels, and the metabolic changes and related signaling pathways in skeletal muscle induced by fasting overlap with those induced by exercise. The reduction of fat disposal has been shown to extend to the liver and to white and brown adipose tissue and to involve an increase in their metabolic activities...
October 11, 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
Antoine Heni Chaanine, Erik Kohlbrenner, Scott I Gamb, Adam J Guenzel, Katherine A Klaus, Ahmed U Fayyaz, K Sreekumaran Nair, Roger J Hajjar, Margaret M Redfield
The Forkhead box O3a (FOXO3a) transcription factor has been shown to regulate glucose metabolism, muscle atrophy and cell death in post-mitotic cells. Its role in regulating mitochondrial and myocardial function is not well studied. Based on previous work, we hypothesized that FOXO3a, through BNIP3, modulates mitochondrial morphology and function in HF. We modulated the FOXO3a-BNIP3 pathway in normal and phenylephrine (PE) stressed adult cardiac myocytes (ACM) in vitro and developed a cardiotropic adeno-associated virus serotype 9 encoding dominant-negative FOXO3a (AAV9...
September 30, 2016: American Journal of Physiology. Heart and Circulatory Physiology
Savita Saini, Ayan Kumar Ghosh, Ruby Singh, Sushmita Das, Kumar Abhishek, Ajay Kumar, Sudha Verma, Abhishek Mandal, Abul Hasan Sardar, Bidyut Purkait, Ashish Kumar, Kislay Kumar Sinha, Pradeep Das
Various physiological stimuli trigger the conversion of non-infective L. donovani promastigotes to the infective form. Here we present the first evidence of the effect of glucose starvation, on virulence and survival of these parasites. Glucose starvation resulted in a decrease in metabolically active parasites and their proliferation. However, this was reversed by supplementation of gluconeogenic amino acids. Glucose starvation induced metacyclogenesis and enhanced virulence through protein kinase A regulatory subunit (LdPKAR1) mediated autophagy...
September 24, 2016: Molecular Microbiology
Regina Helena Pires, Thaís Regiani Cataldi, Livia Maria Franceschini, Mônica Veneziano Labate, Ana Marisa Fusco-Almeida, Carlos Alberto Labate, Mario Sérgio Palma, Maria José Soares Mendes-Giannini
AIM: This study aims to understand which Candida orthopsilosis protein aids fungus adaptation upon its switching from planktonic growth to biofilm. MATERIALS & METHODS: Ion mobility separation within mass spectrometry analysis combination were used. RESULTS: Proteins mapped for different biosynthetic pathways showed that selective ribosome autophagy might occur in biofilms. Glucose, used as a carbon source in the glycolytic flux, changed to glycogen and trehalose...
October 2016: Future Microbiology
Laura M Lashinger, Ciara H O'Flanagan, Sarah M Dunlap, Audrey J Rasmussen, Shannon Sweeney, Jessie Yangxiang Guo, Alessia Lodi, Stefano Tiziani, Eileen White, Stephen D Hursting
BACKGROUND: Calorie restriction (CR) prevents obesity and exerts anticancer effects in many preclinical models. CR is also increasingly being used in cancer patients as a sensitizing strategy prior to chemotherapy regimens. While the beneficial effects of CR are widely accepted, the mechanisms through which CR affects tumor growth are incompletely understood. In many cell types, CR and other nutrient stressors can induce autophagy, which provides energy and metabolic substrates critical for cancer cell survival...
2016: Cancer & Metabolism
Lucie Brisson, Piotr Bański, Martina Sboarina, Coralie Dethier, Pierre Danhier, Marie-Joséphine Fontenille, Vincent F Van Hée, Thibaut Vazeille, Morgane Tardy, Jorge Falces, Caroline Bouzin, Paolo E Porporato, Raphaël Frédérick, Carine Michiels, Tamara Copetti, Pierre Sonveaux
Metabolic adaptability is essential for tumor progression and includes cooperation between cancer cells with different metabolic phenotypes. Optimal glucose supply to glycolytic cancer cells occurs when oxidative cancer cells use lactate preferentially to glucose. However, using lactate instead of glucose mimics glucose deprivation, and glucose starvation induces autophagy. We report that lactate sustains autophagy in cancer. In cancer cells preferentially to normal cells, lactate dehydrogenase B (LDHB), catalyzing the conversion of lactate and NAD(+) to pyruvate, NADH and H(+), controls lysosomal acidification, vesicle maturation, and intracellular proteolysis...
September 12, 2016: Cancer Cell
Theodora Tzanavari, Aimilia Varela, Stamatis Theocharis, Elpinickie Ninou, Alkistis Kapelouzou, Dennis V Cokkinos, Maria I Kontaridis, Katia P Karalis
BACKGROUND AND PURPOSE: Metformin administration is associated with myocardial protection during ischemia and/or reperfusion, possibly via inhibition of inflammatory responses in the heart. Exposure to pathogens, in addition to the activation of the immune system and the associated metabolic dysfunction, often results in compromised myocardial function. We examined whether metformin administration could maintain the normal myocardial function in experimental moderate Gram negative infection, induced by lipopolysaccharide (LPS) administration...
October 2016: Metabolism: Clinical and Experimental
Adrien Moya, Nathanaël Larochette, Joseph Paquet, Mickael Deschepper, Morad Bensidhoum, Valentina Izzo, Guido Kroemer, Hervé Petite, Delphine Logeart-Avramoglou
A major impediment to the development of therapies with mesenchymal stem cells/multipotent stromal cells (MSC) is the poor survival and engraftment of MSCs at the site of injury. We hypothesized that lowering the energetic demand of MSCs by driving them into a quiescent state would enhance their survival under ischemic conditions. Human MSCs were induced into quiescence by serum deprivation (SD) for 48h. Such preconditioned cells (SD-hMCs) exhibited reduced nucleotide and protein syntheses compared to unpreconditioned hMSCs...
August 31, 2016: Stem Cells
Xiao-Dan Guo, Guang-Long Sun, Ting-Ting Zhou, Xin Xu, Zhi-Yuan Zhu, Vatcharin Rukachaisirikul, Li-Hong Hu, Xu Shen
AIM: Streptozotocin (STZ) is widely used to induce oxidative damage and to impair glucose metabolism, apoptosis, and tau/Aβ pathology, eventually leading to cognitive deficits in both in vitro and in vivo models of Alzheimer's disease (AD). In this study, we constructed a cell-based platform using STZ to induce stress conditions mimicking the complicated pathologies of AD in vitro, and evaluated the anti-amyloid effects of a small molecule, N-(1,3-benzodioxol-5-yl)-2-[5-chloro-2-methoxy(phenylsulfonyl)anilino]acetamide (LX2343) in the amelioration of cognitive deficits in AD model mice...
September 2016: Acta Pharmacologica Sinica
Zhengtang Qi, Jie Xia, Xiangli Xue, Qiang He, Liu Ji, Shuzhe Ding
Nicotinamide (NAM), or vitamin B3, is an essential coenzyme for ATP synthesis and an inhibitor of sirtuin 1. Recently, conflicting results were reported regarding the treatment of NAM in type 2 diabetes and obesity. The aim of this study was to determine whether and how long-term treatment with NAM at lower dose would affect insulin sensitivity in mice fed chow diet. We treated mice with NAM (100 mg/kg/day) and normal chow for 8 weeks. Strikingly, NAM induced glucose intolerance and skeletal muscle lipid accumulation in nonobese mice...
October 2016: Journal of Nutritional Biochemistry
Navneet Agnihotri, Kapil Mehta
The ability of cancer cells to metastasize represents the most devastating feature of cancer. Currently, there are no specific biomarkers or therapeutic targets that can be used to predict the risk or to treat metastatic cancer. Many recent reports have demonstrated elevated expression of transglutaminase 2 (TG2) in multiple drug-resistant and metastatic cancer cells. TG2 is a multifunctional protein mostly known for catalyzing Ca(2+)-dependent -acyl transferase reaction to form protein crosslinks. Besides this transamidase activity, many Ca(2+)-independent and non-enzymatic activities of TG2 have been identified...
August 25, 2016: Amino Acids
Lara Kern, Johanne Spreckels, Andrea Nist, Thorsten Stiewe, Chrysanthi Skevaki, Brandon Greene, Marco Mernberger, Hans-Peter Elsässer
Autophagy is a lysosomal degradation process involved in the turnover of organelles or other cell constituents, in providing sources for energy production under starving conditions and in cell metabolism. A key protein in the macroautophagic machinery is the autophagy-related protein (Atg) 7. Constitutive deletion of Atg7 is lethal at birth. A conditional deletion of Atg7 in hepatocytes leads to hepatomegaly and in aged animals to liver tumors. With this study, we aim at analyzing the hepatomegaly development in more detail...
August 23, 2016: Cell and Tissue Research
C H Wilson, A Nikolic, S J Kentish, S Shalini, G Hatzinikolas, A J Page, L Dorstyn, S Kumar
Gender-specific differences are commonly found in metabolic pathways and in response to nutritional manipulation. Previously, we identified a role for caspase-2 in age-related glucose homeostasis and lipid metabolism using male caspase-2-deficient (Casp2 (-/-) ) mice. Here we show that the resistance to age-induced glucose tolerance does not occur in female Casp2 (-/-) mice and it appears to be independent of insulin sensitivity in males. Using fasting (18 h) as a means to further investigate the role of caspase-2 in energy and lipid metabolism, we identified sex-specific differences in the fasting response and lipid mobilization...
2016: Cell Death Discovery
Han Sung Kim, Yeong-Min Yoo
Autophagy appears to be involved in maintaining normal intracellular insulin content by accelerating the insulin degradation rate in β-cells (Marsh et al., 2007) [1]. 2-deoxy-d-glucose (2-DG) is metabolized by hexokinase, and acts as an inhibitor of glycolysis. 2-DG triggers glucose deprivation without altering other nutrients or metabolic pathways (Aghaee et al., 2012) [2], and appears to be an ideal tool for studying autophagy. Rapamycin induced upregulation of autophagy in both cultured isolated islets and pancreatic β-cells (Tanemura et al...
September 2016: Data in Brief
Yoon Kyung Jo, Na Yeon Park, So Jung Park, Byung-Gyu Kim, Ji Hyun Shin, Doo Sin Jo, Dong-Jun Bae, Young-Ah Suh, Jeong Ho Chang, Eun Kyung Lee, Sang-Yeob Kim, Jin Cheon Kim, Dong-Hyung Cho
Autophagy is a catabolic degradation process and maintains cellular homeostasis. And autophagy is activated in response to various stress conditions. Although O-GlcNAcylation functions a sensor for nutrient and stress, the relationship between O-GlcNAcylation and autophagy is largely unknown. Here, we identified that ATG4B is novel target for O-GlcNAcylation under metabolic stress condition. Treatment with PugNAc, an O-GlcNAcase inhibitor increased activation of autophagy in SH-SY5Y cells. Both bimolecular fluorescence complementation and immunoprecipitation assay indicated that OGT directly interacts with ATG4B in SH-SY5Y cells...
August 5, 2016: Oncotarget
Cristovão M Sousa, Douglas E Biancur, Xiaoxu Wang, Christopher J Halbrook, Mara H Sherman, Li Zhang, Daniel Kremer, Rosa F Hwang, Agnes K Witkiewicz, Haoqiang Ying, John M Asara, Ronald M Evans, Lewis C Cantley, Costas A Lyssiotis, Alec C Kimmelman
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease characterized by an intense fibrotic stromal response and deregulated metabolism. The role of the stroma in PDAC biology is complex and it has been shown to play critical roles that differ depending on the biological context. The stromal reaction also impairs the vasculature, leading to a highly hypoxic, nutrient-poor environment. As such, these tumours must alter how they capture and use nutrients to support their metabolic needs. Here we show that stroma-associated pancreatic stellate cells (PSCs) are critical for PDAC metabolism through the secretion of non-essential amino acids (NEAA)...
August 25, 2016: Nature
Han Sung Kim, Tae-Young Han, Yeong-Min Yoo
2-DG triggers glucose deprivation without altering other nutrients or metabolic pathways and then activates autophagy via activation of AMPK and endoplasmic reticulum (ER) stress. We investigated whether 2-DG reduced intracellular insulin increased by melatonin via autophagy/EDC3 in insulinoma INS-1E cells. p-AMPK and GRP78/BiP level were significantly increased by 2-DG in the presence/absence of melatonin, but IRE1α level was reduced in 2-DG treatment. Levels of p85α, p110, p-Akt (Ser473, Thr308), and p-mTOR (Ser2481) were also significantly reduced by 2-DG in the presence/absence of melatonin...
2016: Oxidative Medicine and Cellular Longevity
Ferdinando Chiaradonna, Yuri Pirola, Francesca Ricciardiello, Roberta Palorini
Forskolin (FSK) induces activation of protein kinase A (PKA). This activation protects specifically some cancer cells from death induced by glucose starvation. Cell effects upon FSK treatment prompted us to investigate in detail the physiological role of PKA in the activation of pro-survival mechanisms in glucose starvation. In this regard we performed a microarray analysis of normal NIH3T3 and transformed NIH3T3-K-ras mouse fibroblasts cultured at 1 mM glucose and daily treated or not with 10 μM FSK until 72 h of growth, when the samples were collected...
September 2016: Genomics Data
Hidetoshi Mori, Ramray Bhat, Alexandre Bruni-Cardoso, Emily I Chen, Danielle M Jorgens, Kester Coutinho, Katherine Louie, Benjamin Ben Bowen, Jamie L Inman, Victoria Tecca, Sarah J Lee, Sabine Becker-Weimann, Trent Northen, Motoharu Seiki, Alexander D Borowsky, Manfred Auer, Mina J Bissell
Membrane-anchored matrix metalloproteinase 14 (MMP14) is involved broadly in organ development through both its proteolytic and signal-transducing functions. Knockout of Mmp14 (KO) in mice results in a dramatic reduction of body size and wasting followed by premature death, the mechanism of which is poorly understood. Since the mammary gland develops after birth and is thus dependent for its functional progression on systemic and local cues, we chose it as an organ model for understanding why KO mice fail to thrive...
2016: PeerJ
Bo Li, Xinzhe Li, Zhenhong Ni, Yan Zhang, Yijun Zeng, Xiaohuan Yan, Yan Huang, Jintao He, Xilin Lyu, Yaran Wu, Yuting Wang, Yingru Zheng, Fengtian He
Both dichloroacetate (DCA) and metformin (Met) have shown promising antitumor efficacy by regulating cancer cell metabolism. However, the DCA-mediated protective autophagy and Met-induced lactate accumulation limit their tumor-killing potential respectively. So overcoming the corresponding shortages will improve their therapeutic effects. In the present study, we found that DCA and Met synergistically inhibited the growth and enhanced the apoptosis of ovarian cancer cells. Interestingly, we for the first time revealed that Met sensitized DCA via dramatically attenuating DCA-induced Mcl-1 protein and protective autophagy, while DCA sensitized Met through markedly alleviating Met-induced excessive lactate accumulation and glucose consumption...
July 19, 2016: Oncotarget
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