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AMPKα

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https://www.readbyqxmd.com/read/29785900/insulin-suppresses-the-ampk-signaling-pathway-to-regulate-lipid-metabolism-in-primary-cultured-hepatocytes-of-dairy-cows
#1
Xinwei Li, Yu Li, Hongyan Ding, Jihong Dong, Renhe Zhang, Dan Huang, Lin Lei, Zhe Wang, Guowen Liu, Xiaobing Li
Dairy cows with type II ketosis display hepatic fat accumulation and hyperinsulinemia, but the underlying mechanism is not completely clear. This study aimed to clarify the regulation of lipid metabolism by insulin in cow hepatocytes. In vitro, cow hepatocytes were treated with 0, 1, 10, or 100 nm insulin in the presence or absence of AICAR (an AMP-activated protein kinase alpha (AMPKα) activator). The results showed that insulin decreased AMPKα phosphorylation. This inactivation of AMPKα increased the gene and protein expression levels of carbohydrate responsive element-binding protein (ChREBP) and sterol regulatory element-binding protein-1c (SREBP-1c), which downregulated the expression of lipogenic genes, thereby decreasing lipid biosynthesis...
May 2018: Journal of Dairy Research
https://www.readbyqxmd.com/read/29771332/mechanisms-of-skeletal-muscle-wasting-in-a-mouse-model-for-myotonic-dystrophy-type-1
#2
Ginny R Morriss, Kimal Rajapakshe, Shixia Huang, Cristian Coarfa, Thomas A Cooper
Myotonic dystrophy type 1 (DM1) is a multisystemic disease resulting in severe muscle weakening and wasting. DM1 is caused by expansion of CTG repeats in the 3'-UTR of the DMPK gene. We have developed an inducible, skeletal muscle-specific mouse model of DM1 (CUG960) that expresses 960 CUG repeats in the context of human DMPK exons 11-15. CUG960 RNA-expressing mice induced at PN1, as well as adult-onset animals, show clear, measurable muscle wasting accompanied by severe histological defects including central myonuclei, reduced fiber cross sectional area, increased percentage of oxidative myofibers, and the presence of nuclear RNA foci that colocalize with Mbnl1 protein...
May 16, 2018: Human Molecular Genetics
https://www.readbyqxmd.com/read/29732320/activation-of-host-ire1%C3%AE-dependent-signaling-axis-contributes-the-intracellular-parasitism-of-brucella-melitensis
#3
Aseem Pandey, Furong Lin, Ana L Cabello, Luciana F da Costa, Xuehuan Feng, Hui-Qiang Feng, Ming-Zhe Zhang, Takao Iwawaki, Allison Rice-Ficht, Thomas A Ficht, Paul de Figueiredo, Qing-Ming Qin
Brucella spp. are intracellular vacuolar pathogens that causes brucellosis, a worldwide zoonosis of profound importance. We previously demonstrated that the activity of host unfolded protein response (UPR) sensor IRE1α (inositol-requiring enzyme 1) and ER-associated autophagy confer susceptibility to Brucella melitensis and Brucella abortus intracellular replication. However, the mechanism by which host IRE1α regulates the pathogen intracellular lifestyle remains elusive. In this study, by employing a diverse array of molecular approaches, including biochemical analyses, fluorescence microscopy imaging, and infection assays using primary cells derived from Ern1 (encoding IRE1) conditional knockout mice, we address this gap in our understanding by demonstrating that a novel IRE1α to ULK1, an important component for autophagy initiation, signaling axis confers susceptibility to Brucella intracellular parasitism...
2018: Frontiers in Cellular and Infection Microbiology
https://www.readbyqxmd.com/read/29695972/exercise-protects-against-defective-insulin-signaling-and-insulin-resistance-of-glucose-transport-in-skeletal-muscle-of-angiotensin-ii-infused-rat
#4
Juthamard Surapongchai, Yupaporn Rattanavichit, Jariya Buniam, Vitoon Saengsirisuwan
Objectives: The present study investigated the impact of voluntary exercise on insulin-stimulated glucose transport and the protein expression and phosphorylation status of the signaling molecules known to be involved in the glucose transport process in the soleus muscle as well as other cardiometabolic risks in a rat model with insulin resistance syndrome induced by chronic angiotensin II (ANGII) infusion. Materials and Methods: Male Sprague-Dawley rats were assigned to sedentary or voluntary wheel running (VWR) groups...
2018: Frontiers in Physiology
https://www.readbyqxmd.com/read/29679571/metformin-ameliorates-tgf-%C3%AE-1-induced-osteoblastic-differentiation-of-human-aortic-valve-interstitial-cells-by-inhibiting-%C3%AE-catenin-signaling
#5
Liu Fayuan, Chu Chong, Wei Qinyu, Shi Jiawei, Li Huadong, Dong Nianguo
Osteoblastic differentiation of aortic valve interstitial cells (AVICs) is the central process in the development of calcific aortic valve disease (CAVD). Metformin is a widely used first-line antidiabetic drug, and recently, pleiotropic benefits of metformin beyond hypoglycemia have been reported in the cardiovascular system. Here, we examined the effect of metformin on the osteoblastic differentiation of human AVICs. Our results showed that metformin ameliorated TGF-β1-induced production of osteogenic proteins Runx2 and osteopontin as well as calcium deposition in the cultured human AVICs...
April 18, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29674687/celecoxib-exerts-protective-effects-in-the-vascular-endothelium-via-cox-2-independent-activation-of-ampk-creb-nrf2-signalling
#6
Fahad Al-Rashed, Damien Calay, Marie Lang, Clare C Thornton, Andrea Bauer, Allan Kiprianos, Dorian O Haskard, Anusha Seneviratne, Joseph J Boyle, Alex H Schönthal, Caroline P Wheeler-Jones, Justin C Mason
Although concern remains about the athero-thrombotic risk posed by cyclo-oxygenase (COX)-2-selective inhibitors, recent data implicates rofecoxib, while celecoxib appears equivalent to NSAIDs naproxen and ibuprofen. We investigated the hypothesis that celecoxib activates AMP kinase (AMPK) signalling to enhance vascular endothelial protection. In human arterial and venous endothelial cells (EC), and in contrast to ibuprofen and naproxen, celecoxib induced the protective protein heme oxygenase-1 (HO-1). Celecoxib derivative 2,5-dimethyl-celecoxib (DMC) which lacks COX-2 inhibition also upregulated HO-1, implicating a COX-2-independent mechanism...
April 19, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29669730/drug-induced-alterations-of-mitochondrial-dna-homeostasis-in-steatotic-and-non-steatotic-heparg-cells
#7
Dounia Le Guillou, Simon Bucher, Karima Begriche, Delphine Hoet, Anne Lombes, Gilles Labbe, Bernard Fromenty
Although mitochondriotoxicity plays a major role in drug-induced hepatotoxicity, alteration of mitochondrial DNA (mtDNA) homeostasis has been described only with a few drugs. Because it requires long drug exposure, this mechanism of toxicity cannot be detected with investigations performed in isolated liver mitochondria or cultured cells exposed to drugs for several hours, or a few days. Thus, a first aim of this study was to determine whether a 2-week treatment with 9 hepatotoxic drugs could affect mtDNA homeostasis in HepaRG cells...
April 18, 2018: Journal of Pharmacology and Experimental Therapeutics
https://www.readbyqxmd.com/read/29663481/the-ampk-v-atpase-ph-axis-a-key-regulator-of-the-pro-fibrogenic-phenotype-of-human-hepatic-stellate-cells
#8
Giusi Marrone, Francesco De Chiara, Katrin Böttcher, Ana Levi, Dipok Dhar, Lisa Longato, Giuseppe Mazza, Zhenzhen Zhang, Martina Marrali, Anabel Fernández- Iglesias, Andrew Hall, Tu Vinh Luong, Benoit Viollet, Massimo Pinzani, Krista Rombouts
Liver fibrosis and cirrhosis are characterized by activation of hepatic stellate cells (HSC) which is associated with higher intracellular pH (pHi). The vacuolar H+ adenosine-tri-phosphatase (v-ATPase) multi-subunit complex is a key regulator of intracellular pH homeostasis. The present work was aimed at investigating the functional role of v-ATPase in primary human HSC (hHSC) activation and its modulation by specific AMPK subunits. Here, we demonstrated that the expression of different v-ATPase subunits was increased in in vivo and in vitro activated hHSC, compared to non-activated hHSC...
April 17, 2018: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/29659128/activation-of-dna-demethylases-attenuates-aging-associated-arterial-stiffening-and-hypertension
#9
Kai Chen, Zhongjie Sun
DNA methylation increases with age. The objective of this study was to investigate whether compound H, a potential activator of DNA demethylases, attenuates aging-related arterial stiffness and hypertension. Aged mice (24-27 months) and adult mice (12 months) were used. Pulse wave velocity (PWV), a direct measure of arterial stiffness, and blood pressure (BP) were increased significantly in aged mice. Notably, daily treatments with compound H (15 mg/kg, IP) for 2 weeks significantly attenuated the aging-related increases in PWV and BP...
April 16, 2018: Aging Cell
https://www.readbyqxmd.com/read/29655602/overexpression-of-ctrp3-protects-against-sepsis-induced-myocardial-dysfunction-in-mice
#10
Wen-Ying Wei, Zhen-Guo Ma, Ning Zhang, Si-Chi Xu, Yu-Pei Yuan, Xiao-Feng Zeng, Qi-Zhu Tang
C1q/tumor necrosis factor-related protein-3 (CTRP3) shows striking homologies of genomic structure to the adiponectin. In this study, we aimed to investigate the protective role of CTRP3 against sepsis-induced cardiomyopathy. Here, we overexpressed CTRP3 in myocardium by direct intramyocardial injection and constructed a model of lipopolysaccharide (LPS)-induced sepsis in mice. Our results demonstrated that cardiac-specific overexpression of CTRP3 remarkably attenuated myocardial dysfunction and increased the phosphorylation level of AMPKα during LPS-induced sepsis...
April 12, 2018: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/29627983/fish-oil-supplementation-alleviates-the-altered-lipid-homeostasis-in-blood-liver-and-adipose-tissues-in-high-fat-diet-fed-rats
#11
Chen-Yuan Chiu, Lou-Pin Wang, Shing-Hwa Liu, Meng Tsan Chiang
This study investigated the effects of dietary supplementation of fish oil on the signals of lipid metabolism involved in hepatic cholesterol and triglyceride influx and excretion in high-fat diet (HFD)-fed rats. Fish oil (FO) repressed body (HFD: 533±18.2 g, HFD+FO: 488±28.0 g, p<0.05) and liver weights (HFD: 5.7±0.6 g/100 g body weight, HFD+FO: 4.8±0.4 g/100 g body weight, p<0.05) in HFD-fed rats. Fish oil could also improve HFD-induced imbalance of lipid metabolism in blood, liver, and adipose tissues including the significant decreases in plasma and liver total cholesterol (TC) (plasma-HFD: 113±33...
April 7, 2018: Journal of Agricultural and Food Chemistry
https://www.readbyqxmd.com/read/29615720/involvement-of-amp-activated-protein-kinase-and-death-receptor-5-in-trail-berberine-induced-apoptosis-of-cancer-cells
#12
Rong Ke, Kanchan Vishnoi, Navin Viswakarma, Sreevidya Santha, Subhasis Das, Ajay Rana, Basabi Rana
Our previous studies indicated that combination of Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and PPARγ ligand Troglitazone (TZD), can induce significant apoptosis in various TRAIL-resistant prostate and hepatocellular carcinoma (HCC) cells. These also suggested serine/threonine kinase AMP-activated protein kinase (AMPK) to be a mediator of TRAIL-TZD-induced apoptosis. To further validate AMPK's role in TRAIL sensitization, we determined the apoptotic potential of TRAIL in combination with the natural compound Berberine (BBR), the latter being a potent activator of AMPK...
April 3, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29615536/protective-effects-of-melatonin-against-nicotine-induced-disorder-of-mouse-early-folliculogenesis
#13
Yu-Feng Wang, Xiao-Feng Sun, Ze-Li Han, Lan Li, Wei Ge, Yong Zhao, Massimo De Felici, Wei Shen, Shun-Feng Cheng
In this paper, we show that neonatal mice injected for five consecutive days with nicotine display impaired germ cell cyst breakdown and primordial follicle assembly resulting in decreased ovarian reserve lasting until sex maturation age. The effects of nicotine on the pups ovaries were associated with decreased expression of oocyte specific genes such as Nobox , Lhx8 , Figlα and Sohlh2 . Moreover, the ovaries of pups injected with nicotine showed increased level of cell oxidative stress and autophagic markers (upregulation of AMPKα-1, increased ratio LC3-II/LC3-I, downregulation of AKT and mTOR)...
March 28, 2018: Aging
https://www.readbyqxmd.com/read/29611102/11%C3%AE-hsd1-inhibition-by-rl-118-promotes-autophagy-and-correlates-with-reduced-oxidative-stress-and-inflammation-enhancing-cognitive-performance-in-samp8-mouse-model
#14
Dolors Puigoriol-Illamola, Christian Griñán-Ferré, Foteini Vasilopoulou, Rosana Leiva, Santiago Vázquez, Mercè Pallàs
Elevated glucocorticoid (GC) exposure is widely accepted as a key factor in the age-related cognitive decline in rodents and humans. 11β-HSD1 is a key enzyme in the GCs pathway, catalyzing the conversion of 11β-dehydrocorticosterone to corticosterone in mice, with possible implications in neurodegenerative processes and cognitive impairment. Here, we determined the effect of a new 11β-HSD1 inhibitor, RL-118, administered to 12-month-old senescence-accelerated mouse-prone 8 (SAMP8) mice with neuropathological AD-like hallmarks and widely used as a rodent model of cognitive dysfunction...
April 2, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29610348/activation-of-ampk-by-metformin-improves-withdrawal-signs-precipitated-by-nicotine-withdrawal
#15
Julia K Brynildsen, Bridgin G Lee, Isaac J Perron, Sunghee Jin, Sangwon F Kim, Julie A Blendy
Cigarette smoking is the leading cause of preventable disease and death in the United States, with more persons dying from nicotine addiction than any other preventable cause of death. Even though smoking cessation incurs multiple health benefits, the abstinence rate remains low with current medications. Here we show that the AMP-activated protein kinase (AMPK) pathway in the hippocampus is activated following chronic nicotine use, an effect that is rapidly reversed by nicotine withdrawal. Increasing pAMPK levels and, consequently, downstream AMPK signaling pharmacologically attenuate anxiety-like behavior following nicotine withdrawal...
April 2, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29577356/ser-486-491-phosphorylation-and-inhibition-of-ampk%C3%AE-activity-is-positively-associated-with-gleason-score-metastasis-and-castration-resistance-in-prostate-cancer-a-retrospective-clinical-study
#16
Melissa A Babcook, Mahmut Akgul, Seunghee Margevicius, Gregory T MacLennan, Pingfu Fu, Robert Abouassaly, Sanjay Gupta
BACKGROUND: We previously demonstrated that adenosine monophosphate-activated protein kinase (AMPKα) activity is significantly inhibited by Ser-486/491 phosphorylation in cell culture and in vivo models of metastatic and castration-resistant prostate cancer, and hypothesized these findings may translate to clinical specimens. METHODS: In this retrospective, single-institution pilot study, 45 metastatic prostate cancer cases were identified within the University Hospitals Cleveland Medical Center Pathology Archive with both metastasis and matched primary prostate tumor specimens in formalin-fixed, paraffin-embedded blocks, and complete electronic medical records...
March 26, 2018: Prostate
https://www.readbyqxmd.com/read/29576467/apelin-and-apelin-receptor-at-different-stages-of-corpus-luteum-development-and-effect-of-apelin-on-progesterone-secretion-and-3%C3%AE-hydroxysteroid-dehydrogenase-3%C3%AE-hsd-in-pigs
#17
Marta Różycka, Patrycja Kurowska, Małgorzata Grzesiak, Małgorzata Kotula-Balak, Wacław Tworzydło, Christelle Rame, Ewa Gregoraszczuk, Joelle Dupont, Agnieszka Rak
Recent studies have suggested that apelin has a role in controlling female reproduction. The aims of the present study were, firstly, to investigate the gene expression (mRNA and protein) and immunolocalization of apelin and its receptor APJ in corpora lutea (CL) of pigs collected during the early (CL1), middle (CL2) and late (CL3) luteal phase. Using real time PCR and immunoblotting techniques, it was observed that apelin gene expression was similar in CL1 and CL2, and less in CL3, while relative abundance APJ mRNA and abundance of the protein were similar in CL1 and CL3 and greater in CL2...
March 20, 2018: Animal Reproduction Science
https://www.readbyqxmd.com/read/29570193/phytol-stimulates-the-browning-of-white-adipocytes-through-the-activation-of-amp-activated-protein-kinase-ampk-%C3%AE-in-mice-fed-high-fat-diet
#18
Fenglin Zhang, Wei Ai, Xiaoquan Hu, Yingying Meng, Cong Yuan, Han Su, Lina Wang, Xiaotong Zhu, Ping Gao, Gang Shu, Qingyan Jiang, Songbo Wang
Stimulating the browning of white adipocytes contributes to the restriction of obesity and related metabolic disorders. This study aimed to investigate the browning effects of phytol on mice inguinal subcutaneous white adipose tissue (iWAT) and explore the underlying mechanisms. Our results demonstrated that phytol administration decreased body weight gain and iWAT index, and stimulated the browning of mice iWAT, with the increased expression of brown adipocyte marker genes (UCP1, PRDM16, PGC1α, PDH, and Cyto C)...
March 23, 2018: Food & Function
https://www.readbyqxmd.com/read/29554648/high-glucose-induced-podocyte-injury-involves-activation-of-mammalian-target-of-rapamycin-mtor-induced-endoplasmic-reticulum-er-stress
#19
Jie Lei, Lei Zhao, Yujing Zhang, Yanfeng Wu, Yanbo Liu
BACKGROUND/AIMS: The mechanisms by which high glucose (HG) results in podocyte damage remains unclear. We investigated the potential role of endoplasmic reticulum (ER) stress and mTOR signaling in HG injured podocyte. METHODS: In cultured mouse podocytes, cellular apoptosis was assessed using FITC-Annexin V and propidium iodide staining followed by flow cytometry analysis. Apoptosis-related proteins as well as the ER stress and the mTOR signals were evaluated using immunoblot assay...
2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29547701/mangiferin-enhances-endochondral-ossification-based-bone-repair-in-massive-bone-defect-by-inducing-autophagy-through-activating-amp-activated-protein-kinase-signaling-pathway
#20
Yun Bai, Chuan Liu, Lei Fu, Xiaoshan Gong, Ce Dou, Zhen Cao, Hongyu Quan, Jianmei Li, Fei Kang, Jingjin Dai, Chunrong Zhao, Shiwu Dong
Endochondral ossification is crucial for bone formation in both adult bone repair process and embryo long-bone development. In endochondral ossification, bone marrow-derived mesenchymal stem cells (BMSCs) first differentiate to chondrocyte, BMSC-derived chondrocyte then endure a hypertrophic process to generate new bone. Endochondral ossification-based bone repair is a promising strategy to cure massive bone defect, which is a major clinical issue in orthopedics. However, challenges still remain for this novel strategy...
March 16, 2018: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
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