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Metformin AND AMPK

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https://www.readbyqxmd.com/read/28099155/metformin-promotes-apoptosis-in-hepatocellular-carcinoma-through-the-cebpd-induced-autophagy-pathway
#1
Hsin-Hwa Tsai, Hong-Yue Lai, Yueh-Chiu Chen, Chien-Feng Li, Huei-Sheng Huang, Hsiao-Sheng Liu, Yau-Sheng Tsai, Ju-Ming Wang
Metformin, as an AMP-activated protein kinase (AMPK) activator, can activate autophagy. A study showed that metformin decreased the risk of hepatocellular carcinoma (HCC) in diabetic patients. However, the detailed mechanism in the metformin-mediated anticancer effect remains an open question. Transcription factor CCAAT/enhancer-binding protein delta (CEBPD) has been suggested to serve as a tumor suppressor and is responsive to multiple anticancer drugs in HCC. In this study, we found that CEBPD and autophagy are involved in metformin-induced cell apoptosis in Huh7 cells...
January 13, 2017: Oncotarget
https://www.readbyqxmd.com/read/28092166/subchronic-metformin-pretreatment-enhances-novel-object-recognition-memory-task-in-forebrain-ischemia-behavioural-molecular-and-electrophysiological-studies
#2
Ghorbangol Ashabi, Alireza Sarkaki, Fariba Khodagholi, Shima Zareh Shahamati, Mahdi Goudarzvand, Yaghoob Farbood, Mohammad Badavi, Leila Khalaj
Metformin exerts its effect via AMP-activated protein kinase (AMPK), which is a key sensor for energy homeostasis that regulates different intracellular pathways. Metformin attenuates oxidative stress and cognitive impairment. In our experiment, rats were divided into 8 groups; some were pretreated with metformin (Met, 200 mg/kg) and (or) the AMPK inhibitor Compound C (CC) for 14 days. On day 14, rats underwent transient forebrain global ischemia. Data indicated that pretreatment of ischemic rats with metformin reduced working memory deficits in a novel object recognition test compared to group with ischemia-reperfusion (I-R) (P < 0...
November 4, 2016: Canadian Journal of Physiology and Pharmacology
https://www.readbyqxmd.com/read/28089566/metformin-inhibits-hepatic-mtorc1-signaling-via-dose-dependent-mechanisms-involving-ampk-and-the-tsc-complex
#3
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/28087254/anti-diabetic-drug-metformin-dilates-retinal-blood-vessels-through-activation-of-amp-activated-protein-kinase-in-rats
#4
Asami Mori, Eriko Ishikawa, Tomoyo Amano, Kenji Sakamoto, Tsutomu Nakahara
The aim of this study was to examine whether metformin, a biguanide anti-hyperglycemic drug, dilates retinal blood vessels in rats. Ocular fundus images were captured with an original high-resolution digital fundus camera in vivo and diameters of retinal blood vessels were measured. Both systemic blood pressure and heart rate were continuously recorded. Metformin (0.01-0.3mg/kg/min) increased diameters of retinal blood vessels in a dose-dependent manner. This retinal vasodilator effect of metformin was abolished by compound C, an inhibitor of AMP-activated protein kinase (AMPK), and N(G)-nitro-L-arginine methyl ester, an inhibitor of nitric oxide (NO) synthase...
January 10, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28074493/ampk-does-not-play-a-requisite-role-in-regulation-of-ppargc1a-gene-expression-via-the-alternative-promoter-in-endurance-trained-human-skeletal-muscle
#5
Daniil V Popov, Evgeny A Lysenko, Alexey D Butkov, Tatiana F Vepkhvadze, Dmitriy V Perfilov, Olga L Vinogradova
In human skeletal muscle, PGC-1α is constitutively expressed via the canonical promoter. By contrast, the expression of PGC-1α mRNA via the alternative promoter was found to be highly dependent on the intensity of exercise and to contribute largely to the post-exercise increase of total PGC-1α mRNA. This study investigated the role of AMPK in regulating PGC-1α gene expression via the alternative promoter through a cAMP responsive element-binding protein-1 (CREB1)-dependent mechanism in human skeletal muscle...
January 10, 2017: Experimental Physiology
https://www.readbyqxmd.com/read/28068384/hypoxia-regulates-mtorc1-mediated-keratinocyte-motility-and-migration-via-the-ampk-pathway
#6
Tiantian Yan, Junhui Zhang, Di Tang, Xingyue Zhang, Xupin Jiang, Liping Zhao, Qiong Zhang, Dongxia Zhang, Yuesheng Huang
Keratinocyte migration, the initial event and rate-limiting step in wound healing, plays a vital role in restoration of the intact skin barrier, also known as re-epithelialization. After acute tissue injury, hypoxic microenvironment gradually develops and acts as an early stimulus to initiate the healing process. Although we have previously found that hypoxia induces keratinocyte migration, the underlying mechanism remains unknown. Here, we first observed that hypoxia increased mTORC1 activity. Recombinant lentivirus vector and Rapamycin were used for silencing mTORC1 in HaCaT cells and primary mouse keratinocytes (MKs)...
2017: PloS One
https://www.readbyqxmd.com/read/28065882/rescue-of-mutant-rhodopsin-traffic-by-metformin-induced-ampk-activation-accelerates-photoreceptor-degeneration
#7
Dimitra Athanasiou, Monica Aguila, Chikwado A Opefi, Kieron South, James Bellingham, Dalila Bevilacqua, Peter M Munro, Naheed Kanuga, Francesca E Mackenzie, Adam M Dubis, Anastasios Georgiadis, Anna B Graca, Rachael A Pearson, Robin R Ali, Sanae Sakami, Krzysztof Palczewski, Michael Y Sherman, Philip J Reeves, Michael E Cheetham
Protein misfolding caused by inherited mutations leads to loss of protein function and potentially toxic 'gain of function', such as the dominant P23H rhodopsin mutation that causes retinitis pigmentosa (RP). Here, we tested whether the AMPK activator metformin could affect the P23H rhodopsin synthesis and folding. In cell models, metformin treatment improved P23H rhodopsin folding and traffic. In animal models of P23H RP, metformin treatment successfully enhanced P23H traffic to the rod outer segment, but this led to reduced photoreceptor function and increased photoreceptor cell death...
January 7, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28062414/a-novel-complex-i-inhibitor-protects-against-hypertension-induced-left-ventricular-hypertrophy
#8
Nobutoshi Matsumura, Ian M Robertson, Shereen M Hamza, Carrie-Lynn M Soltys, Miranda M Sung, Grant Masson, Donna L Beker, Jason R B Dyck
Since left ventricular hypertrophy (LVH) increases the susceptibility for the development of other cardiac conditions, pharmacotherapy that mitigates pathological cardiac remodeling may prove to be beneficial in patients with LVH. Previous work has shown that the activation of the energy-sensing kinase, AMP-activated protein kinase (AMPK), can inhibit some of the molecular mechanisms that are involved in LVH. Of interest, metformin activates AMPK through its inhibition of mitochondrial complex 1 in the electron transport chain, and can prevent LVH induced by pressure overload...
January 6, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28054981/the-root-extract-of-pueraria-lobata-and-its-main-compound-puerarin-prevent-obesity-by-increasing-the-energy-metabolism-in-skeletal-muscle
#9
Hyo Won Jung, An Na Kang, Seok Yong Kang, Yong-Ki Park, Mi Young Song
Radix Pueraria lobata (RP) has been reported to prevent obesity and improve glucose metabolism; however, the mechanism responsible for these effects has not been elucidated. The mechanism underlying anti-obesity effect of RP was investigated in high-fat diet (HFD) induced obese mice and skeletal muscle cells (C2C12). Five-week-old C5BL/6 mice were fed a HFD containing or not containing RP (100 or 300 mg/kg) or metformin (250 mg/kg) for 16 weeks. RP reduced body weight gain, lipid accumulation in liver, and adipocyte and blood lipid levels...
January 4, 2017: Nutrients
https://www.readbyqxmd.com/read/28042024/metformin-ameliorates-high-uric-acid-induced-insulin-resistance-in-skeletal-muscle-cells
#10
Huier Yuan, Yaqiu Hu, Yuzhang Zhu, Yongneng Zhang, Chaohuan Luo, Zhi Li, Tengfei Wen, Wanling Zhuang, Jinfang Zou, Liangli Hong, Xin Zhang, Ichiro Hisatome, Tetsuya Yamamoto, Jidong Cheng
Hyperuricemia occurs together with abnormal glucose metabolism and insulin resistance. Skeletal muscle is an important organ of glucose uptake, disposal, and storage. Metformin activates adenosine monophosphate-activated protein kinase (AMPK) to regulate insulin signaling and promote the translocation of glucose transporter type 4 (GLUT4), thereby stimulating glucose uptake to maintain energy balance. Our previous study showed that high uric acid (HUA) induced insulin resistance in skeletal muscle tissue. However, the mechanism of metformin ameliorating UA-induced insulin resistance in muscle cells is unknown and we aimed to determine it...
December 29, 2016: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/28035400/ampk-activators-suppress-breast-cancer-cell-growth-by-inhibiting-dvl3-facilitated-wnt-%C3%AE-catenin-signaling-pathway-activity
#11
Yu-Feng Zou, Chun-Wei Xie, Shi-Xin Yang, Jian-Ping Xiong
Adenosine monophosphate-activated protein kinase (AMPK) is a principal regulator of metabolism and the conservation of energy in cells, and protects them from exposure to various stressors. AMPK activators may exhibit therapeutic potential as suppressors of cell growth; however, the molecular mechanism underlying this phenomenon in various cancer cells remains to be fully elucidated. The present study investigated the effects of AMPK activators on breast cancer cell growth and specified the underlying molecular mechanism...
February 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28030813/stattic-and-metformin-inhibit-brain-tumor-initiating-cells-by-reducing-stat3-phosphorylation
#12
Verena Leidgens, Judith Proske, Lisa Rauer, Sylvia Moeckel, Kathrin Renner, Ulrich Bogdahn, Markus J Riemenschneider, Martin Proescholdt, Arabel Vollmann-Zwerenz, Peter Hau, Corinna Seliger
Glioblastoma (GBM) is the most common and malignant type of primary brain tumor and associated with a devastating prognosis. Signal transducer and activator of transcription number 3 (STAT3) is an important pathogenic factor in GBM and can be specifically inhibited with Stattic. Metformin inhibits GBM cell proliferation and migration. Evidence from other tumor models suggests that metformin inhibits STAT3, but there is no specific data on brain tumor initiating cells (BTICs).We explored proliferation and migration of 7 BTICs and their differentiated counterparts (TCs) after treatment with Stattic, metformin or the combination thereof...
December 24, 2016: Oncotarget
https://www.readbyqxmd.com/read/28018360/atp-induced-inflammasome-activation-and-pyroptosis-is-regulated-by-amp-activated-protein-kinase-in-macrophages
#13
Qing-Bing Zha, Hong-Xia Wei, Chen-Guang Li, Yi-Dan Liang, Li-Hui Xu, Wen-Jing Bai, Hao Pan, Xian-Hui He, Dong-Yun Ouyang
Adenosine triphosphate (ATP) is released by bacteria and host cells during bacterial infection as well as sterile tissue injury, acting as an inducer of inflammasome activation. Previous studies have shown that ATP treatment leads to AMP-activated protein kinase (AMPK) activation. However, it is unclear whether AMPK signaling has been involved in the regulation of ATP-induced inflammasome activation and subsequent pyroptosis. In this study, we aimed to investigate this issue in lipopolysaccharide-activated murine macrophages...
2016: Frontiers in Immunology
https://www.readbyqxmd.com/read/28011481/metformin-exerts-antiproliferative-and-anti-metastatic-effects-against-cholangiocarcinoma-cells-by-targeting-stat3-and-nf-%C3%A4-b
#14
Charupong Saengboonmee, Wunchana Seubwai, Ubon Cha'on, Kanlayanee Sawanyawisuth, Sopit Wongkham, Chaisiri Wongkham
BACKGROUND/AIM: Cholangiocarcinoma (CCA) is an aggressive cancer for which standard treatments are still ineffective. This study demonstrated the antiproliferative and anti-metastatic activity of metformin, an anti-diabetic drug, in CCA cells. MATERIALS AND METHODS: Cell proliferation, migration/invasion and anoikis resistance were determined. The underlying mechanisms were identified using western blotting and immunocytofluorescence. RESULTS: Metformin significantly suppressed proliferation of CCA cells in a dose- and time-dependent manner, regardless of glucose present in the medium...
January 2017: Anticancer Research
https://www.readbyqxmd.com/read/28009869/the-protective-effect-of-betulinic-acid-ba-diabetic-nephropathy-on-streptozotocin-stz-induced-diabetic-rats
#15
Rui Xie, Hong Zhang, Xing-Zhou Wang, Xiao-Zhong Yang, Shang-Nong Wu, Hong-Gang Wang, Peng Shen, Tian-Heng Ma
The present study was designed to investigate the protective effect of betulinic acid (BA) on streptozotocin (STZ)-induced diabetic rats. The rats were intraperitoneally injected with STZ (35 mg kg(-1)). 7 days later, the animals were intragastrically administered with metformin (MET, 150 mg kg(-1)), BA (20 mg kg(-1)) or BA (40 mg kg(-1)) once daily for consecutive 30 days. The blood glucose, the contents of insulin, interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in serum were examined...
December 23, 2016: Food & Function
https://www.readbyqxmd.com/read/28002460/metformin-improves-ileal-epithelial-barrier-function-in-interleukin-10-deficient-mice
#16
Yansong Xue, Hanying Zhang, Xiaofei Sun, Mei-Jun Zhu
BACKGROUND AND AIMS: The impairment of intestinal epithelial barrier is the main etiologic factor of inflammatory bowel disease. The proper intestinal epithelial proliferation and differentiation is crucial for maintaining intestinal integrity. Metformin is a common anti-diabetic drug. The objective is to evaluate the protective effects of metformin on ileal epithelial barrier integrity using interleukin-10 deficient (IL10KO) mice. METHODS: Wild-type and IL10KO mice were fed with/without metformin for 6 weeks and then ileum was collected for analyses...
2016: PloS One
https://www.readbyqxmd.com/read/27988363/in-vitro-antiglioma-action-of-indomethacin-is-mediated-via-amp-activated-protein-kinase-mtor-complex-1-signalling-pathway
#17
Aleksandar Pantovic, Mihajlo Bosnjak, Katarina Arsikin, Milica Kosic, Milos Mandic, Biljana Ristic, Jelena Tosic, Danica Grujicic, Aleksandra Isakovic, Nikola Micic, Vladimir Trajkovic, Ljubica Harhaji-Trajkovic
We investigated the role of the intracellular energy-sensing AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway in the in vitro antiglioma effect of the cyclooxygenase (COX) inhibitor indomethacin. Indomethacin was more potent than COX inhibitors diclofenac, naproxen, and ketoprofen in reducing the viability of U251 human glioma cells. Antiglioma effect of the drug was associated with p21 increase and G2M cell cycle arrest, as well as with oxidative stress, mitochondrial depolarization, caspase activation, and the induction of apoptosis...
December 14, 2016: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/27957796/involvement-of-ampk-in-regulating-the-degradation-of-mad2b-under-high-glucose-in-neuronal-cells
#18
Xianfang Meng, Guangpin Chu, Chen Ye, Hui Tang, Ping Qiu, Yue Hu, Man Li, Chun Zhang
Although our recent study has demonstrated that mitotic spindle assembly checkpoint protein (MAD2B) mediates high glucose-induced neuronal apoptosis, the mechanisms for MAD2B degradation under hyperglycaemia have not yet been elucidated. In this study, we first found that the activation of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) was decreased in neurons, accompanied with the increased expression of MAD2B. Mechanistically, we demonstrated that activation of AMPK with its activators such as AICAR and metformin decreased the expression of MAD2B, indicating a role of AMPK in regulating the expression of MAD2B...
December 13, 2016: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/27941340/salvianolic-acid-b-ameliorates-hyperglycemia-and-dyslipidemia-in-db-db-mice-through-the-ampk-pathway
#19
Ming-Qing Huang, Cai-Jie Zhou, Yi-Ping Zhang, Xiao-Qin Zhang, Wen Xu, Jing Lin, Pei-Jian Wang
BACKGROUND/AIMS: Salvianolic acid B (Sal B), a major polyphenolic compound of Salvia miltiorrhiza Bunge, has been shown to possess potential antidiabetic activities. However, the action mechanism of SalB in type 2 diabetes has not been investigated extensively. The present study was designed to investigate the effects of Sal B on diabetes-related metabolic changes in a spontaneous model of type 2 diabetes, as well as its potential molecular mechanism. METHODS: Male C57BL/KsJ-db/db mice were orally treated with Sal B (50 and 100 mg/kg) or metformin (positive drug, 300 mg/kg) for 6 weeks...
2016: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/27923278/ampk-serves-as-a-therapeutic-target-against-anemia-of-inflammation
#20
Minjun Wang, Hong Xin, Wenbo Tang, Yiming Li, Zhaoyun Zhang, Linling Fan, Lei Miao, Bo Tan, Xiling Wang, Yi Zhun Zhu
AIMS: Anemia of inflammation (AI), the second prevalent anemia, is associated with worse prognosis and increased mortality in numerous chronic diseases. We recently reported that the gasotransmitter hydrogen sulfide (H2S) suppressed the inflammatory activation of signal transducer and activator of transcription 3 (STAT3) and hepcidin, the critical mediators of AI. Adenosine 5'-monophosphate-activated protein kinase (AMPK) is a novel inflammatory regulator and might be activated by H2S...
January 18, 2017: Antioxidants & Redox Signaling
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