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https://www.readbyqxmd.com/read/28089623/which-treatment-for-type-2-diabetes-associated-with-non-alcoholic-fatty-liver-disease
#1
REVIEW
Arianna Mazzotti, Maria Turchese Caletti, Francesca Marchignoli, Giulia Forlani, Giulio Marchesini
Type 2 diabetes (T2DM) and nonalcoholic fatty liver disease (NAFLD) are highly prevalent in the community, and share common pathogenic mechanisms. There is also evidence that T2DM may be favored by hepatic fat accumulation; in turn the presence of T2DM is a risk factor for liver disease progression. The treatment of T2DM has considerably changed in the past few years; new drug classes, promoting glucose-lowering through mechanisms different from classical insulin-sensitizing or insulin-secreting action, have been added to continuing lifestyle intervention...
December 30, 2016: Digestive and Liver Disease
https://www.readbyqxmd.com/read/28089566/metformin-inhibits-hepatic-mtorc1-signaling-via-dose-dependent-mechanisms-involving-ampk-and-the-tsc-complex
#2
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/28088698/metformin-enhancing-the-antitumor-efficacy-of-carboplatin-against-ehrlich-solid-carcinoma-grown-in-diabetic-mice-effect-on-igf-1-and-tumoral-expression-of-igf-1-receptors
#3
Dina M Abo-Elmatty, Eman A Ahmed, Mona K Tawfik, Seham A Helmy
Diabetes has been listed as a risk factor for various types of cancer. Cancer cell development can be promoted by increased levels of IGF-1 and hyperinsulinemia that are associated with diabetes type II. Metformin is an anti-diabetic agent and its potential antitumor impact has become the objective of numerous studies. In this vein, we hypothesize that using metformin in diabetes type II mice may synergistic with carboplatin for reducing the risk of cancer. Therefore, the study aimed to evaluate the in vivo antitumor activity of metformin against solid EAC tumor growth in female diabetic mice and its potential pro-apoptotic and anti-proliferative effects with clarification of its inconclusive biological mechanisms...
January 12, 2017: International Immunopharmacology
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
#4
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
#5
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/28068351/phenotype-and-tissue-expression-as-a-function-of-genetic-risk-in-polycystic-ovary-syndrome
#6
Cindy T Pau, Tim Mosbruger, Richa Saxena, Corrine K Welt
Genome-wide association studies and replication analyses have identified (n = 5) or replicated (n = 10) DNA variants associated with risk for polycystic ovary syndrome (PCOS) in European women. However, the causal gene and underlying mechanism for PCOS risk at these loci have not been determined. We hypothesized that analysis of phenotype, gene expression and metformin response as a function of genotype would identify candidate genes and pathways that could provide insight into the underlying mechanism for risk at these loci...
2017: PloS One
https://www.readbyqxmd.com/read/28062414/a-novel-complex-i-inhibitor-protects-against-hypertension-induced-left-ventricular-hypertrophy
#7
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/28060743/2017-update-on-the-relationship-between-diabetes-and-colorectal-cancer-epidemiology-potential-molecular-mechanisms-and-therapeutic-implications
#8
REVIEW
Nieves González, Isabel Prieto, Laura Del Puerto-Nevado, Sergio Portal-Nuñez, Juan Antonio Ardura, Marta Corton, Beatriz Fernández-Fernández, Oscar Aguilera, Carmen Gomez-Guerrero, Sebastián Mas, Juan Antonio Moreno, Marta Ruiz-Ortega, Ana Belen Sanz, Maria Dolores Sanchez-Niño, Federico Rojo, Fernando Vivanco, Pedro Esbrit, Carmen Ayuso, Gloria Alvarez-Llamas, Jesús Egido, Jesús García-Foncillas, Alberto Ortiz, Diabetes Cancer Connect Consortium
Worldwide deaths from diabetes mellitus (DM) and colorectal cancer increased by 90% and 57%, respectively, over the past 20 years. The risk of colorectal cancer was estimated to be 27% higher in patients with type 2 DM than in non-diabetic controls. However, there are potential confounders, information from lower income countries is scarce, across the globe there is no correlation between DM prevalence and colorectal cancer incidence and the association has evolved over time, suggesting the impact of additional environmental factors...
January 3, 2017: Oncotarget
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/28052534/metformin-a-review-of-its-history-and-future-from-lilac-to-longevity
#10
REVIEW
Inas Thomas, Brigid Gregg
Metformin is a widely prescribed medication that has been used to treat children with type 2 diabetes in the United States for the past 15 years. Metformin now has a variety of clinical applications in pediatrics, and its potential clinical uses continue to expand. In addition to reviewing the current understanding of its mechanisms of action including the newly discovered effects on the gastrointestinal tract, we will also discuss current clinical uses in pediatrics, including in type 1 diabetes. Finally, we examine the existing state of monitoring for metformin efficacy and side effects and discuss prospective future clinical uses...
February 2017: Pediatric Diabetes
https://www.readbyqxmd.com/read/28052008/targeting-p-glycoprotein-function-p53-and-energy-metabolism-combination-of-metformin-and-2-deoxyglucose-reverses-the-multidrug-resistance-of-mcf-7-dox-cells-to-doxorubicin
#11
Chaojun Xue, Changyuan Wang, Yaoting Sun, Qiang Meng, Zhihao Liu, Xiaokui Huo, Pengyuan Sun, Huijun Sun, Xiaodong Ma, Xiaochi Ma, Jinyong Peng, Kexin Liu
Multidrug resistance(MDR) is a major obstacle to efficiency of breast cancer chemotherapy. We investigated whether combination of metformin and 2-deoxyglucose reverses MDR of MCF-7/Dox cells and tried to elucidate the possible mechanisms. The combination of metformin and 2-deoxyglucose selectively enhanced cytotoxicity of doxorubicin against MCF-7/Dox cells. Combination of the two drugs resumed p53 function via inhibiting overexpression of murine doubleminute 2(MDM2) and murine doubleminute 4(MDM4) leading to G2/M arrest and apoptosis in MCF-7/Dox cells...
December 30, 2016: Oncotarget
https://www.readbyqxmd.com/read/28049772/placing-the-nuclear-pore-in-the-metformin-mechanism-of-action
#12
Nancy R Gough
No abstract text is available yet for this article.
January 3, 2017: Science Signaling
https://www.readbyqxmd.com/read/28045889/metformin-induces-growth-inhibition-and-cell-cycle-arrest-by-upregulating-microrna34a-in-renal-cancer-cells
#13
Wei Xie, Lei Wang, Halei Sheng, Jing Qiu, Di Zhang, Le Zhang, Fan Yang, Dahai Tang, Kebin Zhang
BACKGROUND Metformin is a widely used biguanide drug for the treatment of type 2 diabetes. It has been revaluated as a potential anti-cancer drug with promising activity in various tumors. However, the precise mechanisms underlying the suppression of cancer cells by metformin remain not well understood. MATERIAL AND METHODS In this study, human renal cell carcinoma cell line ACHN was used to investigate the anti-proliferation effect of metformin. A cell counting kit-8 assay was used to detect the cell viability...
January 3, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/28042024/metformin-ameliorates-high-uric-acid-induced-insulin-resistance-in-skeletal-muscle-cells
#14
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
#15
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/28025449/metformin-enhances-osteogenesis-and-suppresses-adipogenesis-of-human-chorionic-villous-mesenchymal-stem-cells
#16
Qiaoli Gu, Yanzheng Gu, Huilin Yang, Qin Shi
Metformin is the first-line anti-hyperglycemic drugs commonly used to treat type 2 diabetes. Recent studies have shown that metformin can enhance bone formation through induction of endothelial nitric oxide synthase (eNOS). Human chorionic villous mesenchymal stem cells (CV-MSCs) are promising candidates for regenerative medicine. The present study aimed to investigate the effects of metformin on the osteogenic and adipocytic differentiation of human CV-MSCs, and to elucidate the underlying mechanism. CV-MSCs, prepared from human term placentae, were cultured with different concentrations of metformin...
2017: Tohoku Journal of Experimental Medicine
https://www.readbyqxmd.com/read/28017679/metformin-protects-the-brain-against-ischemia-reperfusion-injury-through-pi3k-akt1-jnk3-signaling-pathways-in-rats
#17
Xu-Hua Ge, Guo-Ji Zhu, De-Qin Geng, Han-Zhi Zhang, Juan-Mei He, Ai-Zhen Guo, Lin-Lin Ma, De-Hua Yu
Although Metformin, a first-line antidiabetic drug, can ameliorate ischemia/reperfusion (I/R) induced brain damage, but how metformin benefits injured hippocampus and the mechanisms are still largely unknown. Therefore, the aim of this study was to investigate the neuroprotective mechanisms of metformin against ischemic brain damage induced by cerebral I/R and to explore whether the Akt-mediated down-regulation of the phosphorylation of JNK3 signaling pathway contributed to the protection provided by metformin...
December 23, 2016: Physiology & Behavior
https://www.readbyqxmd.com/read/28011481/metformin-exerts-antiproliferative-and-anti-metastatic-effects-against-cholangiocarcinoma-cells-by-targeting-stat3-and-nf-%C3%A4-b
#18
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/27990091/novel-applications-of-cox-2-inhibitors-metformin-and-statins-for-the-primary-chemoprevention-of-breast-cancer
#19
REVIEW
Darren Micallef, Sarah Micallef, Pierre Schembri-Wismayer, Jean Calleja-Agius
Recent evidence shows that commonly prescribed drugs, such as non-steroidal anti-inflammatory drugs (NSAIDs), metformin, and statins, may have beneficial roles in the primary chemoprevention of breast cancer. Therefore, these drugs could potentially be used in addition to the hormonal drugs currently used for this purpose (namely, selective estrogen receptor modulators and aromatase inhibitors) due to their alternative mechanisms of action.
2016: Journal of the Turkish German Gynecological Association
https://www.readbyqxmd.com/read/27987248/understanding-and-overcoming-metformin-gastrointestinal-intolerance
#20
REVIEW
Fabrice Bonnet, André Scheen
Metformin is the most widely prescribed drug for patients with type 2 diabetes mellitus and the first-line pharmacologic option as supported by multiple international guidelines, yet a rather large proportion of patients cannot tolerate metformin in adequate amounts because of its associated gastrointestinal (GI) adverse events (AEs). GI AEs typically encountered with metformin therapy include diarrhoea, nausea, flatulence, indigestion, vomiting, and abdominal discomfort, with diarrhoea and nausea being the most common...
December 17, 2016: Diabetes, Obesity & Metabolism
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