Statins And Metformin For Chemoprevention Of Hepatocellular Carcinoma
Hepatocellular carcinoma (HCC) is the sixth most common cancer and the second or third leading cause of death from cancer worldwide, with the uncertainty reflecting the paucity or absence of reliable and accurate estimates in high-incidence countries.[1, 2] Most HCC cases occur in hepatitis B virus (HBV) endemic areas such as East Asia and sub-Saharan Africa.[3] However, the incidence of HCC has been increasing in Western countries over the past several decades, mainly as a result of increasing incidences of chronic hepatitis C, nonalcoholic fatty liver disease, diabetes, and obesity, which are known risk factors for HCC.[4] Although several curative treatment modalities, including surgical resection, radiofrequency ablation, and liver transplantation have been developed to improve the prognosis of HCC, because of the lack of effective surveillance systems for early diagnosis of HCC in both low- and high-resource countries, the 5-year survival rate of HCC is still poor. Because of the dismal prognosis of HCC, chemoprevention is an appealing approach but is unproven at the present time. In this review, we highlight two promising drugs—statins and metformin—for the chemoprevention of HCC. Statins Mechanisms Statins, 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors, are widely used for prevention of cardiovascular and cerebrovascular events because of their lipid-lowering effects. Thus, statins are the second most common prescription drug in the United States, and one in four Americans aged 45 years or older are prescribed statins for cardiovascular disease.[5] Statins have antitumor effects through the following mechanisms: (1) they down-regulate the RAF/mitogen-activated protein kinase 1/extracellular signal-regulated kinase (ERK) pathway, thus reducing ce Continue reading >>
A Molecular Mechanism Whereby Metformin Protects Against Liver Cancer
A molecular mechanism whereby metformin protects against liver cancer A molecular mechanism whereby metformin protects against liver cancer DESCRIPTION (provided by applicant): Nonalcoholic fatty liver disease (NAFLD) and type-2 diabetes (T2D) are associated with increased risk of hepatocellular carcinoma (HCC), and individuals with T2D treated with metformin have a reduced risk of HCC incidence and mortality. Although several factors have been reported to probably mediate the preventive effect of metformin on the risk of several types of cancers, a precise mechanism by which metformin reduces HCC risk remains largely unknown. Specifically, it is not known what cellular factors, targeted by metformin, are critical in the development of HCC in diabetic patients, and which sub- population of patients may be more responsive to metformin treatment. Our long-term goal is to understand the molecular basis of HCC. The objective of this proposal is to unveil the mechanism by which metformin inhibits spontaneous HCC development in mice bearing a heterozygous deletion of the nuclear receptor coactivator-5 (Ncoa5) gene and improve current tools utilizing identified genes and signatures to predict prognosis and response to metformin in patients with HCC. The central hypothesis is that reduced Ncoa5 expression is a key risk factor for HCC development in the context of a diabetic condition, and metformin protects mice against HCC development by reducing hepatic insulin resistance and steatosis, in part by positively regulating the expression of Ncoa5. The rationale for the proposed research is that therapeutic strategies, aimed at increasing Ncoa5 expression or targeting Ncoa5 deficiency driven oncogenic pathways, are potentially effective in protecting against HCC. This hypothesis Continue reading >>
Metformin Effects On The Liver
Physicians commonly prescribe Metformin if you have Type 2 diabetes and need help controlling your blood sugar. It reduces how much glucose you absorb from food and the amount your liver produces. On rare occasions, however, Metformin causes liver dysfunction and a serious metabolic condition involving the liver. For this reason, physicians exercise caution when prescribing Metformin to patients with liver disease. Video of the Day In healthy individuals, the liver produces glucose to keep blood sugar stable when you haven't eaten for several hours. Uncontrolled glucose production in the liver may cause high blood sugar in individuals with Type 2 diabetes. Researchers discovered that Metformin blocks critical enzymes involved in signaling the liver to produce glucose, thereby decreasing blood sugar levels. Their work was reported in the February 2013 edition of the journal "Nature." Lactic Acid Production Your muscles, brain, skin and other tissues produce a substance called lactic acid. Under normal circumstances, your liver and kidneys remove lactic acid from the blood and convert some of it to glucose. If a life-threatening metabolic condition known as lactic acidosis occurs, lactic acid levels increase faster than the liver can keep up with. Though its mechanism is unclear, Metformin causes lactic acidosis in a small segment -- up to 1 percent -- of patients, according to NYU Langone Medical Center. Almost all reported cases occurred in patients with underlying metabolic issues, such as liver or kidney disease. According to LiverTox, a publication of the U.S. National Library of Science drug database, Metformin may occasionally cause mild liver toxicity, characterized by minor elevations in liver enzymes. It occurs in less than 1 percent of the patients taking Metfo Continue reading >>
War On Cancer: Diabetes Drug May Help
All cells possess cell polarity. Its what allows them to perform specific tasks. Polarity lets epithelial cells form protective walls in cavities and organs. The walls protect against toxins, pathogens, and inflammatory triggers. Any crack in the wall can open the door to cancer. The research team identified the mechanism that helps keep the wall strong. Researchers already knew about something called the stress-polarity pathway. As stated in the researchers press release , its a specialized pathway mobilized only during periods of stress. It is orchestrated by a protein kinase called AMPK that protects cellular polarity when epithelial cells are under energetic stress and an activator of AMPK called LBK1. LBK1 is a tumor suppressor. LBK1 mutations are associated with loss of cell polarity and cancer. The mystery was in how the LKB1-AMPK pathway preserves cell polarity during stress. The new research found that the stress-polarity pathway relies on a protein called GIV/Girdin. Metformin affects this protein. "In summary, by identifying GIV/Girdin as a key layer within the stress-polarity pathway we've peeled another layer of the proverbial onion," Dr. Pradipta Ghosh, the studys senior author, said in the press release. Ghosh explained that the research provided new insights into the epithelium-protecting and tumor-suppressive actions of metformin. Read more: Can a positive attitude help defeat cancer? Dr. Timothy Byun is a medical oncologist with the Center for Cancer Prevention and Treatment at St. Joseph Hospital in Southern California. He told Healthline that metformin has several mechanisms that may contribute to its anticancer property. Byun said multiple epidemiologic studies show an association between metformin use and reduced cancer incidence and mortality. It Continue reading >>
Metformin For Liver Cancer Prevention In Patients With Type 2 Diabetes: A Systematic Review And Meta-analysis
Metformin for Liver Cancer Prevention in Patients with Type 2 Diabetes: A Systematic Review and Meta-Analysis Departments of Epidemiology and Biostatistics (Z.-J.Zha., Z.-J.Zhe.), Shanghai 200025, China Address all correspondence and requests for reprints to: Zhi-Jiang Zhang, M.D., Ph.D., Department of Epidemiology, School of Public Health, Shanghai Jiao Tong University, 227 South Chongqing Road, Shanghai 200025, China Search for other works by this author on: Departments of Epidemiology and Biostatistics (Z.-J.Zha., Z.-J.Zhe.), Shanghai 200025, China Search for other works by this author on: Preventive Medicine (R.S.), School of Public Health, Shanghai Jiao Tong University, Shanghai 200025, China Search for other works by this author on: Department of Endocrinology (Q.S.), Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China Search for other works by this author on: Department of Epidemiology (Q.J.), School of Public Health, Fudan University, Shanghai 200032, China Search for other works by this author on: College of Nursing (K.E.K.), University of South Florida, Tampa, Florida 33612 Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 97, Issue 7, 1 July 2012, Pages 23472353, Zhi-Jiang Zhang, Zhi-Jie Zheng, Rong Shi, Qing Su, Qingwu Jiang, Kevin E. Kip; Metformin for Liver Cancer Prevention in Patients with Type 2 Diabetes: A Systematic Review and Meta-Analysis, The Journal of Clinical Endocrinology & Metabolism, Volume 97, Issue 7, 1 July 2012, Pages 23472353, Data on the potential effect of metformin on the risk of liver cancer are limited and inconsistent. The objective of this study was to review the evidence currently available to examine the potential role of metformin in chemo Continue reading >>
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Metformin-induced Hepatotoxicity
Metformin is the first choice oral antidiabetic drug for type 2 diabetes and currently the most consumed. Although gastrointestinal intolerance is frequent, metformin-induced hepatotoxicity is rare. Fewer than 10 cases have been reported (1). In all of those cases, metformin was associated with concomitant intake of other potentially hepatotoxic drugs. We present what we feel may be the first documented case of hepatotoxicity due to metformin with no other drug interference. A 61-year-old man was admitted to the hospital with a 3-day history of painless jaundice. He had no history of liver disease or toxic habits and denied previous consumption of drugs or herbal products, but had been taking metformin (1,700 mg/day for 6 weeks) after being diagnosed with type 2 diabetes. Laboratory tests showed a mixed pattern of liver damage (total bilirubin 2.9 mg/dL, direct bilirubin 2.4 mg/dL, aspartate aminotransferase [AST] 290 units/L [≤40], alanine aminotransferase [ALT] 861 units/L [≤35], γ-glutamyltransferase [GGT] 861 units/L [≤35], and alkaline phosphatase [ALP] 622 units/L [≤120]). International normalized ratio and eosinophil counts were normal. Diagnostic work-up ruled out viral hepatitis A, B, and C, as well as autoimmune and metabolic liver disease (negative antinuclear antibodies, anti-mitochondrial antibodies, smooth muscle antibodies, anti-liver/kidney microsomal antibodies; normal ceruloplasmin, α-1 antitrypsin, copper). Abdominal ultrasound and cholangio-MRI showed no pathological findings. The patient refused a liver biopsy. After stopping metformin, the patient's clinical condition progressively improved and liver enzymes normalized in 30 days. He was discharged with only recommendations to modify his lifestyle. Six weeks after discharge, the patient a Continue reading >>
Metformin Therapy And Risk Of Cancer In Patients With Type 2 Diabetes: Systematic Review
Metformin Therapy and Risk of Cancer in Patients with Type 2 Diabetes: Systematic Review 1 Department of Clinical Pharmacology and Epidemiology, Consorzio Mario Negri Sud, S. Maria Imbaro (CH), Chieti, Italy, 1 Department of Clinical Pharmacology and Epidemiology, Consorzio Mario Negri Sud, S. Maria Imbaro (CH), Chieti, Italy, 1 Department of Clinical Pharmacology and Epidemiology, Consorzio Mario Negri Sud, S. Maria Imbaro (CH), Chieti, Italy, 3 Diaverum Medical Scientific Office, Lund, Sweden, 4 School of Public Health, University of Sydney, Darlington, Australia, 1 Department of Clinical Pharmacology and Epidemiology, Consorzio Mario Negri Sud, S. Maria Imbaro (CH), Chieti, Italy, 1 Department of Clinical Pharmacology and Epidemiology, Consorzio Mario Negri Sud, S. Maria Imbaro (CH), Chieti, Italy, 1 Department of Clinical Pharmacology and Epidemiology, Consorzio Mario Negri Sud, S. Maria Imbaro (CH), Chieti, Italy, 2 Department of Clinical and Experimental Medicine, University of Naples Federico II, Naples, Italy, 3 Diaverum Medical Scientific Office, Lund, Sweden, 4 School of Public Health, University of Sydney, Darlington, Australia, Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: MF AN. Performed the experiments: MF EL. Analyzed the data: MF GL EL FP AN. Wrote the manuscript: MF GL AN GFMS. Statistical analysis: GL FP. Administrative, technical, or material support: MF EL. Study supervision: AN. Received 2013 May 8; Accepted 2013 Jul 1. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. This article Continue reading >>
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- Olive oil in the prevention and management of type 2 diabetes mellitus: a systematic review and meta-analysis of cohort studies and intervention trials
Deptor-related Mtor Suppression Is Involved In Metformin's Anti-cancer Action In Human Liver Cancer Cells
Volume 460, Issue 4 , 15 May 2015, Pages 1047-1052 DEPTOR-related mTOR suppression is involved in metformin's anti-cancer action in human liver cancer cells We elucidated a novel pathway of metformin's anti-cancer action in HCC cells. DEPTOR is involved in the suppressing effect of metformin on mTOR signaling. Metformin increases DEPTOR protein levels via suppression of proteasome activity. DEPTOR-related mTOR suppression is involved in metformin's anti-cancer action. Metformin, one of the most commonly used drugs for patients with type 2 diabetes, recently has received much attention regarding its anti-cancer action. It is thought that the suppression of mTOR signaling is involved in metformin's anti-cancer action. Although liver cancer is one of the most responsive types of cancer for reduction of incidence by metformin, the molecular mechanism of the suppression of mTOR in liver remains unknown. In this study, we investigated the mechanism of the suppressing effect of metformin on mTOR signaling and cell proliferation using human liver cancer cells. Metformin suppressed phosphorylation of p70-S6 kinase, and ribosome protein S6, downstream targets of mTOR, and suppressed cell proliferation. We found that DEPTOR, an endogenous substrate of mTOR suppression, is involved in the suppressing effect of metformin on mTOR signaling and cell proliferation in human liver cancer cells. Metformin increases the protein levels of DEPTOR, intensifies binding to mTOR, and exerts a suppressing effect on mTOR signaling. This increasing effect of DEPTOR by metformin is regulated by the proteasome degradation system; the suppressing effect of metformin on mTOR signaling and cell proliferation is in a DEPTOR-dependent manner. Furthermore, metformin exerts a suppressing effect on proteaso Continue reading >>
Metformin Use Improves Survival Of Diabetic Liver Cancer Patients: Systematic Review And Meta-analysis
Metformin use improves survival of diabetic liver cancer patients: systematic review and meta-analysis 1 Department of Epidemiology and Health Statistics, Xiangya School of Public Health, Central South University, Changsha, China 2 Department of Infectious Disease, Viral Hepatitis Key Laboratory of Hunan Province, Xiangya Hospital, Central South University, Changsha, China 2 Department of Infectious Disease, Viral Hepatitis Key Laboratory of Hunan Province, Xiangya Hospital, Central South University, Changsha, China 1 Department of Epidemiology and Health Statistics, Xiangya School of Public Health, Central South University, Changsha, China 1 Department of Epidemiology and Health Statistics, Xiangya School of Public Health, Central South University, Changsha, China 1 Department of Epidemiology and Health Statistics, Xiangya School of Public Health, Central South University, Changsha, China 2 Department of Infectious Disease, Viral Hepatitis Key Laboratory of Hunan Province, Xiangya Hospital, Central South University, Changsha, China Correspondence to:Hong-Zhuan Tan,Email: [email protected] Received 2016 May 22; Accepted 2016 Jul 19. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. This article has been cited by other articles in PMC. Metformin has garnered considerable interest as a chemo-preventive and chemo-therapeutic agent given the increased risk of liver cancer among diabetic patients. This work was performed to illustrate the association between metformin use and survival of diabetic liver cancer patients. We conducted a comprehensive literature search of PubMed, Web of Science, Em Continue reading >>
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Metformin, The Liver, And Diabetes
Most people think diabetes comes from pancreas damage, due to autoimmune problems or insulin resistance. But for many people diagnosed “Type 2,” the big problems are in the liver. What are these problems, and what can we do about them? First, some basic physiology you may already know. The liver is one of the most complicated organs in the body, and possibly the least understood. It plays a huge role in handling sugars and starches, making sure our bodies have enough fuel to function. When there’s a lot of sugar in the system, it stores some of the excess in a storage form of carbohydrate called glycogen. When blood sugar levels get low, as in times of hunger or at night, it converts some of the glycogen to glucose and makes it available for the body to use. Easy to say, but how does the liver know what to do and when to do it? Scientists have found a “molecular switch” called CRTC2 that controls this process. When the CRTC2 switch is on, the liver pours sugar into the system. When there’s enough sugar circulating, CRTC2 should be turned off. The turnoff signal is thought to be insulin. This may be an oversimplification, though. According to Salk Institute researchers quoted on RxPG news, “In many patients with type II diabetes, CRTC2 no longer responds to rising insulin levels, and as a result, the liver acts like a sugar factory on overtime, churning out glucose [day and night], even when blood sugar levels are high.” Because of this, the “average” person with Type 2 diabetes has three times the normal rate of glucose production by the liver, according to a Diabetes Care article. Diabetes Self-Management reader Jim Snell brought the whole “leaky liver” phenomenon to my attention. He has frequently posted here about his own struggles with soarin Continue reading >>
Metformin Supplementation And Cancer Treatment
Home > Articles > Supplements and Botanicals > Metformin Supplementation and Cancer Treatment Metformin Supplementation and Cancer Treatment The Oncology Association of Naturopathic Physicians (OncANP) annual conference was chock-full of excellent talks on the use of a variety of supplements that may be useful in helping to reduce the risk of cancer development, progression and recurrence. I wrote a blog post, yesterday, on Dr Dugald Seelys talk on the use of melatonin supplementation in cancer treatment . Today, I will update you on the latest information on Metformin. Metformin is a medication derived from the herbGalega officinalis, also known asFrench lilac. (Also check out my previous blog article on Metformin .) The talk on metformin was given by Dr Davis Lamson, MS, ND ( Tahoma Clinic and Bastyr University .) He made a compelling case for why this commonly prescribed, inexpensive (and safe) diabetes medication might want to be added to the care plan for patients with any one of a variety of cancer types. First of all, metformin has been used for over 50 years in the management of diabetes. So, we have lots of safety information on it. It is also available as a generic prescription, so its relatively cheap. The challenge for many patients who might want to use it is that most physicians will not write a prescription for it unless you have diabetes (as metformin is only approved by the FDA for this indication.) You might ask your physician to read this article to help convince them to prescribe it to you. Metformin is such a promising anti-cancer medication that there are approximately 150 clinical trials (see ClinicalTrials.Gov ) investigating its use in cancer treatment and prevention. Cancer loves sugar ( see our blog post on this here .) So, if you reduce the Continue reading >>
Oncotarget | Metformin Use Improves Survival Of Diabetic Liver Cancer Patients: Systematic Review And Meta-analysis
Metformin use improves survival of diabetic liver cancer patients: systematic review and meta-analysis Shu-Juan Ma, Yi-Xiang Zheng, Peng-Cheng Zhou, Yan-Ni Xiao, Hong-Zhuan Tan _ Metrics: PDF 672 views | HTML 478 views | ? Shu-Juan Ma1, Yi-Xiang Zheng2, Peng-Cheng Zhou2, Yan-Ni Xiao1 and Hong-Zhuan Tan1 1 Department of Epidemiology and Health Statistics, Xiangya School of Public Health, Central South University, Changsha, China 2 Department of Infectious Disease, Viral Hepatitis Key Laboratory of Hunan Province, Xiangya Hospital, Central South University, Changsha, China Keywords: metformin, liver cancer, survival, diabetes mellitus, meta-analysis Received: May 22, 2016 Accepted: July 19, 2016 Published: August 02, 2016 Metformin has garnered considerable interest as a chemo-preventive and chemo-therapeutic agent given the increased risk of liver cancer among diabetic patients. This work was performed to illustrate the association between metformin use and survival of diabetic liver cancer patients. We conducted a comprehensive literature search of PubMed, Web of Science, Embase, BIOSIS Previews, Cochrane Library from inception to 12 May 2016. Meta-analyses were performed using Stata (version 12.0), with hazard ratios (HRs) and corresponding 95% confidence intervals (CIs) as effect measures. Eleven cohort studies involving 3452 liver cancer patients fulfilled the inclusion criteria. Meta-analyses showed that metformin use was associated with better survival (HR = 0.59; 95% CI, 0.42-0.83; p = 0.002) of liver cancer patients, and the beneficial effect persisted (HR = 0.64; 95% CI, 0.42-0.97; p = 0.035) when the population was restricted to diabetic liver cancer patients. After adjusting for age, etiology, index of tumor severity and treatment of liver cancer, the associa Continue reading >>
- Metformin Improves Overall Survival of Colorectal Cancer Patients with Diabetes: A Meta-Analysis
- Glycaemic control in people with type 2 diabetes mellitus during and after cancer treatment: A systematic review and meta-analysis
- Caffeinated and Decaffeinated Coffee Consumption and Risk of Type 2 Diabetes: A Systematic Review and a Dose-Response Meta-analysis
Risk Of Cancer In Diabetes: The Effect Of Metformin
Risk of Cancer in Diabetes: The Effect of Metformin Endocrine Research Center (Firouzgar), Institute of Endocrinology and Metabolism, Tehran University of Medical Sciences, Tehran 15937-48711, Iran Received 20 July 2013; Accepted 16 August 2013 Academic Editors: A. Kautzky-Willer and N. Tentolouris Copyright © 2013 Mojtaba Malek et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Cancer is the second cause of death. Association of diabetes as a growing and costly disease with cancer is a major health concern. Meanwhile, preexisting diabetes is associated with an increased risk of all-cause and cancer-specific mortalities. Presence of diabetes related comorbidities, poorer response to cancer treatment, and excess mortality related to diabetes are among the most important explanations. Although diabetes appear to be a risk factor for cancer and is associated with the mortality risk in cancer patients, several factors such as diabetes duration, multiple drug therapy, and the presence of diabetes comorbidities make the assessment of the effect of diabetes treatment on cancer risk and mortality difficult. Metformin is the drug of choice for the treatment of type 2 diabetes. The available evidence from basic science, clinical, and population-based research supports the anticancer effect of metformin. However, randomized controlled clinical trials do not provide enough evidence for a strong protective effect of metformin on cancer incidence or mortality. One of the most important limitations of these trials is the short duration of the followup. Further long-term randomized controlled clinical trials spec Continue reading >>
Syrosingopine Sensitizes Cancer Cells To Killing By Metformin
Syrosingopine sensitizes cancer cells to killing by metformin 1Biozentrum, University of Basel, 4056 Basel, Switzerland. 2Basilea Pharmaceutica International Ltd., Basel, Switzerland. 3Institute for Medical Microbiology, University of Basel, 4003 Basel, Switzerland. 4Molecular Pathology, University Hospital Basel, 4003 Basel, Switzerland. 5Stem Cell Center of Competence, University of Basel, 4056 Basel, Switzerland. *Corresponding author. Email: m.hall{at}unibas.ch We report that the anticancer activity of the widely used diabetic drug metformin is strongly potentiated by syrosingopine. Synthetic lethality elicited by combining the two drugs is synergistic and specific to transformed cells. This effect is unrelated to syrosingopines known role as an inhibitor of the vesicular monoamine transporters. Syrosingopine binds to the glycolytic enzyme -enolase in vitro, and the expression of the -enolase isoform correlates with nonresponsiveness to the drug combination. Syrosingopine sensitized cancer cells to metformin and its more potent derivative phenformin far below the individual toxic threshold of each compound. Thus, combining syrosingopine and codrugs is a promising therapeutic strategy for clinical application for the treatment of cancer. Metformin, an oral antidiabetic of the biguanide class, is the most widely prescribed drug for type 2 diabetes. It acts as a mild mitochondrial inhibitor, and its impact on key metabolic organs, such as the liver and muscle, results in reduced blood glucose levels and restoration of insulin responsiveness at the whole-body level. Metformin is a well-tolerated drug that can be taken for years with few adverse effects, such as rare cases of lactic acidosis. There is increasing evidence that metformin, in addition to its antidiabetic e Continue reading >>
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Understanding The Benefit Of Metformin Use In Cancer Treatment
Understanding the benefit of metformin use in cancer treatment Dowling et al; licensee BioMed Central Ltd.2011 Biguanides have been developed for the treatment of hyperglycemia and type 2 diabetes. Recently, metformin, the most widely prescribed biguanide, has emerged as a potential anticancer agent. Epidemiological, preclinical and clinical evidence supports the use of metformin as a cancer therapeutic. The ability of metformin to lower circulating insulin may be particularly important for the treatment of cancers known to be associated with hyperinsulinemia, such as those of the breast and colon. Moreover, metformin may exhibit direct inhibitory effects on cancer cells by inhibiting mammalian target of rapamycin (mTOR) signaling and protein synthesis. The evidence supporting a role for metformin in cancer therapy and its potential molecular mechanisms of action are discussed. MetforminmTOR SignalingPhenforminMetformin ActionPotential Anticancer Effect The biguanides metformin, phenformin and buformin are derived from the herb Galega officinalis (French lilac, also known as Goat's Rue or Italian Fitch) and were originally developed for the treatment of hyperglycemia and type 2 diabetes. Use of tea infused with French lilac for relief of frequent urination (polyuria) and halitosis (a sweet odor on breath), both now well known symptoms of diabetes, dates back to ancient Egypt and medieval Europe [ 1 3 ]. Work in the 1920 s identified biguanides as the active compounds from the French lilac and led to their development as therapeutics in the 1950 s [ 1 , 3 , 4 ]. While phenformin and buformin were withdrawn from the market in the 1970 s due to toxicity related to lactic acidosis, metformin (N',N'-dimethylbiguanide) remains one of the most commonly prescribed drugs, with Continue reading >>
