PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27079349-4 2016 We investigated improved survival, lower risks of recurrences, and lower, more stable levels of prostate-specific antigen (PSA) in patients with DM2 along with prostate cancer on metformin. Metformin 179-188 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 145-148 27079349-5 2016 METHODS: Patients with prostate cancer along with DM2 who remained on metformin were compared with controls who were not on metformin matched by age, weight, race and Gleason score cancer staging. Metformin 70-79 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 50-53 25468944-9 2015 Glucose rate of disappearance relative to baseline increased more in CON (31 +- 3%) than in DM2 (6 +- 1%) and DM2+Met (21 +- 2%), showing a small increase caused by metformin. Metformin 165-174 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 92-95 25683794-11 2015 The association of glimepiride/metformin, both due to cost as well as effectiveness and safety, may be the preferential treatment for most DM2 patients, and it offers a potential advantage in refractory hyperglycemic populations, tolerant to treatment. Metformin 31-40 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 139-142 25468944-9 2015 Glucose rate of disappearance relative to baseline increased more in CON (31 +- 3%) than in DM2 (6 +- 1%) and DM2+Met (21 +- 2%), showing a small increase caused by metformin. Metformin 165-174 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 110-117 20331505-11 2010 In DM2 patients with HCC, metformin therapy is associated with a reduced HCC risk and seems to have a protective effect on HCC development. Metformin 26-35 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 3-6 24308813-8 2013 A decrease in ER expression was noted in women with EC and DM2 receiving metformin as compared to women treated with insulin (p = 0.004). Metformin 73-82 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 59-62 23983487-3 2013 We report on a case of metformin-induced mixed hepatocellular and cholestatic liver injury in an elderly patient with DM-2 as well as review and summarize case reports of metformin hepatotoxicity available in English on the PubMed database. Metformin 23-32 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 118-122 23983487-8 2013 CONCLUSION: Metformin is an important drug for the treatment of DM-2, which is also used for treatment of patients with fatty liver. Metformin 12-21 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 64-68 23808738-4 2013 In the case of pharmacotherapy there was confirmed efficiency of metformin, which could be used in states with high risk of DM2 conversion and some antihypertensive drugs, mainly sartans. Metformin 65-74 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 124-127 24082827-19 2013 CONCLUSION: Modification of lifestyle, such as diet and increased physical activity or use of metformin may improve glycemic regulation, reduce obesity and prevent or delay the onset of developing DM 2. Metformin 94-103 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 197-201 23983487-1 2013 INTRODUCTION: Metformin is a first-line drug choice for the treatment of type 2 diabetes mellitus (DM-2). Metformin 14-23 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 99-103 21298495-6 2012 Additionally, DM2 patients without cancer, who had parents or siblings with DM2, received biguanide metformin versus sulfonylurea derivatives more often than those with breast or endometrial cancer, either with or without family history of DM2. Metformin 100-109 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 14-17 21298495-6 2012 Additionally, DM2 patients without cancer, who had parents or siblings with DM2, received biguanide metformin versus sulfonylurea derivatives more often than those with breast or endometrial cancer, either with or without family history of DM2. Metformin 100-109 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 76-79 21298495-6 2012 Additionally, DM2 patients without cancer, who had parents or siblings with DM2, received biguanide metformin versus sulfonylurea derivatives more often than those with breast or endometrial cancer, either with or without family history of DM2. Metformin 100-109 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 76-79 20572306-8 2010 Antidiabetic treatment with metformin was more common among cirrhotic and control DM2 subjects than among cases with HCC. Metformin 28-37 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 82-85 20572306-12 2010 CONCLUSION: In patients with preexisting DM2, the risk of HCC is positively associated with poor chronic glycemic control and significantly decreased by metformin therapy. Metformin 153-162 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 41-44 18399062-1 2007 A case-control study was carried out on a sample of 15 Mexican patients (40-56 years old) with type 2 diabetes mellitus (DM2) that had developed five years and been treated with oral hypoglycemic drugs (sulfonylurea and/or metformin), with no microvascular or macrovascular complications. Metformin 223-232 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 121-124 18062354-7 2007 Metformin, Thiazolidinediones and Acarbose are anti-hyperglycemic drugs of choice: they reduce the incidence of DM2 and IR (or improve insulin sensitivity) and they decrease or stabilize the visceral adipose tissue mass (Thiazolidinediones increases subcutaneous fat only). Metformin 0-9 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 112-122 18837086-5 2008 Compared to controls, males DM2 with HCC were more frequently treated with insulin (38.1% vs 17.6%, P = 0.009) and with sulfonylurea with or without metformin than with diet with or without metformin (84% vs 68.3%, P = 0.049). Metformin 149-158 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 28-31 18401838-2 2008 Our first aim was to investigate the prevalence of risk determinants in subjects with type 2 diabetes mellitus (DM2) taking metformin compared to subjects with nonmetformin treatment. Metformin 124-133 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 112-115 18401838-11 2008 Improved selection of patients can result in safe metformin utilization in one quarter of subjects on DM2 related drug treatment. Metformin 50-59 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 102-105 18038714-9 2007 After 8 months of treatment with metformin he developed DM2. Metformin 33-42 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 56-59 18038714-17 2007 CONCLUSION: We suggest that early initiation of combined therapy comprising a high dose of metformin plus rosiglitazone may be valuable in managing insulin resistance and DM2 in children with AS. Metformin 91-100 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 171-174 31627625-6 2007 In patients with DM-2, metformin exerted a positive effect on fasting glycemia (p = 0.001) and postprandial hyperglycemia (absolute and relative areas under the curve in the oral glucose tolerance test (OGTT)). Metformin 23-32 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 17-21 31627625-9 2007 In patients with DM-2, metformin therapy enhanced a low-calorie diet-induced body weight loss, most markedly within the first three months of therapy. Metformin 23-32 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 17-21 16503324-1 2005 BACKGROUND: Metformin hydrochloride is widely used for the treatment of type 2 diabetes mellitus (DM-2). Metformin 12-35 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 98-102 16503324-3 2005 OBJECTIVE: The aim of this article was to report a case of serious hepatotoxicity possibly associated with metformin use in an elderly patient with DM-2. Metformin 107-116 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 148-152 16503324-9 2005 CONCLUSIONS: In this case of an elderly woman with DM-2 who presented with symptoms of hepatotoxicity after 3 weeks of metformin treatment, metformin appeared to have caused a mixed-type (hepatocellular and cholestatic) hepatic damage. Metformin 119-128 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 51-55 16503324-4 2005 METHODS: After receiving metformin 500 mg/d for 3 weeks, a 73-year-old Japanese woman weighing 33.5 kg with poorly controlled DM-2 presented with fatigue, jaundice, nausea, vomiting, anorexia, and abdominal pain. Metformin 25-34 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 126-130 16503324-9 2005 CONCLUSIONS: In this case of an elderly woman with DM-2 who presented with symptoms of hepatotoxicity after 3 weeks of metformin treatment, metformin appeared to have caused a mixed-type (hepatocellular and cholestatic) hepatic damage. Metformin 140-149 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 51-55 12769787-1 2003 Although a number of assessments disagree, the preponderance of the evidence indicates that the major therapeutic action of metformin in type 2 diabetes (DM2) is on the liver, and glucose production (EGP) in particular. Metformin 124-133 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 154-157 15506677-10 2004 CONCLUSIONS: Metformin was often ineffective in our adolescents with DM2 and compliance was a major factor. Metformin 13-22 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 69-72 12769787-9 2003 Sites of metformin action can therefore be considered as a compilation of valid therapeutic targets in DM2. Metformin 9-18 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 103-106 12769787-12 2003 (iii) unifying concepts: reported actions of metformin on the mitochondrial respiratory chain, free fatty acid metabolism, AMP-activated protein kinase, and on membrane proteins directly may all explain subsets of actions that are seen, providing more integrated targets for consideration in the therapy of DM2. Metformin 45-54 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 307-310 29456855-1 2018 Metformin, the drug of choice in the treatment of type 2 diabetes mellitus (DM2), in addition to aspirin (ASA), the drug prescribed for cardioprotection of diabetic and non-diabetic patients, have an inhibitory effect on cancer cell survival. Metformin 0-9 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 76-79 30918874-9 2018 In the multivariate analysis, metformin use and age were independent predictors of the b/T ratio in both DM1 and DM2 patients, while the type of basal insulin was an independent predictor only in DM1. Metformin 30-39 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 113-116 29456855-5 2018 A total of 515 CRC patients without DM2 and 156 with DM2 treated with metformin were enrolled in the study. Metformin 70-79 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 53-56 29456855-7 2018 The five-year relative survival for stage III CRC was 101% [95% confidence interval (CI)=76-126] in the 18 patients with DM2 treated with metformin and ASA, 55% (95% CI=31-78) in the 23 without DM2 treated with ASA, 55% (95% CI=45-65) in the 150 without DM2 not taking ASA, and 29% (95% CI=13-45) in the 43 with DM2 treated with metformin, however not with ASA. Metformin 138-147 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 121-124 30684325-1 2018 OBJECTIVE: Introduction: The paper presents the findings of our own study on the changes of the systemic inflammation in patients with type 2 diabetes mellitus (DM2) and ischemic heart disease (IHD) during the combination treatment with metformin and pioglitazone. Metformin 237-246 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 161-164 28985579-1 2017 PURPOSE: In 2015, we published a study on a small series of patients with hepatocellular carcinoma (HCC) treated chronically with metformin for type II diabetes mellitus (DM2) who showed a poorer response to sorafenib. Metformin 130-139 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 171-174 29047344-1 2017 BACKGROUND: Metformin is usually prescribed as first line therapy for type 2 diabetes mellitus (DM2). Metformin 12-21 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 96-99 29047344-3 2017 This systematic review examined the available evidence on the safety and efficacy of metformin in the management of DM2 in older adults. Metformin 85-94 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 116-119 29047344-7 2017 Studies were included if they reported safety or efficacy outcomes with metformin (alone or in combination) for the management of DM2 compared to placebo, usual or no treatment, or other antidiabetics. Metformin 72-81 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 130-133 29047344-14 2017 Four recommendations were developed suggesting to discontinue the use of metformin for the management of DM2 in older adults with risk factors such as age > 80, gastrointestinal complaints during the last year and/or GFR <=60 ml/min. Metformin 73-82 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 105-108 29047344-15 2017 CONCLUSIONS: On the evidence available, the safety and efficacy profiles of metformin appear to be better, and certainly no worse, than other treatments for the management of DM2 in older adults. Metformin 76-85 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 175-178