Metformin prevents liver tumourigenesis by attenuating fibrosis in a transgenic mouse model of hepatocellular carcinoma (original) (raw)

Preventive Role of Metformin Against Hepatocellular Carcinoma in Patients with Diabetes Mellitus -A Systematic Review

JOMENAS Press, 2021

Diabetes mellitus (DM) and hepatocellular carcinoma (HCC) are very challenging health conditions. Although the relation between them is not completely understood, many factors contribute to this relation, including hyperinsulinemia, inflammatory reactions, and other co-modifiers as obesity. This study is designed to detect the role of metformin in preventing HCC in patients with DM compared to other anti-diabetic medications. We have screened the articles systemically in three databases such as PubMed, PubMed Central (PMC), and Medical Literature Analysis and Retrieval System Online (MEDLINE), using specific keywords and Medical Subject Heading (MeSH) terms for related published articles. Moreover, we have used Google Scholar, International Diabetes Federation (IDF), and American Diabetes Association (ADA). We have applied our inclusion/ exclusion criteria, and we have also applied the quality check assessment using Cochrane bias assessment, AMSTAR checklist, SANRA checklist, and New-Castle Ottawa tool. In the end, we reviewed ten studies that were strictly reviewed and analyzed. Based on our study, we reported that the major factor in the development of HCC in patients with DM is the duration, especially more than ten years. We concluded that the risk of development of HCC is directly proportional to the longer duration of DM. Our results show that metformin plays an important role in preventing HCC in patients with DM by decreasing insulin resistance. In contrast, the use of Insulin and drugs that promote insulin secretion is associated with increased incidence of HCC.

Metformin Improves Biochemical and Pathophysiological Changes in Hepatocellular Carcinoma with Pre-Existed Diabetes Mellitus Rats

Pathogens, 2021

Hepatocellular carcinoma (HCC) is one of the world’s most widely recognized malignant tumors that accounts for 90% of all the primary liver cancers and is a major cause of death from cancer, representing half a million deaths per year. Obesity and associated metabolic irregularities, particularly diabetes mellitus (DM) and insulin resistance, are important risk factors for the advancement of HCC. Recently, retrospective studies showed that metformin (MET) could protect the hepatic tissues in pre-existing diabetes mellitus from HCC. The purpose of this study was to assess the role of MET treatment in the pre-existing diabetic rats before and after HCC induction by diethylnitrosamine (DEN). Thirty-five male Sprague Dawley albino rats were partitioned into the following groups: Group 1 (Gp1) was the control. Gp2 was injected intraperitoneally (i.p) with streptozotocin (STZ) (80 mg/kg) and DEN (50 mg/kg/7 weeks). Gp3, Gp4, and Gp5 were injected as in Gp2 and treated with MET (150 mg/kg)...

Metformin and hepatocellular carcinoma

Journal of symptoms and signs, 2015

There is ample evidence that type 2 diabetes is an independent risk factor for the development of various cancers including hepatocellular carcinoma (HCC). Metformin, a widely used antidiabetic agent, has been shown to have chemopreventive properties that may reduce the risk of cancer in diabetes. Here we summarize clinical and experimental data concerning the role of metformin in diabetes-associated hepatocarcinogenesis and review the key molecular mechanisms implicated in this action. By modulating mitochondrial function, metformin activates adenosine monophosphate-activated protein kinase (AMPK), a master regulator of energy metabolism that corrects most diabetes-associated derangements and mitigates the impact of insulin resistance on tumor growth. Moreover, metformin acts through additional AMPK targets in various pathways of oncogenesis and tumor suppression. Finally, metformin may also hinder hepatocarcinogenesis through AMPK-independent mechanisms. Controversies about the us...