Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase01:27

Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase

20
Phase II biotransformation reactions are essential for detoxifying and eliminating xenobiotics, including many pharmaceutical compounds. These reactions typically involve conjugation, the covalent attachment of polar endogenous groups such as glucuronic acid, sulfate, methyl, or acetyl moieties to functional groups introduced during Phase I metabolism. The resulting conjugates are more water-soluble, enabling efficient renal or biliary excretion.The major classes of Phase II enzymes include...
20
Drug toxicity: Drug–Drug Interaction01:30

Drug toxicity: Drug–Drug Interaction

67
Drug–drug interactions can precipitate toxicity through multiple mechanisms. Absorption interactions alter how drugs enter the body, exemplified when ranitidine increases the absorption of basic drugs, while cholestyramine decreases the levels of propranolol. Protein binding interactions occur when drugs share the same binding sites on plasma proteins. Drugs like aspirin and warfarin, when bound in excess, can lead to increased free drug concentrations, enhancing the potential for...
67
Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test01:22

Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test

225
In clinical practice, the direct measurement of hepatic blood flow to evaluate liver function presents significant challenges due to the intricate and specialized nature of the necessary techniques. Consequently, healthcare professionals often rely on empirical estimates derived from thorough patient examinations and liver function tests to gauge liver health. Among the tools at their disposal, the Child–Pugh and MELD scoring systems stand out for their ability to categorize and assess...
225
Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

712
Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood...
712
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

2.0K
Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
2.0K
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

621
α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
Acarbose and miglitol are...
621

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Diet-microbiome synergy underlies obesity-associated immunotherapy efficacy.

Nature·2026
Same author

Mitochondrial ETF insufficiency drives neoplastic growth by selectively optimizing cancer bioenergetics.

eLife·2026
Same author

ASO Visual Abstract: Adherence to Endocrine Prevention in Patients with Atypical Hyperplasia and Lobular Carcinoma In Situ: Promising Trends from Real-World Use of Low-Dose Tamoxifen.

Annals of surgical oncology·2026
Same author

Systematic assessment of obesity-related risk factors in renal cancer etiology: A longitudinal risk and Mendelian randomization analysis.

PLoS medicine·2026
Same author

Adherence to Endocrine Prevention in Patients with Atypical Hyperplasia and Lobular Carcinoma In Situ: Promising Trends from Real-World Use of Low-Dose Tamoxifen.

Annals of surgical oncology·2026
Same author

Inflammation and insulin profiles in men assigned to exercise vs. usual care for prostate cancer: results from the active surveillance exercise (ASX) randomized controlled trial.

Cancer causes & control : CCC·2026

Related Experiment Video

Updated: Feb 22, 2026

Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer
06:21

Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer

Published on: May 10, 2024

1.3K

Metformin and hepatic carcinogenesis.

Michael Pollak1, Ana M Gonzalez-Angulo

  • 1Lady Davis Research Institute and McGill University, Montreal, Quebec, 3999 Chemin Cote Sainte Catherine, Montreal Quebec H3T 1E2, Canada. michael.pollak@mcgill.ca

Cancer Prevention Research (Philadelphia, Pa.)
|April 3, 2012
PubMed
Summary

Metformin, a diabetes drug, shows promise in reducing liver cancer (hepatoma) risk in both human population studies and mouse models. Further research is needed to optimize its use for hepatoma prevention.

More Related Videos

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
07:29

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies

Published on: June 20, 2015

20.2K
Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module
10:39

Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module

Published on: June 18, 2015

13.9K

Related Experiment Videos

Last Updated: Feb 22, 2026

Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer
06:21

Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer

Published on: May 10, 2024

1.3K
Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
07:29

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies

Published on: June 20, 2015

20.2K
Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module
10:39

Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module

Published on: June 18, 2015

13.9K

Area of Science:

  • Hepatocellular carcinoma (HCC) research
  • Cancer prevention strategies
  • Pharmacological interventions in oncology

Background:

  • Observational studies suggest metformin use in diabetic patients correlates with reduced incidence of several cancers, including hepatoma.
  • Hepatoma (liver cancer) presents a growing clinical challenge due to increasing prevalence and poor patient prognosis.
  • Metformin, a common antidiabetic medication, is being investigated for potential anticancer properties.

Purpose of the Study:

  • To investigate the effect of metformin on carcinogen-induced hepatoma in a preclinical mouse model.
  • To contribute experimental data supporting the hypothesis that metformin may possess chemopreventive properties against liver cancer.
  • To inform future clinical trial design for metformin-based hepatoma prevention strategies.

Main Methods:

  • Utilized a mouse model to study carcinogen-induced hepatoma.
  • Administered metformin to assess its impact on tumor development.
  • Evaluated the efficacy of metformin in an experimental carcinogenesis setting.

Main Results:

  • Bhalla and colleagues demonstrated a reduction in carcinogen-induced hepatoma in mice treated with metformin.
  • The study provides experimental evidence supporting metformin's potential role in hepatoma prevention.
  • Results align with retrospective population studies linking metformin to lower cancer risk in diabetics.

Conclusions:

  • Metformin shows potential as a preventive agent for hepatoma in experimental models.
  • Further research into metformin's mechanism of action, pharmacokinetics, and efficacy predictors is warranted.
  • Optimizing clinical trial design for hepatoma prevention using metformin requires additional data.