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

Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

994
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...
994
Oral Hypoglycemic Agents: Glinides01:06

Oral Hypoglycemic Agents: Glinides

996
Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively...
996
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

914
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...
914
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

1.1K
Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
1.1K
Oral Hypoglycemic Agents: Sulfonylureas01:17

Oral Hypoglycemic Agents: Sulfonylureas

1.7K
Sulfonylureas are oral hypoglycemic agents utilized in treating type 2 diabetes. They are characterized by their unique sulfonylurea chemical structure. The family of sulfonylureas is divided into generations. First-generation sulfonylureas, including tolbutamide (Orinase), chlorpropamide (Diabinese), and tolazamide (Tolinase), trigger insulin release from pancreatic β cells and enhance peripheral tissues' insulin sensitivity. The second-generation members, such as glipizide...
1.7K
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

1.4K
Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
1.4K

You might also read

Related Articles

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

Sort by
Same author

Targeting negative phosphorylation to activate AMPK.

Endocrine connections·2025
Same author

In vivo glycerol metabolism in patients with glycerol kinase deficiency.

JIMD reports·2024
Same author

Single-cell profiling of brain pericyte heterogeneity following ischemic stroke unveils distinct pericyte subtype-targeted neural reprogramming potential and its underlying mechanisms.

Theranostics·2024
Same author

Regulation of hypothalamic reactive oxygen species and feeding behavior by phosphorylation of the beta 2 thyroid hormone receptor isoform.

Scientific reports·2024
Same author

Protocol for measuring mitochondrial size in mouse and human liver tissues.

STAR protocols·2024
Same author

Leukemia inhibitory factor suppresses hepatic de novo lipogenesis and induces cachexia in mice.

Nature communications·2024
Same journal

AARS1 promotes tumor progression and immune evasion via ATF6 lactylation-mediated tryptophan metabolism in hepatocellular carcinoma.

Cell metabolism·2026
Same journal

Reactive species as regulators of immune cell metabolism, tolerance, and autoimmunity.

Cell metabolism·2026
Same journal

The interplay between the microbiome and immune cells in metabolic homeostasis and disease.

Cell metabolism·2026
Same journal

The metabolic basis of regulated cell death.

Cell metabolism·2026
Same journal

Gut microbiota-derived lysine phenylacetylation impairs mitochondrial function and is alleviated by SIRT3.

Cell metabolism·2026
Same journal

Methionine-supplemented longevity diet increases growth hormone, GLP-1, and FGF21; reduces frailty; and promotes healthspan.

Cell metabolism·2026
See all related articles

Related Experiment Video

Updated: Apr 17, 2026

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

20.3K

Metformin action: concentrations matter.

Ling He1, Fredric E Wondisford1

  • 1Division of Metabolism, Departments of Pediatrics, Physiology and Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.

Cell Metabolism
|February 5, 2015
PubMed
Summary
This summary is machine-generated.

Metformin

More Related Videos

Understanding the Changes in Mitochondrial Morphology through Dynamic and Three-dimensional Fluorescence Micrographs
08:15

Understanding the Changes in Mitochondrial Morphology through Dynamic and Three-dimensional Fluorescence Micrographs

Published on: August 15, 2025

1.3K
Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion
07:30

Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion

Published on: May 10, 2018

9.9K

Related Experiment Videos

Last Updated: Apr 17, 2026

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

20.3K
Understanding the Changes in Mitochondrial Morphology through Dynamic and Three-dimensional Fluorescence Micrographs
08:15

Understanding the Changes in Mitochondrial Morphology through Dynamic and Three-dimensional Fluorescence Micrographs

Published on: August 15, 2025

1.3K
Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion
07:30

Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion

Published on: May 10, 2018

9.9K

Area of Science:

  • Pharmacology and Endocrinology
  • Type 2 Diabetes Mellitus Research

Background:

  • Metformin is a widely prescribed oral anti-diabetic agent.
  • Its precise mechanism of action is not fully understood.
  • Previous studies used supra-pharmacological concentrations of metformin.

Purpose of the Study:

  • To investigate the mechanism of action of metformin.
  • To understand metformin's effects at therapeutic concentrations relevant to type 2 diabetes mellitus patients.

Main Methods:

  • Review of existing literature on metformin.
  • Analysis of studies using varying concentrations of metformin.
  • Comparison of results from pharmacological and supra-pharmacological studies.

Main Results:

  • Most prior research utilized metformin doses significantly higher than therapeutic levels.
  • This discrepancy may explain the controversy and incomplete understanding of metformin's action.
  • Therapeutic concentrations might reveal distinct or more nuanced effects.

Conclusions:

  • Understanding metformin's action requires studies at clinically relevant concentrations.
  • Further research is needed to elucidate the precise mechanisms of metformin in type 2 diabetes mellitus.
  • Re-evaluating existing data and conducting new studies at therapeutic doses is crucial.