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

187
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...
187
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

169
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...
169
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

180
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...
180
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

313
Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
313
Insulin: Dosing Regimen and Adverse Effects01:16

Insulin: Dosing Regimen and Adverse Effects

165
Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
165
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

254
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...
254

You might also read

Related Articles

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

Sort by
Same author

Irgm1 Restrains CD8<sup>+</sup> T Cell Cytokine Production and Apoptosis via Cell-Extrinsic Regulation of Type I Interferon Signaling.

European journal of immunology·2026
Same author

Obesity and Tumor Development Reprogram the Proteome and Metabolic Effects of Adipose- and Tumor-Derived Extracellular Vesicles.

bioRxiv : the preprint server for biology·2026
Same author

Targeting IL-6 receptor mediated metabolic pathways to control Th17 cell differentiation and inflammatory responses.

Frontiers in immunology·2025
Same author

Minimally Invasive Staged Endoscopic CO2 Laser Repair of Type III Laryngo-Tracheo-Esophageal Clefts: When and How.

The Laryngoscope·2025
Same author

Pulmonary and Radiographic Findings in Pediatric Type 1 Laryngeal Cleft.

The Laryngoscope·2025
Same author

Type I interferon signaling and peroxisomal dysfunction contribute to enhanced inflammatory cytokine production in IRGM1-deficient macrophages.

The Journal of biological chemistry·2024

Related Experiment Video

Updated: Jun 21, 2025

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test OGTT and Insulin Tolerance Test ITT
08:13

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test OGTT and Insulin Tolerance Test ITT

Published on: January 7, 2018

68.2K

Metformin as a Therapeutic Agent for Obesity-Associated Immune Dysfunction.

Devika Rajeev1, Nancie J MacIver2

  • 1Department of Nutrition, University of North Carolina at Chapel Hill, NC, United States.

The Journal of Nutrition
|July 7, 2024
PubMed
Summary

Obesity impairs immune function, and weight loss may not fully restore it. Metformin, an antidiabetic drug, shows promise in modulating immune responses and reducing obesity-related inflammation.

Keywords:
autoimmunityimmunitymetforminobesitytumor immunityviral infection

More Related Videos

Isolation of Adipose Tissue Immune Cells
07:09

Isolation of Adipose Tissue Immune Cells

Published on: May 22, 2013

36.2K
Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
08:47

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy

Published on: December 7, 2017

9.7K

Related Experiment Videos

Last Updated: Jun 21, 2025

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test OGTT and Insulin Tolerance Test ITT
08:13

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test OGTT and Insulin Tolerance Test ITT

Published on: January 7, 2018

68.2K
Isolation of Adipose Tissue Immune Cells
07:09

Isolation of Adipose Tissue Immune Cells

Published on: May 22, 2013

36.2K
Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
08:47

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy

Published on: December 7, 2017

9.7K

Area of Science:

  • Immunology
  • Metabolic Disease Research
  • Pharmacology

Background:

  • Obesity is linked to chronic inflammation and immune dysfunction, increasing risks for infections, autoimmune diseases, and cancer.
  • Immune deficits in obesity may persist even after weight loss, necessitating novel therapeutic strategies.
  • Targeting obesity-associated inflammation is crucial for improving health outcomes.

Purpose of the Study:

  • To review the potential of metformin as a therapeutic agent for obesity-associated immune dysfunction.
  • To explore the immunomodulatory effects of metformin in the context of obesity.
  • To summarize the evidence supporting metformin's role in mitigating obesity-related immune impairments.

Main Methods:

  • Review of existing scientific literature on metformin's effects on the immune system in obesity.
  • Analysis of studies investigating metformin's impact on immune cell function and cytokine production.
  • Examination of evidence for both AMP-activated protein kinase (AMPK)-dependent and independent mechanisms.

Main Results:

  • Metformin exhibits immunomodulatory properties, affecting immune responses in a cell- and disease-specific manner.
  • Evidence suggests metformin enters immune cells, disrupting electron transport and influencing immune cell differentiation and cytokine profiles.
  • Metformin's actions on immune cells have demonstrated potential benefits in infection, autoimmunity, and cancer models.

Conclusions:

  • Metformin may serve as a viable therapeutic option to counteract obesity-induced immune dysfunction and inflammation.
  • Further research into metformin's precise mechanisms of action on the immune system is warranted.
  • Metformin's immunomodulatory effects offer a promising avenue for improving health in individuals with obesity-related complications.