Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Glucagon-like Receptor Agonists

Glucagon-like Receptor Agonists

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...

You might also read

Related Articles

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

Sort by

Same author

Yeast-Based Bio-Valorization of Whey for Sustainable and Functional Bread Development: A Step Toward Next-Generation Food Products.

Journal of food science·2026

Same author

CATS-A tool to contextualize cancer hallmarks to specific cancer types.

iScience·2026

Same author

Chronic semaglutide alters ingestive behavior without impairing taste function in mice.

Molecular metabolism·2026

Same author

Attenuated hypothalamic response to fructose via a dedicated gut-brain pathway.

Neuron·2026

Same author

Effect of Hull-Less Pumpkin Seed Powder on Dough Farinograph Behavior, Bread Quality, and Antioxidant Properties: A Multivariate Analysis Approach.

Journal of food science·2026

Same author

Ozonation as a Green Approach to Improve the Dough Rheology, Farinograph, Baking Characteristics, and Textural Attributes of Whole Wheat Flour Bread.

Journal of texture studies·2026

Search research articles

Related Experiment Video

Updated: Jun 16, 2025

Neo-Islet Formation in Liver of Diabetic Mice by Helper-dependent Adenoviral Vector-Mediated Gene Transfer

Neo-Islet Formation in Liver of Diabetic Mice by Helper-dependent Adenoviral Vector-Mediated Gene Transfer

Published on: October 10, 2012

Transcriptome-guided GLP-1 receptor therapy rescues metabolic and behavioral disruptions in a Bardet-Biedl syndrome

Arashdeep Singh^1,2,3, Naila Haq⁴, Mingxin Yang^2,3

¹Monell Chemical Senses Center, Philadelphia, Pennsylvania, USA.

The Journal of Clinical Investigation

|April 15, 2025

Summary

Bardet-Biedl Syndrome (BBS) causes obesity and learning issues. A new BBS5 mouse model shows GLP-1R agonists can treat BBS-related metabolic problems, including hyperphagia and weight gain.

Keywords:

Endocrinology Macrophages Metabolism Monogenic diseases Obesity

More Related Videos

Lentiviral Mediated Gene Silencing in Human Pseudoislet Prepared in Low Attachment Plates

Lentiviral Mediated Gene Silencing in Human Pseudoislet Prepared in Low Attachment Plates

Published on: May 14, 2019

Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets

Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets

Published on: May 11, 2015

Related Experiment Videos

Last Updated: Jun 16, 2025

Neo-Islet Formation in Liver of Diabetic Mice by Helper-dependent Adenoviral Vector-Mediated Gene Transfer

Neo-Islet Formation in Liver of Diabetic Mice by Helper-dependent Adenoviral Vector-Mediated Gene Transfer

Published on: October 10, 2012

Lentiviral Mediated Gene Silencing in Human Pseudoislet Prepared in Low Attachment Plates

Lentiviral Mediated Gene Silencing in Human Pseudoislet Prepared in Low Attachment Plates

Published on: May 14, 2019

Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets

Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets

Published on: May 11, 2015

Area of Science:

Ciliopathies
Metabolic disorders
Obesity pathogenesis

Background:

Bardet-Biedl Syndrome (BBS) is a ciliopathy linked to obesity and learning deficits due to BBS gene mutations.
Mutations in BBSome genes exacerbate BBS symptoms, affecting primary cilia function.
Understanding BBS-induced obesity mechanisms is crucial for developing targeted therapies.

Purpose of the Study:

To investigate the mechanisms of BBS-induced obesity using a novel BBS5 knockout (BBS5-/-) mouse model.
To characterize the metabolic and immunophenotypic alterations in BBS5-/- mice.
To evaluate the therapeutic potential of GLP-1R agonists in BBS.

Main Methods:

Generation and characterization of BBS5 knockout (BBS5-/-) mice.
Phenotypic analysis including metabolic testing, glucose/insulin tolerance, and hormone level assessment.
Hypothalamic transcriptomics and functional analysis of endocrine signaling pathways.
Treatment of BBS5-/- mice with a GLP-1R agonist.

Main Results:

BBS5-/- mice exhibited key BBS symptoms: hyperphagia, learning deficits, glucose intolerance, and altered metabolic hormones.
Unique immunophenotype in white adipose tissue with proinflammatory macrophages and dysfunctional regulatory T cells.
Hypothalamic transcriptomics revealed defects in insulin, leptin, and CCK signaling, but preserved GLP-1R responsiveness.
GLP-1R agonist treatment improved hyperphagia, weight gain, glucose tolerance, and metabolic hormone profiles in BBS5-/- mice.

Conclusions:

BBS5-/- mice serve as a valuable translational model for BBS research.
GLP-1R agonists show significant therapeutic potential for managing metabolic dysregulation in BBS.
Targeting GLP-1R pathways offers a promising strategy for BBS treatment.