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

Glucose Absorption Into the Small Intestine

Glucose Absorption Into the Small Intestine

Complex carbohydrates consumed cannot be absorbed into the small intestine in their original form. First, they must be hydrolyzed to a monosaccharide form such as glucose or galactose. These monosaccharides are then transported across the intestinal membrane and into the blood via transcellular transport. The intestinal epithelial cells allow the movement of these monosaccharides with a defined 'entry' through membrane transporter proteins present on their apical membrane and 'exit' via the...

Glucose Homeostasis: Regulation of Blood Glucose

Glucose Homeostasis: Regulation of Blood Glucose

Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...

Glucose Transporters

Glucose Transporters

Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:

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 the...

Gut-Brain Axis

Gut-Brain Axis

The gut–brain axis is a bidirectional communication system that connects the gastrointestinal tract and the brain. This interaction is mediated through multiple pathways, including the vagus nerve, hormonal signals, immune responses, and chemical messengers produced by gut microbes.Microbial Contributions to Brain FunctionGut microbiota contributes significantly to brain function by producing neuroactive compounds. These include neuroactive compounds that influence neurotransmitters such as...

You might also read

Related Articles

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

Sort by

Same author

Enhanced lysosomal glycogen breakdown is associated with liver tumorigenesis in glycogen storage disease type III.

JHEP reports : innovation in hepatology·2026

Same author

[Intestinal gluconeogenesis : When the intestine produces glucose to prevent obesity and hepatic steatosis].

Medecine sciences : M/S·2025

Same author

Loss of atrial natriuretic peptide signaling causes insulin resistance, mitochondrial dysfunction, and low endurance capacity.

Science advances·2024

Same author

Intestinal gluconeogenesis controls the neonatal development of hypothalamic feeding circuits.

Molecular metabolism·2024

Same author

Impaired Glucose Metabolism, Primary Cilium Defects, and Kidney Cystogenesis in Glycogen Storage Disease Type Ia.

Journal of the American Society of Nephrology : JASN·2024

Same author

Long-term trajectories of weight loss and health outcomes: protocol of the SCOOP-RNPC nationwide observational study.

BMJ open·2024

Search research articles

Related Experiment Video

Updated: Jul 7, 2026

Real-time Analysis of Gut-brain Neural Communication: Cortex wide Calcium Dynamics in Response to Intestinal Glucose Stimulation

Real-time Analysis of Gut-brain Neural Communication: Cortex wide Calcium Dynamics in Response to Intestinal Glucose Stimulation

Published on: December 29, 2023

[Glucose sensing: from gut to brain].

Gilles Mithieux¹

¹Inserm 855, UCBLyon 1.

Bulletin De L'Academie Nationale De Medecine

|January 30, 2008

Summary

High portal vein glucose, often from protein-rich meals, suppresses appetite by activating brain regions. This effect is mediated by the portal nervous system, explaining how protein intake promotes satiety.

Area of Science:

Metabolism and Endocrinology
Neuroscience
Gastroenterology

Background:

Glucose and energy homeostasis are closely linked, with portal vein glucose levels known to influence food intake.
Nerves within the portal vein wall are suspected to play a role in glucose sensing.

Purpose of the Study:

To investigate the role of intestinal gluconeogenesis in regulating food intake.
To elucidate the mechanism by which portal glucose concentration affects satiety, particularly after a protein-rich meal.

Main Methods:

Examined gluconeogenic gene expression (mRNA, protein, enzyme activity) in rat and human intestines.
Quantified intestinal glucose production using radiolabeled glucose tracers and arterio-venous balance.
Studied the effects of portal glucose infusion on food intake and hypothalamic activation (c-Fos) in conscious rats.

More Related Videos

Measuring Uptake of the Glucose Analog, 6-(N-(7-Nitrobenz-2-Oxa-1,3-Diazol-4-yl)Amino)-6-Deoxyglucose, in Intact Murine Neural Retina

Measuring Uptake of the Glucose Analog, 6-(N-(7-Nitrobenz-2-Oxa-1,3-Diazol-4-yl)Amino)-6-Deoxyglucose, in Intact Murine Neural Retina

Published on: March 14, 2025

Visualizing Monocarboxylates and Other Relevant Metabolites in the Ex Vivo Drosophila Larval Brain Using Genetically Encoded Sensors

Visualizing Monocarboxylates and Other Relevant Metabolites in the Ex Vivo Drosophila Larval Brain Using Genetically Encoded Sensors

Published on: October 27, 2023

Related Experiment Videos

Last Updated: Jul 7, 2026

Real-time Analysis of Gut-brain Neural Communication: Cortex wide Calcium Dynamics in Response to Intestinal Glucose Stimulation

Real-time Analysis of Gut-brain Neural Communication: Cortex wide Calcium Dynamics in Response to Intestinal Glucose Stimulation

Published on: December 29, 2023

Measuring Uptake of the Glucose Analog, 6-(N-(7-Nitrobenz-2-Oxa-1,3-Diazol-4-yl)Amino)-6-Deoxyglucose, in Intact Murine Neural Retina

Measuring Uptake of the Glucose Analog, 6-(N-(7-Nitrobenz-2-Oxa-1,3-Diazol-4-yl)Amino)-6-Deoxyglucose, in Intact Murine Neural Retina

Published on: March 14, 2025

Visualizing Monocarboxylates and Other Relevant Metabolites in the Ex Vivo Drosophila Larval Brain Using Genetically Encoded Sensors

Visualizing Monocarboxylates and Other Relevant Metabolites in the Ex Vivo Drosophila Larval Brain Using Genetically Encoded Sensors

Published on: October 27, 2023

Investigated the role of the portal nervous system by inactivating it.

Main Results:

Fasting and protein-rich diets strongly induced gluconeogenic gene expression, increasing portal vein glucose levels.
Intraportal glucose infusion decreased food intake and activated hypothalamic appetite-regulating centers.
These effects mimicked those of a protein-rich diet and were abolished by portal nervous system inactivation.

Conclusions:

Intestinal glucose production and subsequent increases in portal vein glucose contribute to satiety.
The portal nervous system is crucial for mediating the appetite-suppressing effects of elevated portal glucose and protein-rich diets.
Provides a mechanistic link between high-protein diets, portal glucose sensing, and the sensation of fullness.