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

Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids

Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids

Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2 (COX-2),...

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel Disease...

Antiasthma Drugs: Inhaled Corticosteroids and Glucocorticoids

Antiasthma Drugs: Inhaled Corticosteroids and Glucocorticoids

Inhaled corticosteroids (ICS) are anti-inflammatory drugs used primarily in treating persistent asthma and providing long-term maintenance. They target the bronchial mucosa, the lining of the airways, to control inflammation, a critical factor in asthma progression and exacerbation.
ICS work through a multifaceted mechanism of action. They suppress the inflammatory response caused by the proliferation of TH cells. They also reduce the transcription of the IL-2 gene, which is involved in the...

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...

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

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

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...

Inflammatory Bowel Disease IV: Pharmacological Management

Inflammatory Bowel Disease IV: Pharmacological Management

Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...

You might also read

Related Articles

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

Sort by

Same author

Open-Label 9-Year Follow-Up Extension Phase 2 Study of Once-Weekly Somatrogon in Children With Growth Hormone Deficiency.

The Journal of clinical endocrinology and metabolism·2026

Same author

Low handgrip strength as a potential factor linking diabetes and worse outcomes at hospital - Reply to Liu J et al. "Interpreting diabetic nutritional phenotypes: Preserved mass, impaired strength, or complication burden?"

Clinical nutrition ESPEN·2026

Same author

Adaptive response of breastmilk metabotype and miRNAs patterns in a rat model of gestational diabetes and its postpartum evolution.

The Journal of nutritional biochemistry·2026

Same author

Antenatal N-acetylcysteine supplementation in pregnant women with impending preterm birth: a prospective randomized placebo-controlled trial.

Pediatric research·2026

Same author

From childhood to adulthood in chronic intestinal failure: A nationwide study.

Clinical nutrition (Edinburgh, Scotland)·2026

Same author

The MAIA trial: Protocol of a prospective randomized controlled trial to evaluate the impact of an omega-3 polyunsaturated fatty acids-enriched diet on the loss of independence in nursing home residents.

Clinical nutrition ESPEN·2026

Search research articles

Related Experiment Video

Updated: Jul 8, 2026

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer

Published on: November 15, 2024

Corticosteroids increase glutamine utilization in human splanchnic bed.

Ronan Thibault¹, Susan Welch, Nelly Mauras

¹INRA, UMR 1280, Physiologie des Adaptations Nutritionnelles, Université de Nantes, 44093 Nantes cedex 1, France.

American Journal of Physiology. Gastrointestinal and Liver Physiology

|December 29, 2007

Summary

This summary is machine-generated.

Glucocorticosteroids like prednisone increase the body's need for glutamine in the splanchnic bed. This study shows prednisone alters glutamine metabolism, highlighting potential impacts for patients on long-term steroid therapy.

More Related Videos

Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids

Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids

Published on: April 25, 2016

Related Experiment Videos

Last Updated: Jul 8, 2026

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer

Published on: November 15, 2024

Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids

Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids

Published on: April 25, 2016

Area of Science:

Metabolic research
Endocrinology
Nutritional science

Background:

Glutamine is the most abundant amino acid, crucial for gut and liver metabolism in healthy individuals.
Glucocorticosteroids are potent anti-inflammatory drugs with known metabolic effects.
The impact of glucocorticosteroids on splanchnic glutamine metabolism is not fully understood.

Purpose of the Study:

To investigate how prednisone, a glucocorticosteroid, affects splanchnic glutamine metabolism in healthy adults.
To quantify changes in glutamine synthesis, appearance, and extraction in response to prednisone treatment.

Main Methods:

Healthy adults underwent 5-hour intravenous infusions of labeled leucine and glutamine.
Oral tracer doses of labeled glutamine were administered to assess splanchnic extraction.
Prednisone treatment (0.8 mg/kg/day for 6 days) was compared to a baseline control period.
Isotope tracer methods were used to measure amino acid appearance rates and oxidation.

Main Results:

Prednisone did not alter leucine metabolism (appearance or oxidation).
Prednisone significantly increased plasma glutamine appearance rate, primarily due to enhanced de novo synthesis.
Prednisone increased the splanchnic bed's extraction of glutamine without changing the fraction oxidized.

Conclusions:

High-dose glucocorticosteroids, exemplified by prednisone, increase glutamine requirements in the splanchnic bed.
These findings suggest altered glutamine dynamics under glucocorticosteroid influence.
Further research is needed to determine the clinical relevance for patients on chronic corticoid therapy or with severe illnesses.