Related Experiment Video

Updated: Sep 3, 2025

Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
08:58

Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis

Published on: March 11, 2017

16.1K

Inulin may prevent steatosis by suppressing cannabinoid receptor-1 and patatin-like phospholipase-3 expression in

İsmail Mücahit Alptekin1, Funda Pınar Çakıroğlu1, Saba Kiremitci2

  • 1Department of Nutrition and Dietetics, Faculty of Health Sciences, Ankara University, Ankara, Turkey.

Nutrition (Burbank, Los Angeles County, Calif.)
|July 31, 2022
PubMed
Abstract

Insights

Inulin supplementation effectively prevented non-alcoholic fatty liver disease (NAFLD) development in rats. This dietary intervention impacted the endocannabinoid system, suggesting inulin as a potential NAFLD treatment.

Area of Science:

  • Hepatology
  • Metabolic Diseases
  • Nutritional Science

Background:

  • Non-alcoholic fatty liver disease (NAFLD) is a prevalent global liver condition with incompletely understood molecular pathways.
  • Emerging evidence implicates the endocannabinoid system in NAFLD pathogenesis.
  • Inulin, a prebiotic fiber, has demonstrated potential benefits for NAFLD management.

Purpose of the Study:

  • To investigate the therapeutic effects of inulin on NAFLD.
  • To explore the role of the endocannabinoid system in mediating inulin's effects on NAFLD.
  • To evaluate inulin's impact on NAFLD progression in a rat model.

Main Methods:

  • Male Wistar rats were assigned to control or high-fat diets, with or without 15% inulin, for 12 weeks.
  • Evaluated biochemical markers, insulin, adiponectin, liver histology (steatosis, inflammation, NAS), and liver endocannabinoid levels (anandamide, 2-arachidonylglycerol).
  • Assessed gene expression of cannabinoid receptor-1 and Patatin-like phospholipase-3 via quantitative PCR.

Main Results:

  • High-fat diet significantly increased NAFLD activity scores (NAS).
  • Inulin supplementation reduced NAS, insulin resistance (HOMA-IR), and levels of triacylglycerol, total cholesterol, and AST.
  • Inulin decreased hepatic cannabinoid receptor-1 and Patatin-like phospholipase-3 gene expression and 2-arachidonylglycerol levels.

Conclusions:

  • Inulin supplementation effectively prevented NAFLD development in rats.
  • Inulin's protective effects appear mediated through modulation of the endocannabinoid system and related gene expression in the liver.
  • Inulin shows promise as a therapeutic or preventative agent for non-alcoholic fatty liver disease.
Keywords:
2-ArachidonylglycerolAnandamideHigh fat dietInulinNon-alcoholic fatty liver diseaseSteatosis

More Related Videos

A Model of Experimental Steatosis In Vitro: Hepatocyte Cell Culture in Lipid Overload-Conditioned Medium08:35

A Model of Experimental Steatosis In Vitro: Hepatocyte Cell Culture in Lipid Overload-Conditioned Medium

Published on: May 18, 2021

6.6K
Author Spotlight: Establishing MASLD Cell Models for Investigating Disease Mechanisms and the Lipid-Lowering Effects of Koumiss07:03

Author Spotlight: Establishing MASLD Cell Models for Investigating Disease Mechanisms and the Lipid-Lowering Effects of Koumiss

Published on: July 19, 2024

1.0K

Related Concept Videos

Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

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...
239
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

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...
247
Glucagon-like Receptor Agonists01:24

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...
400
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
1.4K