Ginsenoside Rg1 attenuates hepatic insulin resistance induced by high-fat and high-sugar by inhibiting inflammation.

Abstract

Ginsenoside Rg1 is the active ingredient of Chinese herbal medicine ginseng and sanqi, which has remarkable effects on anti-inflammation and anti-diabetes. In this study, we explored the molecular mechanism of ginsenoside Rg1 against diabetes in rat subjected to insulin resistance induced by high-fat and high-sugar (HFHS). Biochemical analysis revealed that ginsenoside Rg1 significantly decreased the serum levels of alanine transaminase, aspartate transaminase, alkaline phosphatase, total cholesterol, triglyceride, low-density lipoprotein and increased the serum levels of high-density lipoprotein, which indicated ginsenoside Rg1 improved the extent of hepatic steatosis. Furthermore, ginsenoside Rg1 suppressed the expression of IL-1β, IL-6,TNF-α,NF-κB and G6Pase, however, p-Akt was up-regulated. These results suggested that ginsenosideRg1 improved insulin resistance through suppressing inflammatory response and glucose output, which may be a potential therapeutic strategy in protecting hepatic steatosis.

• Authors: Xiaoming Fan, Chao Zhang, Shiwei Niu, Biao Fan, Danshan Gu, Kerong Jiang, Ruonan Li, Shude Li
• Journal: European journal of pharmacology (Eur J Pharmacol) Vol. 854 Pg. 247-255 (Jul 05 2019) ISSN: 1879-0712 [Electronic] Netherlands
• PMID: 31002778 (Publication Type: Journal Article)
• Copyright: Copyright © 2019 Elsevier B.V. All rights reserved.

Chemical References

• Dietary Fats
• Dietary Sugars
• Ginsenosides
• Insulin Receptor Substrate Proteins
• Irs1 protein, rat
• NF-kappa B
• Phosphatidylinositol 3-Kinases
• Proto-Oncogene Proteins c-akt
• Glucose-6-Phosphatase
• ginsenoside Rg1

Topics

• Active Transport, Cell Nucleus (drug effects)
• Animals
• Cell Nucleus (drug effects, metabolism)
• Dietary Fats (adverse effects)
• Dietary Sugars (adverse effects)
• Gene Expression Regulation, Enzymologic (drug effects)
• Ginsenosides (pharmacology, therapeutic use)
• Glucose-6-Phosphatase (genetics)
• Inflammation (drug therapy)
• Insulin Receptor Substrate Proteins (genetics)
• Insulin Resistance
• Liver (drug effects, metabolism)
• NF-kappa B (metabolism)
• Phosphatidylinositol 3-Kinases (metabolism)
• Phosphorylation (drug effects)
• Proto-Oncogene Proteins c-akt (metabolism)
• Rats
• Rats, Sprague-Dawley
• Signal Transduction (drug effects)