Journal
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
Volume 69, Issue 30, Pages 8428-8439Publisher
AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.1c02476
Keywords
ginsenoside Rg5; T2DM; insulin sensitivity; mitochondrial dysfunction; Sirt1
Funding
- National Natural Science Foundation of China [21776228, 21978236, 21978229]
- Key Research and Development Program of Shaanxi [2019ZDLSF03-01-02]
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The research discovered that Rg5 can enhance liver mitochondrial biogenesis and insulin sensitivity in db/db mice by activating specific signaling pathways, indicating its potential as a natural product for T2DM interventions.
Type 2 diabetes mellitus (T2DM) is a common metabolic syndrome that decreases insulin sensitivity and mitochondrial biogenesis in the liver. Our previous study demonstrated that ginsenoside Rg5 (Rg5) could attenuate renal injury in diabetic mice but its underlying mechanism in mitochondrial biogenesis and insulin sensitivity remains poorly understood. In this study, we found that Rg5 intervention significantly inhibited blood glucose increases in db/db mice, improved liver function damage and hepatocyte apoptosis, and activated the IRS-1/phosphatidylinositol 3-kinase/AKT insulin metabolism signaling pathway. Rg5 treatment also increased the level of glycogen synthesis and activated sirtuin1 (Sirt1) to increase glucose uptake and insulin sensitivity in insulin-resistant HepG2 (IR-HepG2) cells. Rg5 intervention also effectively improved liver oxidative stress and inflammation in db/db mice and increased mitochondrial biogenesis caused by T2DM. Additionally, the Rg5 treatment increased the mitochondrial mass in IR-HepG2 cells and activated Sirt1 to regulate the Sirt1/PGC-1 alpha/mitofusin-2 mitochondrial biosynthesis pathway. Our findings demonstrated that Rg5 enhanced liver mitochondrial biogenesis and insulin sensitivity in db/db mice by activating the Sirt1/PGC-1 alpha signaling pathway, suggesting the potential of Rg5 as a natural product for T2DM interventions.
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