Ginsenoside Rb1 improves leptin sensitivity in the prefrontal cortex in obese mice
Yizhen Wu1, Xu-Feng Huang1,2, Christopher Bell1
1School of Medicine, University of Wollongong, and Illawarra Health and Medical Research Institute, Wollongong, NSW, Australia.
CNS Neuroscience & Therapeutics
|November 14, 2017
Summary
Ginsenoside Rb1 (Rb1) reverses obesity-induced leptin resistance in the brain. This improves brain-derived neurotrophic factor (BDNF) signaling and synaptogenesis, potentially treating neurodegenerative disorders.
Area of Science:
- Neuroscience
- Metabolism
- Pharmacology
Background:
- Obesity impairs leptin signaling, affecting brain-derived neurotrophic factor (BDNF) and synaptogenesis.
- This impairment is linked to cognitive decline, depression, and neurodegenerative diseases.
- Ginsenoside Rb1 (Rb1), from ginseng, has anti-obesity and cognitive-enhancing properties.
Purpose of the Study:
- To investigate if Rb1 can restore leptin's effects on BDNF expression and synaptogenesis in the prefrontal cortex during obesity.
- To examine Rb1's efficacy in both in vivo and in vitro models of obesity.
Main Methods:
- Utilized high-fat diet-induced obese mice and cultured prefrontal cortical neurons.
- Administered chronic Rb1 treatment to obese mice.
- Exposed cultured neurons to palmitic acid and Rb1 to assess effects on leptin signaling, BDNF, and synaptic proteins.
Main Results:
- Chronic Rb1 treatment enhanced central leptin sensitivity and JAK2-STAT3 signaling in obese mice.
- Palmitic acid impaired leptin-induced BDNF expression, synaptic protein levels, and neurite outgrowth in neurons.
- Rb1 treatment significantly protected neurons against palmitic acid-induced damage.
Conclusions:
- Rb1 reverses central leptin resistance and restores leptin-BDNF-synaptogenesis pathways in the prefrontal cortex.
- Rb1 improves synaptic plasticity and neuronal function compromised by obesity.
- Rb1 supplementation shows promise for treating obesity-related neurodegenerative disorders.


