Central inflammation and leptin resistance are attenuated by ginsenoside Rb1 treatment in obese mice fed a high-fat diet

PLoS One. 2014 Mar 27;9(3):e92618. doi: 10.1371/journal.pone.0092618. eCollection 2014.


A low-grade pro-inflammatory state is at the pathogenic core of obesity and type 2 diabetes. We tested the hypothesis that the plant terpenoid compound ginsenoside Rb1 (Rb1), known to exert anti-inflammatory effects, would ameliorate obesity, obesity-associated inflammation and glucose intolerance in the high-fat diet-induced obese mouse model. Furthermore, we examined the effect of Rb1 treatment on central leptin sensitivity and the leptin signaling pathway in the hypothalamus. We found that intraperitoneal injections of Rb1 (14 mg/kg, daily) for 21 days significantly reduced body weight gain, fat mass accumulation, and improved glucose tolerance in obese mice on a HF diet compared to vehicle treatment. Importantly, Rb1 treatment also reduced levels of pro-inflammatory cytokines (TNF-α, IL-6 and/or IL-1β) and NF-κB pathway molecules (p-IKK and p-IκBα) in adipose tissue and liver. In the hypothalamus, Rb1 treatment decreased the expression of inflammatory markers (IL-6, IL-1β and p-IKK) and negative regulators of leptin signaling (SOCS3 and PTP1B). Furthermore, Rb1 treatment also restored the anorexic effect of leptin in high-fat fed mice as well as leptin pSTAT3 signaling in the hypothalamus. Ginsenoside Rb1 has potential for use as an anti-obesity therapeutic agent that modulates obesity-induced inflammation and improves central leptin sensitivity in HF diet-induced obesity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiposity / drug effects
  • Animals
  • Body Weight / drug effects
  • Diet, High-Fat
  • Energy Metabolism / drug effects
  • Ginsenosides / administration & dosage
  • Ginsenosides / pharmacology*
  • Glucose / metabolism
  • Glucose Tolerance Test
  • Hormones / blood
  • Hypothalamus / metabolism
  • Hypothalamus / pathology
  • Inflammation / drug therapy
  • Inflammation / etiology*
  • Inflammation / metabolism*
  • Leptin / metabolism*
  • Male
  • Mice
  • Mice, Obese
  • Neuropeptides / metabolism
  • Obesity / complications*
  • Obesity / etiology
  • Signal Transduction / drug effects
  • Time Factors


  • Ginsenosides
  • Hormones
  • Leptin
  • Neuropeptides
  • ginsenoside Rb1
  • Glucose

Grant support

This study was supported by Diabetes Australia Research Trust Research Projects to XFH and YHY. YHY is supported by the National Health and Medical Research Council of Australia (NHMRC 573441). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.