Uncoupled protein 3 and p38 signal pathways are involved in anti-obesity activity of Solanum tuberosum L. cv. Bora Valley

J Ethnopharmacol. 2008 Aug 13;118(3):396-404. doi: 10.1016/j.jep.2008.05.014. Epub 2008 May 20.

Abstract

Aim of study: This study was undertaken to elucidate the anti-obesity mechanism of a new purple potato variety that has been used for the prevention of metabolic diseases as a folk remedy in Korea.

Materials and methods: Proliferation assay, differentiation assay, Western blotting, were performed in 3T3-L1 adipocytes, while blood chemistry for hyperlipidemic parameters, measurement of body weight and abdominal fats, reverse transcriptase-polymerase chain reaction (RT-PCR) analysis, magnetic resonance image (MRI) scanning were carried out in high fat diet fed Sprague-Dawley rats with ethanol extract of Solanum tuberosum L. cv. Bora Valley (ESTBV).

Results: ESTBV significantly inhibited the proliferation and differentiation of 3T3-L1 cells as well as reduced the cellular leptin level. ESTBV also significantly attenuated the levels of insulin and leptin at 500mg/kg in high fat diet fed rats. In addition, ESTBV significantly reduced total fat and whole body lipid in a therapeutic experiment, which was confirmed by MRI scanning and also significantly inhibited the retroperitoneal and epididymal fats in a preventive experiment compared with control. Similarly, the levels of total cholesterol, triglyceride and low density lipoprotein (LDL) were significantly reduced at a lower dose 200mg/kg of ESTBV in a preventive experiment than at 500mg/kg in a therapeutic experiment. Furthermore, body weight gain was significantly suppressed by over 4 weeks treatment of ESTBV compared with control. Interestingly, the expression of p38 mitogen-activated protein kinase (MAPK) was significantly downregulated in 3T3-L1 cells by ESTBV and the expression of uncoupled protein 3 (UCP-3) was activated in fats and liver tissues of ESTBV treated group compared with high fat diet control.

Conclusion: ESTBV has anti-obesity potential via inhibition of lipid metabolism through p38 MAPK and UCP-3 pathways.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Abdominal Fat / drug effects
  • Animals
  • Anti-Obesity Agents / pharmacology*
  • Cholesterol / blood
  • Ion Channels / genetics
  • Ion Channels / physiology*
  • Leptin
  • Lipid Metabolism / drug effects
  • MAP Kinase Signaling System / drug effects*
  • Magnetic Resonance Imaging
  • Male
  • Mice
  • Mitochondrial Proteins / genetics
  • Mitochondrial Proteins / physiology*
  • Phytotherapy
  • Plant Extracts / analysis
  • Plant Extracts / pharmacology*
  • Rats
  • Rats, Sprague-Dawley
  • Solanum tuberosum*
  • Triglycerides / blood
  • Uncoupling Protein 3
  • p38 Mitogen-Activated Protein Kinases / genetics
  • p38 Mitogen-Activated Protein Kinases / physiology*

Substances

  • Anti-Obesity Agents
  • Ion Channels
  • Leptin
  • Mitochondrial Proteins
  • Plant Extracts
  • Triglycerides
  • Ucp3 protein, mouse
  • Ucp3 protein, rat
  • Uncoupling Protein 3
  • Cholesterol
  • p38 Mitogen-Activated Protein Kinases