Modulatory effects of yerba maté (Ilex paraguariensis) on the PI3K-AKT signaling pathway

Mol Nutr Food Res. 2013 Oct;57(10):1882-5. doi: 10.1002/mnfr.201200834. Epub 2013 May 14.

Abstract

The aim of this study was to evaluate the effects of yerba maté (YM) extract on the phosphatidylinositol 3-kinase (PI3K)-AKT signaling pathway in vivo. The mice were introduced to either standard- or high-fat diet (HFD). After 8 weeks on an HFD, mice were randomly assigned to one of the two treatment conditions, water or yerba maté extract at 1.0 g/kg. After treatment, glucose blood level and hepatic insulin response were evaluated. Liver tissue was examined to determine the mRNA levels using the PI3K-AKT PCR array. The nuclear translocation of forkhead box O1 (FOXO1) was determined by an electrophoretic mobility-shift assay. Our data demonstrated that yerba maté extract significantly decreased the final body weight, glucose blood levels, and insulin resistance of mice. Molecular analysis demonstrated that an HFD downregulated Akt2, Irs1, Irs2, Pi3kca, Pi3kcg, and Pdk1; after yerba maté treatment, the levels of those genes returned to baseline. In addition, an HFD upregulated Pepck and G6pc and increased FOXO1 nuclear translocation. The intervention downregulated these genes by decreasing FOXO1 nuclear translocation. The results obtained demonstrate for the first time the specific action of yerba maté on the PI3K-AKT pathway, which contributed to the observed improvement in hepatic insulin signaling.

Keywords: Insulin resistance; Obesity; PI3K-AKT; Yerba maté.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Glucose / metabolism
  • Body Weight / drug effects
  • Diet, High-Fat
  • Down-Regulation
  • Forkhead Box Protein O1
  • Forkhead Transcription Factors / genetics
  • Forkhead Transcription Factors / metabolism
  • Glucose-6-Phosphatase / genetics
  • Glucose-6-Phosphatase / metabolism
  • Ilex paraguariensis / chemistry*
  • Insulin / blood
  • Insulin Receptor Substrate Proteins / genetics
  • Insulin Receptor Substrate Proteins / metabolism
  • Insulin Resistance
  • Male
  • Mice
  • Phosphatidylinositol 3-Kinase / genetics
  • Phosphatidylinositol 3-Kinase / metabolism*
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Pyruvate Dehydrogenase Acetyl-Transferring Kinase
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Signal Transduction / drug effects*
  • Up-Regulation

Substances

  • Blood Glucose
  • Forkhead Box Protein O1
  • Forkhead Transcription Factors
  • Foxo1 protein, mouse
  • Insulin
  • Insulin Receptor Substrate Proteins
  • Irs1 protein, mouse
  • Irs2 protein, mouse
  • Pdk1 protein, mouse
  • Pyruvate Dehydrogenase Acetyl-Transferring Kinase
  • RNA, Messenger
  • Phosphatidylinositol 3-Kinase
  • Akt2 protein, mouse
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • Glucose-6-Phosphatase
  • G6pc2 protein, mouse