Beneficial effects of IH-901 on glucose and lipid metabolisms via activating adenosine monophosphate-activated protein kinase and phosphatidylinositol-3 kinase pathways.

IH-901 is an intestinal metabolite of ginsenosides found in Panax ginseng. In the present study, effects of IH-901 on glucose and lipid metabolisms were examined using C2C12 myotubes and C57BL/ksJ db/db mice. A significant increase in phosphorylated adenosine monophosphate-activated protein kinase was observed when differentiated C2C12 myotubes were treated with IH-901. Glucose transporter 4 protein expressions were also up-regulated when muscle cells were treated with of IH-901 up to 60 minutes, resulting in stimulation of glucose uptake by 25% as compared with untreated cells. In addition, phosphatidylinositol-3 kinase and Akt protein expressions were increased when C2C12 myotubes were exposed to IH-901 for up to 3 hours; and these effects including glucose uptake were attenuated by pretreatment with LY294002, a selective phosphatidylinositol-3 kinase inhibitor. In animal study, IH-901 at 25 mg/kg lowered the plasma glucose, triglyceride, cholesterol, and nonesterified fatty acid levels by 20.7%, 41.6%, 20.2%, and 24.6%, respectively, compared with control mice. In the meantime, plasma insulin levels were significantly increased by 2.2 and 3.4 times in 10 and 25 mg/kg-treated mice, respectively, compared with control mice, in parallel with the histologic observation showing a preserved architecture of the pancreatic islet. Protein and gene expression patterns for adenosine monophosphate-activated protein kinase, sterol regulatory element binding protein-1a, and glucose transporter 4 in the liver and skeletal muscles were similar to those in cell studies. In summary, IH-901 might be a promising therapeutic agent improving altered glucose and lipid metabolisms revealed in type 2 diabetes mellitus patients.

Laparoscopic and open surgery for right colonic diverticulitis.

The purpose of this study is to evaluate the safety and effectiveness of laparoscopic surgery by comparing laparoscopic and conventional surgery of right colonic diverticulitis (RCD). Among 124 patients who were treated for RCD from January 1997 to July 2007, we enrolled 54 patients who received resection therapy of RCD. Patients were divided into two groups: laparoscopic (LAP; n=19) and conventional (CON; n=35) surgery groups according to the respective surgical modality. The diverticulectomy (DIV; n=46) and right colectomy (COL; n=8) groups were also compared according to operative methods. There were significant differences between preoperative diagnosis and selection of the operative method and between RCD type and selection of operative method. However, there were no significant differences between preoperative diagnosis and selection of laparoscopic surgery and between RCD type and selection of laparoscopic surgery. The Kaplan-Meier estimated recurrence risk for all patients also showed no significant differences between LAP and CON and DIV and COL (P = 0.413). The Kaplan-Meier-estimated RCD-free period after surgery was 92.7 months (limited to 100 months). Laparoscopic surgery of RCD is an effective and safety method as a result of no differences in clinical data between conventional and laparoscopic surgery.

Ginsenoside Rg1 suppresses hepatic glucose production via AMP-activated protein kinase in HepG2 cells.

Panax ginseng is known to have anti-diabetic activity, but the active ingredients are not yet fully identified. In this study, we found the inhibitory effect of Rg(1) on hepatic glucose production through AMP-activated protein kinase (AMPK) activation in HepG2 cells. Rg(1) significantly inhibited hepatic glucose production in a concentration-dependent manner, and this effect was reversed in the presence of compound C, a selective AMPK inhibitor. In addition, Rg(1) markedly induced the phosphorylations of liver kinase B1 (LKB1), AMPK and forkhead box class O1 (FoxO1), a key transcription factor for gluconeogenic enzymes, in time- and concentration-dependent manners. Glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) activities were inhibited by 24% and 21%, respectively, when the cells were exposed to 40 microM of Rg(1), resulting from phosphorylation of FoxO1 and inhibition of gluconeogenic gene expression. Taken together, our results demonstrated the suppressive effect of Rg(1) on hepatic glucose production via LKB1-AMPK-FoxO1 pathway in HepG2 human hepatoma cells.