Glycyrrhizic acid (GA) has been reported to inhibit postprandial blood glucose rise and 11 beta-hydroxysteroid dehydrogenase 1 (11 beta HSD1) activity. As not much work has been done on GA effects on 11 beta HSD1 and 2 and HOMA-IR at different treatment periods, this work was conducted. 60 male Sprague Dawley rats fed ad libitum were assigned into six groups of control and treated that were given GA at different duration namely 12, 24 and 48 h. Treated and control groups were intraperitoneally administered with GA (50 mgkg(-1)) and saline respectively. Blood and subcutaneous (ATS) and visceral adipose tissue (ATV), abdominal (MA) and quadriceps femoris muscle (MT), liver (L) and kidney (K) were examined. HOMA-IR in GA-treated rats decreased in all groups (p <0.05). In the 12-h and 24-h treated rats, 11 beta HSD1 activities decreased in all tissues (p <0.05) except MA and MT (p > 0.05) in the former and ATV (p > 0.05) in the latter. However, 11 beta HSD1 activities decreased significantly in all tissues (p <0.05) in the 48-h treated rats. Significant decrease in 11 beta HSD2 (p > 0.05) activities were observed in the L of all treatment groups and K in the 24-h and 48-h treated rats (p <0.05). Histological analysis on ATS showed increase in the number of small-size adipocytes while ATV adipocytes showed shrinkage after GA administration. Increased glycogen deposition in the L was observed in the GA-administered rats in all the treatment periods. In conclusion, GA treatment showed a decrease in the HOMA-IR and both 11 beta HSD1 and 2 activities in all tissues, with more profound decrease in the 48-h treated rats.
|Pages (from-to)||617 - 624|
|Number of pages||8|
|Journal||Experimental and Clinical Endocrinology and Diabetes|
|Publication status||Published - 2010|