Key result
Glycyrrhetic acid lowers blood glucose and improves lipid profiles via 11β-HSD1 inhibition in rats.
Why the study?
The role of glycyrrhetic acid (GE) in ameliorating metabolic syndrome through effects on gluconeogenic enzymes, lipoprotein lipase, and PPARs was investigated.
Does glycyrrhetic acid improve metabolic parameters in normal rats?
Does glycyrrhetic acid improve metabolic parameters in normal rats?
Glycyrrhetic acid lowers blood glucose and improves lipid profiles in normal rats, likely via 11β-HSD1 inhibition rather than PPAR agonism.
No immediate clinical implications; leaves open whether 11β-HSD1 inhibition by glycyrrhetic acid merits human metabolic trials.
The aim of this study was to examine the role of glycyrrhetic acid (GE) as a potential compound in the amelioration of metabolic syndrome. Rats given intraperitoneal injection of GE were sacrificed after 24 hours. Blood was collected for the determination of glucose, insulin and lipid profiles; while tissues were used for 11β-HSD1, gluconeogenic enzymes activities, PPAR-α/-γ and LPL expression by RT-PCR. Intraperitoneal injection of 50mg/kg GE to normal rats significantly lowered blood glucose while insulin level and HOMA-IR showed no significant changes. H6PDH activities increased in the liver, kidney, subcutaneous and visceral adipose tissues and quadriceps femoris but decreased in the abdominal muscle. PEPCK activities were significantly reduced in the kidney and decreased in the liver but showed an increase in the subcutaneous and visceral adipose tissues. G6Pase activities were found to be reduced in both the liver and kidney. 11β-HSD1 activities increased in the liver but decreased in all other tissues. There were improvements in lipid profiles in GE-treated rats. Up-regulation of LPL activity was seen in all tissues except quadriceps femoris. PPAR-α expression was up-regulated in the liver, heart and abdominal muscle while down-regulated in the kidney and quadriceps femoris but were undetectable in the subcutaneous and visceral adipose tissues. PPAR-γ expression was up-regulated in all tissues except the kidney. GE prevented hyperglycaemia and improved lipid profiles possibly through 11β-HSD1 inhibition instead of via PPAR agonism.
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Yaw et al. (2013) studied Metabolic syndrome (animal model). Glycyrrhetic acid (GE) was evaluated on Blood glucose, insulin, lipid profiles, and tissue enzyme/receptor expression. Glycyrrhetic acid (50mg/kg) significantly lowered blood glucose and improved lipid profiles in normal rats, possibly through 11β-HSD1 inhibition rather than PPAR agonism.
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