Protective effects of Liuweidihuangwan on hepatic insulin resistance in OLETF rats.
- Author:
Hua DU
1
;
Yaoming XUE
;
Bo ZHU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Diabetes Mellitus, Experimental; drug therapy; metabolism; Drugs, Chinese Herbal; pharmacology; therapeutic use; Insulin Receptor Substrate Proteins; metabolism; Insulin Resistance; Intracellular Signaling Peptides and Proteins; metabolism; Liver; drug effects; metabolism; pathology; Male; Phosphoenolpyruvate Carboxykinase (GTP); metabolism; Rats; Rats, Inbred OLETF; Signal Transduction
- From: Journal of Southern Medical University 2012;32(12):1824-1827
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the mechanism through which Liuweidihuangwan improves hepatic insulin resistance in type 2 diabetic rats.
METHODSWith LETO rats as the normal control group, OLETF rats were treated daily with or without Liuweidihuangwan. At 8, 32, and 40 weeks of the treatment, 3 rats were randomly selected from each group for histological examination of the liver tissues and for detection of phosphoenolpyruvate carboxylase kinase (PEPCK) mRNA expression using RT-PCR and insulin receptor substrate-1 (IRS-1) and IRS-2 protein expressions using Western blotting.
RESULTSCompared with LETO rats, OLETF rats showed progressive destruction of the lobular structures and hepatic steatosis in the liver over time. OLETF rats with Liuweidihuangwan treatment had basically normal lobular structure with only mild fatty degeneration in the liver. RT-PCR detection demonstrated a significantly higher PEPCK mRNA expression in untreated OLETF rats than in LETO rats (P<0.01), but a significantly lowered PEPCK expression in OLETF rats after Liuweidihuangwan dosing (P<0.01). Western blotting showed that significantly lower p-IRS-1 and p-IRS-2 protein expressions in untreated OLETF rats than those in LETO rats and treated OLTEF rats (P<0.05).
CONCLUSIONLiuweidihuangwan improves hepatic insulin resistance in OLETF rats by inhibiting the activity of gluconeogenic key enzyme (PEPCK) in the liver and enhancing IRS-1 and IRS-2 expressions in the insulin signaling pathway.
