Effect of Berberine on Expression of Hepatocyte Nuclear Factor-4α in Rats with Fructose-induced Insulin Resistance
- Author:
GAO ZHIQIANG
1
;
LENG SANHUA
;
LU FUER
;
XIE MEIJUAN
;
XU LIJUN
;
WANG KAIFU
Author Information
1. 华中科技大学同济医学院附属同济医院
- Keywords:
insulin resistance;
berberine;
liver;
HNF-4α;
high fructose diet
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2008;28(3):261-265
- CountryChina
- Language:Chinese
-
Abstract:
The effects of berberine on the expression of hepatocyte nuclear factor-4α (HNF-4α) in liver of rats with fructose-induced insulin resistance and the molecular mechanism of berberine preventing insulin resistance were investigated. The experimental animals were divided into two groups of 16 animals each. The control group received a control routine diet containing 60% carbohydrate, and the study group a high-fructose diet containing 60% fructose as the sole source of carbohydrate. At the end of 6 weeks these were each subdivided into two groups. One was administered with berberine [187.5mg/(kg·d) in 5g/L carboxymethyl cellulosel] by intragastric intubation and the other group was treated with a vehicle (5g/L carboxymethyl cellulose). The rats were fed on the same dietary regimen for the next 4 weeks. After the experimental period of 10 weeks, plasma glucose, insulin and triglyceride levels were measured. HOMA insulin resistance index (HOMA-IR) was assayed. Immunohistochemistry, semiquantitative RT-PCR and western blot were used to detect the expression of HNF-4α in liver. Compared with control diet, fructose feeding induced hyperinsulinemia, HOMA-IR and increased triglyceride (all P<0.01). Berberine prevented the rise in plasma insulin (P<0.01), HOMA-IR (P<0.01) and triglyceride (P<0.05) in the fructose-fed rats. No change in plasma glucose was seen among these groups. The mRNA and protein expression of HNF-4α was decreased in the fructose-fed rats, but berberine could promote its expression. It was concluded that berberine could prevent fructose-induced insulin resistance in rats possibly by promoting the expression HNF-4α in liver.
