title: The effects of berberine on hyperhomocysteinemia and hyperlipidemia in rats fed with a long-term high-fat diet.
abstract: BACKGROUND
  The study was undertaken to examine the effects of berberine (BBR) on serum homocysteine, lipids and the aortic lesion in Sprague-Dawley (SD) rats fed with a long-term high-fat diet (HFD).
  
  
  METHODS
  Healthy male SD rats weighing 190-210 g received randomly standard diet or a high-fat diet for 24 weeks. After 8 weeks of feeding, rats fed with HFD were randomized to receive berberine (200 mg · kg-1· day-1) or vehicle by gavage for 16 weeks. After overnight fasting, all rats were sacrificed and total blood samples were also collected for determinant of fasting serum homocysteine (Hcy), total cholesterol (TC) and low density lipoprotein cholesterol (LDL-c) levels. The aorta was stained with hematoxylin and eosin (HE) and Sudan Ш to evaluate aortic lesion. The livers were dissected out and snap-frozen in liquid nitrogen for hepatic TC content and molecular analysis. 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGR), Lipoprotein receptors and apolipoproteins gene expression in the liver were determined by real-time PCR.
  
  
  RESULTS
  Intragastrical administration with berberine for 16 weeks lowered serum Hcy in rats fed with a high-fat diet. In parallel, it also decreased body weight and improved serum TC and LDL-c. Berberine also tended to decrease hepatic cholesterol. Consistently, berberine also upregulated LDL receptor (LDLR) mRNA level and suppressed HMGR gene expression. Meanwhile, upon berberine-treated rats, there was a significant increase in apolipoprotein E (apoE) mRNA, but no change in apoAI and scavenger receptor (SR) mRNA in the liver. Further, no atherosclerotic lesions were developed in berberine-treated rats for 16 weeks.
  
  
  CONCLUSIONS
  Berberine can counteract HFD-elicited hyperhomocysteinemia and hyperlipidemia partially via upregulating LDLR and apoE mRNA levels and suppressing HMGR gene expression.
authors: Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China.
authors: Xin-xia
authors: XX
authors: Chang
authors: Hong-mei
authors: HM
authors: Yan
authors: Qiong
authors: Q
authors: Xu
authors: Ming-feng
authors: MF
authors: Xia
authors: Hua
authors: H
authors: Bian
authors: Teng-fang
authors: TF
authors: Zhu
authors: Xin
authors: X
authors: Gao
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000473:pathology; D001053:Apolipoproteins / Q000235:genetics / Q000378:metabolism; D050197:Atherosclerosis / Q000517:prevention & control; D001599:Berberine / Q000494:pharmacology* / Q000627:therapeutic use; D002784:Cholesterol / Q000378:metabolism; D008078:Cholesterol, LDL / Q000097:blood; D059305:Diet, High-Fat / Q000009:adverse effects; D004353:Drug Evaluation, Preclinical; D006710:Homocysteine / Q000097:blood; D006903:Hydroxymethylglutaryl CoA Reductases / Q000235:genetics / Q000378:metabolism; D020138:Hyperhomocysteinemia / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D006949:Hyperlipidemias / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D000960:Hypolipidemic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D008055:Lipids / Q000097:blood; D008099:Liver / Q000378:metabolism; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D018110:Receptors, Lipoprotein / Q000235:genetics / Q000378:metabolism; D012307:Risk Factors
chemical_list: D001053:Apolipoproteins; D008078:Cholesterol, LDL; D000960:Hypolipidemic Agents; D008055:Lipids; D018110:Receptors, Lipoprotein; D001599:Berberine; D006710:Homocysteine; D002784:Cholesterol; D006903:Hydroxymethylglutaryl CoA Reductases