title: Effect of genistein on insulin resistance, renal lipid metabolism, and antioxidative activities in ovariectomized rats.
abstract: OBJECTIVE
  Postmenopausal women develop obesity, insulin resistance, and potentially renal dysfunction because of decreased serum estrogen levels. We investigated the effects of genistein, an estrogen-like compound thought to exert antioxidative effects, on insulin resistance, renal lipid accumulation, and oxidative stress in ovariectomized rats.
  
  
  METHODS
  Three weeks after an ovariectomy or a sham surgery, rats were put on a high-fat diet containing 0% or 0.1% genistein for 4 wk. We examined the following treatment groups: sham surgery + high-fat diet (sham), ovariectomy + high-fat diet (OVX), and ovariectomy + high-fat diet with 0.1% genistein (OVX + G).
  
  
  RESULTS
  The OVX + G group had increased serum estradiol levels and renal expression of estrogen receptors-alpha and -beta compared with the OVX group. OVX + G rats showed decreases in serum insulin levels and the insulin resistance index. OVX + G rats also exhibited decreased renal triacylglycerol and cholesterol levels, which may have been the result of decreased sterol response element binding protein-1 and -2 expressions, and increased adenosine triphosphate-binding cassette transporter-1 and adiponectin receptor expression. The observed increases in renal lipid levels and serum and renal transforming growth factor-beta in OVX rats may be associated with the increased expression of extracellular matrix proteins, such as fibronectin, and the decreased activity of metalloproteinase-2, an extracellular matrix-degrading enzyme. Ovariectomy also induced oxidative stress by the reduction of antioxidative enzymes, whereas genistein reversed these detrimental ovariectomy-induced effects.
  
  
  CONCLUSIONS
  Genistein may help to maintain normal kidney function through the alleviation of many ovariectomy-induced risk factors for renal damage, including an increased insulin resistance index, renal oxidative stress, lipid accumulation, and extracellular matrix protein expression.
authors.affiliation: Division of Metabolic Disease, Center for Biomedical Sciences, National Institute of Health, Seoul, Korea.
authors.forename: Joo Sun
authors.initials: JS
authors.lastname: Choi
authors.forename: Jihyun
authors.initials: J
authors.lastname: Song
mesh_terms: D000818:Animals; D004041:Dietary Fats / Q000008:administration & dosage; D004958:Estradiol / Q000097:blood; D005260:Female; D019833:Genistein / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D007333:Insulin Resistance; D007668:Kidney / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D050356:Lipid Metabolism / Q000187:drug effects*; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000378:metabolism; D023421:Models, Animal; D010052:Ovariectomy; D010084:Oxidation-Reduction; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D011960:Receptors, Estrogen / Q000378:metabolism
chemical_list: D004041:Dietary Fats; D011960:Receptors, Estrogen; D004958:Estradiol; D019833:Genistein; D005978:Glutathione