title: Supplementing with Opuntia ficus-indica Mill and Dioscorea nipponica Makino extracts synergistically attenuates menopausal symptoms in estrogen-deficient rats.
abstract: BACKGROUND
  Prickly pear cactus grown in Korea (Opuntia ficus-indica Mill, KC) and Buchema (Dioscorea nipponica Makino, B) have been traditionally used in East Asia and South America to treat various metabolic diseases. The aim of the present study was to determine whether the extracts of KC, B, and KC+B can prevent the impairments of energy, glucose, lipid and bone homeostasis in estrogen-deficient ovariectomized (OVX) rats and to explore their mechanisms.
  
  
  METHODS
  OVX rats were divided into 4 groups and fed high fat diets supplemented with either 3% dextrin (control), 3% KC, 3% B or 1.5% KC+1.5% B. Sham rats were fed 3% dextrin. After 12 weeks of diet consumption, energy, lipid, glucose and bone metabolisms were analyzed and Wnt signaling in the femur and hepatic signaling were determined.
  
  
  RESULTS
  OVX impaired energy, glucose and lipid metabolism and decreased uterine and bone masses. B and KC+B prevented the decrease in energy expenditure, especially from fat oxidation, in OVX rats, but did not affect food intake. KC+B and B reduced body weight and visceral fat levels, as compared to the OVX-control, by decreasing fat synthesis and inhibiting FAS and SREBP-1c expression. KC+B and B prevented the increases in serum lipid levels and insulin resistance by improving hepatic insulin signaling (pIRS→pAkt→pGSK-3β). KC and KC+B also prevented decreases in bone mineral density (BMD) in the femur and lumbar spine in OVX rats. This was related to decreased expressions of bone turnover markers such as serum osteocalcin, alkaline phosphatase (ALP) and bone-specific ALP levels, and increased serum P levels. KC and KC+B upregulated low-density lipoprotein receptor-related protein 5 and β-catenin in OVX rats, but suppressed the expression of dickkopf-related protein 1. B alone improved energy, lipid and glucose homeostasis, but not bone loss, whereas KC alone enhanced BMD, but not energy, lipid or glucose homeostasis.
  
  
  CONCLUSIONS
  KC+B synergistically attenuated impairments of bone, energy, lipid and glucose metabolism by OVX, suggesting potential efficacy of the combination for alleviating menopausal symptoms.
authors.affiliation: Korea Institute of Oriental Medicine, Daejeon, South Korea.
authors.forename: Byoung-Seob
authors.initials: BS
authors.lastname: Ko
authors.affiliation: Korea Institute of Oriental Medicine, Daejeon, South Korea.
authors.forename: Hye Won
authors.initials: HW
authors.lastname: Lee
authors.affiliation: Food & Nutrition, Obesity/Diabetes Center, Hoseo University, Asan, South Korea.
authors.forename: Da Sol
authors.initials: DS
authors.lastname: Kim
authors.affiliation: Food & Nutrition, Obesity/Diabetes Center, Hoseo University, Asan, South Korea.
authors.forename: Suna
authors.initials: S
authors.lastname: Kang
authors.affiliation: Korea Institute of Oriental Medicine, Daejeon, South Korea.
authors.forename: Jin Ah
authors.initials: JA
authors.lastname: Ryuk
authors.affiliation: Food & Nutrition, Obesity/Diabetes Center, Hoseo University, Asan, South Korea. Electronic address: smpark@hoseo.edu.
authors.forename: Sunmin
authors.initials: S
authors.lastname: Park
mesh_terms: D000818:Animals; D015519:Bone Density / Q000187:drug effects; D001842:Bone and Bones / Q000187:drug effects / Q000378:metabolism; D019587:Dietary Supplements; D027742:Dioscorea / Q000737:chemistry*; D004357:Drug Synergism; D004734:Energy Metabolism / Q000187:drug effects; D004967:Estrogens / Q000172:deficiency; D005260:Female; D005947:Glucose / Q000378:metabolism; D050356:Lipid Metabolism / Q000187:drug effects; D008593:Menopause; D029747:Opuntia / Q000737:chemistry*; D010052:Ovariectomy; D010936:Plant Extracts / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D056910:Republic of Korea
chemical_list: D004967:Estrogens; D010936:Plant Extracts; D005947:Glucose
keywords: Bone mineral density; Energy expenditure; Glucose homeostasis; Insulin signaling; Serum lipid profiles; Wnt signaling