Biomedical subjects

Do Y Soung

Publications and source records attributed to Do Y Soung.

5 recordsLinked to original sources

PubMed2006

Soy protein supplementation does not cause lymphocytopenia in postmenopausal women.

BACKGROUND: The health benefits of soy isoflavones have been widely investigated; however, there are some concerns as to whether soy isoflavones, similar to ipriflavone, a synthetic isoflavone, cause lymphocytopenia in postmenopausal women. Hence, the purpose of this study was to investigate the extent to which 12-month supplementation of 25 g soy protein containing 60 mg isoflavones alters lymphocyte counts or other hematological parameters in postmenopausal women who were not on hormone replacement therapy. METHODS: Eighty-seven postmenopausal women were randomly assigned to receive either soy protein or an equivalent amount of control protein devoid of isoflavones. Fasting venous blood was collected at baseline and at the end of twelve month study period for complete blood count analyses. RESULTS: Between the two treatment groups, the percent changes in hematological parameters, including lymphocytes, were not different. While women consuming the soy supplement had an increase in mean corpuscular hemoglobin concentration (MCHC) and red cell distribution width index (RDW; a marker of reticulocytes), women consuming the control diet had higher percentage of only MCHC. CONCLUSION: Overall, the results of the present study indicate that consumption of 25 g soy protein containing 60 mg isoflavones daily for one year does not cause lymphocytopenia.

Aged↗

PubMed2006

Soy moderately improves microstructural properties without affecting bone mass in an ovariectomized rat model of osteoporosis.

Soy protein is reported to prevent bone loss in both women and rat models of osteoporosis. However, the role of soy isoflavones on the trabecular microarchitectural properties needs to be explored. In the present study, we examined whether soy protein with graded doses of isoflavones reverses loss of bone mineral density (BMD), bone mineral content (BMC), and trabecular microstructure in an ovariectomized (Ovx) osteopenic rat model. Seventy-eight 9-m old female Sprague-Dawley rats were either sham-operated (Sham; 1 group) or Ovx (5 groups) and fed a semi-purified casein-based diet. After 90 days, the occurrence of bone loss was confirmed using dual energy X-ray absorptiometry. Thereafter, rats were assigned to the following treatments: Sham, Ovx (control), Ovx + 17beta-estradiol (E(2); 10 microg/kg body wt. twice per week), Ovx + soy protein depleted of isoflavones (Soy-; 0.06 mg isoflavones/g protein), Ovx + soy protein with normal isoflavone content (Soy; 3.55 mg isoflavones/g protein), and Ovx + isoflavone-enriched soy protein (Soy+; 7.10 mg isoflavones/g protein). After 125 days of treatment, rats were euthanized, and tibia and lumbar bones were collected for the assessment of BMD, BMC, and trabecular microarchitectural properties using X-ray microcomputed tomography. None of the treatments had an effect on BMD or microarchitectural properties of the lumbar vertebra. However, Soy treatment significantly increased tibial BMC and BMD by 10% and 4.5% compared with Ovx control, but the increase in BMD was not enough to reach the BMD levels of the Sham control group. The Soy+ diet positively affected the tibial architectural properties including trabecular thickness, separation, and number. In summary, our findings suggest that soy protein does not restore bone loss in osteopenic rats; however, higher doses of isoflavones may be required to reverse the loss of tibial microstructural properties.

Absorptiometry, Photon↗

PubMed2006

Wnt induction of chondrocyte hypertrophy through the Runx2 transcription factor.

We investigated the molecular mechanisms underlying canonical Wnt-mediated regulation of chondrocyte hypertrophy using chick upper sternal chondrocytes. Replication competent avian sarcoma (RCAS) viral over-expression of Wnt8c and Wnt9a, upregulated type X collagen (col10a1) and Runx2 mRNA expression thereby inducing chondrocyte hypertrophy. Wnt8c and Wnt9a strongly inhibited mRNA levels of Sox9 and type II collagen (col2a1). Wnt8c further enhanced canonical bone morphogenetic proteins (BMP-2)-induced expression of Runx2 and col10a1 while Wnt8c and Wnt9a inhibited TGF-beta-induced expression of Sox9 and col2a1. Over-expression of beta-catenin mimics the effect of Wnt8c and Wnt9a by upregulating Runx2, col10a1, and alkaline phosphatase (AP) mRNA levels while it inhibits col2a1 transcription. Western blot analysis shows that Wnt8c and beta-catenin also induces Runx2 protein levels in chondrocytes. Thus, our results indicate that activation of the canonical beta-catenin Wnt signaling pathway induces chondrocyte hypertrophy and maturation. We further investigated the effects of beta-catenin-TCF/Lef on Runx2 promoter. Co-transfection of lymphoid enhancer factor (Lef1) and beta-catenin in chicken upper sternal chondrocytes together with deletion constructs of the Runx2 promoter shows that the proximal region spanning the first 128 base pairs of this promoter is responsible for the Wnt-mediated induction of Runx2. Mutation of the TCF/Lef binding site in the -128 fragment of the Runx2 promoter resulted in loss of its responsiveness to beta-catenin. Additionally, gel-shift assay analyses determined the DNA/protein interaction of the TCF/Lef binding sites on the Runx2 promoter. Finally, our site-directed mutagenesis data demonstrated that the Runx2 site on type X collagen promoter is required for canonical Wnt induction of col10a1. Altogether we demonstrate that Wnt/beta-catenin signaling is regulated by TGF-beta and BMP-2 in chick upper sternal chondrocytes, and mediates chondrocyte hypertrophy at least partly through activation of Runx2 which in turn may induce col10a1 expression.

Alkaline Phosphatase↗

PubMed2005

Ipriflavone modulates IGF-I but is unable to restore bone in rats.

Previously it has been reported that ipriflavone can prevent bone loss in ovarian hormone deficient rats. The present study evaluated whether ipriflavone was able to restore bone mass in osteopenic ovariectomized rats. Seventy-two, 90 day-old Sprague-Dawley rats were divided into six groups (sham two groups; ovariectomized four groups). Thirty-five days from the date of surgery, one sham and one ovx group were killed to verify the occurrence of bone loss. The remaining four groups were sham, ovx, ovx + ipriflavone (100 mg[sol ]kg body weight per day), or ovx + 17beta-estradiol (10 microg[sol ]kg body weight daily) for a period of 65 days. Ipriflavone was ineffective in restoring bone density and unlike estrogen did not prevent bone resorption as evidenced by increased (p < 0.05) urinary excretion of hydroxyproline and serum tartrate-resistant acid phosphatase activity. Ipriflavone increased (p < 0.05) the expression of IGF-I in the femur. These observations suggest that higher doses of ipriflavone or longer-term studies may be necessary to restore bone mass.

Animals↗

PubMedDate not supplied

Soy isoflavones prevent ovariectomy-induced atherosclerotic lesions in Golden Syrian hamster model of postmenopausal hyperlipidemia.

OBJECTIVE: Soy isoflavones, as dietary supplements, may reduce the formation of atherosclerotic lesions that increase in women after menopause. The objectives of this study were to determine whether (1) ovariectomized (ovx) hamsters will develop atherosclerotic lesions and (2) soy isoflavones can dose-dependently prevent the ovariectomy-induced rise in plasma cholesterol and atherosclerotic lesions in hamsters. DESIGN: Seventy-two 6-month-old female Golden Syrian hamsters were randomly assigned to six groups: sham-operated; ovx control; ovx + 17beta-estradiol (E(2); 10 microg E(2) per kilogram of body weight); and ovx + 9.5 (low-dose), 19 (medium-dose), or 38 (high-dose) mg isoflavones per kilogram diet. Treatments were initiated immediately after surgery and continued for 120 days. Blood was drawn via abdominal aorta for assessment of circulating lipids, and tissues were collected, including the aortic arch for assessment of atherosclerotic lesions. RESULTS: All three doses of isoflavones prevented the rise in plasma total cholesterol from ovx; and, as the isoflavone dose increases, the cholesterol-lowering effects of isoflavones become more pronounced (7.8%, 11.8%, and 19.6% reductions in total cholesterol for low-dose, medium-dose, and high-dose, respectively). Ovx hamsters developed atherosclerotic lesions without being on an atherogenic diet. Ninety-two percent of hamsters in the ovx control group had atherosclerotic lesions compared with only 8% in sham, 62% in the E(2) group, 29% in the low-dose group, 38% in the medium-dose group, and 58% in the high-dose group. The aortic fatty streak area was approximately 20 times higher in ovx hamsters compared with the sham animals. All doses of isoflavones were able to significantly reduce fatty streak area to that of the sham group. CONCLUSIONS: Soy isoflavones, independent of the protein source, prevent hypercholesterolemia and the formation of atherosclerotic lesions induced by ovarian hormone deficiency in hamsters. The antiatherogenic mechanisms of isoflavones need further investigation.

Animals↗