Hooshmand Shirin, Brisco Jayme R Y, Arjmandi Bahram H
School of Exercise and Nutritional Sciences, San Diego State University,5500 Campanile Drive,San Diego,CA92182-7251,USA.
Nutrition, Food & Exercise Sciences, Florida State University,Tallahassee,FL32306,USA.
Br J Nutr. 2014 Jul 14;112(1):55-60. doi: 10.1017/S0007114514000671. Epub 2014 Apr 29.
Although several studies have confirmed the bone-protective properties of dried plum, its exact mechanisms of action remain unclear. Recent research has shown that osteocytes may control bone formation via the production of sclerostin and bone resorption via the receptor activator of NF-κB ligand (RANKL) and its inhibitor osteoprotegerin (OPG). To investigate the mechanism of action of dried plum in reversing bone loss, we measured serum levels of RANKL, OPG and sclerostin in osteopenic postmenopausal women (n 160). Participants were randomly assigned to the treatment group of either 100 g dried plum/d or 75 g dried apple/d (comparative control) for 1 year. All participants received 500 mg Ca plus 400 IU (10 μg) vitamin D daily. Bone mineral densities (BMD) of the lumbar spine, forearm, hip and whole body were assessed at baseline and at the end of the study using dual-energy X-ray absorptiometry. Blood samples were collected at baseline and after 12 months to assess bone biomarkers. Dried plum significantly increased the BMD of the ulna and spine in comparison with the control group. In comparison with corresponding baseline values, dried plum increased the RANKL levels by only +1·99 v. +18·33% and increased the OPG levels by +4·87 v. - 2·15% in the control group. Serum sclerostin levels were reduced by - 1·12% in the dried plum group v. +3·78% in the control group. Although percentage changes did not reach statistical significance (P≤ 0·05), these preliminary data may indicate that the positive effects of dried plum on bone are in part due to the suppression of RANKL production, the promotion of OPG and the inhibition of sclerostin.
尽管多项研究证实了西梅干的骨骼保护特性,但其确切作用机制仍不清楚。最近的研究表明,骨细胞可能通过分泌硬化蛋白来控制骨形成,并通过核因子κB受体活化因子配体(RANKL)及其抑制剂骨保护素(OPG)来控制骨吸收。为了研究西梅干逆转骨质流失的作用机制,我们测量了骨质疏松绝经后女性(n = 160)血清中RANKL、OPG和硬化蛋白的水平。参与者被随机分配到治疗组,分别食用100克/天的西梅干或75克/天的苹果干(对照),为期1年。所有参与者每天补充500毫克钙和400国际单位(10微克)维生素D。在基线和研究结束时,使用双能X线吸收法评估腰椎、前臂、髋部和全身的骨密度。在基线和12个月后采集血样,以评估骨生物标志物。与对照组相比,西梅干显著增加了尺骨和脊柱的骨密度。与相应的基线值相比,西梅干组RANKL水平仅增加了+1.99%,而对照组增加了+18.33%;西梅干组OPG水平增加了+4.87%,而对照组下降了-2.15%。西梅干组血清硬化蛋白水平下降了-1.12%,而对照组上升了+3.78%。尽管百分比变化未达到统计学显著性(P≤0.05),但这些初步数据可能表明,西梅干对骨骼的积极作用部分归因于其对RANKL分泌的抑制、对OPG的促进以及对硬化蛋白的抑制。