研究报告

益生菌与膳食因子复配对骨质疏松小鼠维生素D活性代谢物水平和骨骼健康的影响

  • 喻喜华 ,
  • 田高 ,
  • 王一 ,
  • 李刘若兰 ,
  • 方海琴 ,
  • 陆文伟 ,
  • 陆守荣 ,
  • 王鸿超
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  • 1(国药控股星鲨制药(厦门)有限公司,福建 厦门,361026)
    2(厦门市母婴健康营养产品重点实验室,福建 厦门,361026)
    3(江南大学 食品学院,江苏 无锡,214122)
    4(国家食品安全风险评估中心,北京,100022)
    5(南京医科大学附属无锡人民医院,江苏 无锡,214122)
第一作者:硕士(王鸿超副教授为通信作者,E-mail:hcwang@jiangnan.edu.cn)

收稿日期: 2025-05-31

  修回日期: 2025-10-17

  网络出版日期: 2026-06-15

基金资助

国家重点研发计划项目 (2022YFF1100403)

Effects of probiotic and dietary factor combination on vitamin D active metabolite levels and bone health in osteoporotic mice

  • YU Xihua ,
  • TIAN Gao ,
  • WANG Yi ,
  • LI Liuruolan ,
  • FANG Haiqin ,
  • LU Wenwei ,
  • LU Shourong ,
  • WANG Hongchao
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  • 1(Sinopharm Xingsha Pharmaceutical (Xiamen) Co.Ltd., Xiamen 361026, China)
    2(Xiamen Key Laboratory of Maternal and Infant Health and Nutrition Products, Xiamen 361026, China)
    3(School of Food Science and Technology, Jiangnan University, Wuxi 214122, China)
    4(China National Center for Food Safety Risk Assessment, Beijing 100022, China)
    5(The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi 214122, China)

Received date: 2025-05-31

  Revised date: 2025-10-17

  Online published: 2026-06-15

摘要

老年人群容易因为皮肤和肝肾功能衰退患骨质疏松症,因此老年人群以及骨质疏松患者需要通过额外摄入维生素D来弥补维生素D合成能力降低。但补充维生素D效果仍较为有限,如何提高1,25二羟基维生素D水平显得更为关键。该研究提供了一种由青春双歧杆菌、长双歧杆菌、姜黄素和低聚半乳糖组成的益生菌和膳食因子复配组合。相较于模型组,使用益生菌膳食复配组合干预骨质疏松小鼠后,小鼠的骨密度与骨体积分数显著提高,其骨小梁结构也得到显著改善。使骨质疏松小鼠血清中1,25二羟基维生素D水平平均提高19.37%(95% CI:4.52%,34.21%),改善血清骨指标;同时其在骨生成、骨代谢和炎症反应相关基因表达水平也有显著改善效果。以上结果表明,此益生菌膳食复配组合起到了缓解骨钙流失,维持骨骼健康,修复骨骼损伤,增加成骨细胞,降低骨质疏松程度的作用。

本文引用格式

喻喜华 , 田高 , 王一 , 李刘若兰 , 方海琴 , 陆文伟 , 陆守荣 , 王鸿超 . 益生菌与膳食因子复配对骨质疏松小鼠维生素D活性代谢物水平和骨骼健康的影响[J]. 食品与发酵工业, 2026 , 52(10) : 59 -68 . DOI: 10.13995/j.cnki.11-1802/ts.043444

Abstract

The elderly population is prone to osteoporosis due to declining skin function and impaired liver and kidney function. Consequently, both the elderly and individuals with osteoporosis require supplemental vitamin D intake to compensate for reduced vitamin D synthesis capacity. While vitamin D supplementation remains relatively limited in efficacy, enhancing levels of its primary active form, 1,25-dihydroxyvitamin D(1,25(OH)2D), is of greater significance. This study aimed to provide a probiotic and dietary factor complex combination consisting of Bifidobacterium adolescentis, Bifidobacterium longum, curcumin, and oligogalactose.Compared with the model group, this combination significantly increased the bone mineral density and bone volume fraction of osteoporotic mice by 27.47% (95% CI:4.15%, 49.49%), and significantly improved the trabecular structure of bone.The combination increased the serum level of 1,25(OH)2D in osteoporotic mice by 19.36% (95% CI:4.52%,34.21%) and improved the serum bone indexes.It also significantly improved the expression level of genes related to bone production, bone metabolism, and inflammatory response.The above results showed that this probiotic dietary combination could alleviate bone calcium loss, maintain bone health, repair bone damage, increase osteoblasts, and reduce the degree of osteoporosis.

参考文献

[1] LEBOFF M S, GREENSPAN S L, INSOGNA K L, et al.The clinician’s guide to prevention and treatment of osteoporosis[J].Osteoporosis International, 2022, 33(10):2049-2102.
[2] KHAN A A, MORRISON A, HANLEY D A, et al.Diagnosis and management of osteonecrosis of the jaw:A systematic review and international consensus[J].Journal of Bone and Mineral Research, 2015, 30(1):3-23.
[3] SHOBACK D, ROSEN C J, BLACK D M, et al.Pharmacological management of osteoporosis in postmenopausal women:An endocrine society guideline update[J].The Journal of Clinical Endocrinology and Metabolism, 2020, 105(3):dgaa048.
[4] CRANDALL C J, HOVEY K M, ANDREWS C, et al.Comparison of clinical outcomes among users of oral and transdermal estrogen therapy in the Women’s Health Initiative Observational Study[J].Menopause, 2017, 24(10):1145-1153.
[5] ROERHOLT C, EIKEN P, ABRAHAMSEN B. Initiation of anti-osteoporotic therapy in patients with recent fractures: A nationwide analysis of prescription rates and persistence[J]. Osteoporosis International, 2009, 20(2):299-307.
[6] LIU S K, MUNSON J C, BELL J E, et al.Quality of osteoporosis care of older Medicare recipients with fragility fractures:2006 to 2010[J].Journal of the American Geriatrics Society, 2013, 61(11):1855-1862.
[7] KIM S C, KIM M S, SANFÉLIX-GIMENO G, et al.Use of osteoporosis medications after hospitalization for hip fracture:A cross-national study[J].The American Journal of Medicine, 2015, 128(5):519-526.e1.
[8] BOUILLON R, MANOUSAKI D, ROSEN C, et al.The health effects of vitamin D supplementation:Evidence from human studies[J].Nature Reviews Endocrinology, 2022, 18(2):96-110.
[9] HARRISON S R, LI D Y, JEFFERY L E, et al.Vitamin D, autoimmune disease and rheumatoid arthritis[J].Calcified Tissue International, 2020, 106(1):58-75.
[10] LATIC N, ERBEN R G.Vitamin D and cardiovascular disease, with emphasis on hypertension, atherosclerosis, and heart failure[J].International Journal of Molecular Sciences, 2020, 21(18):6483.
[11] CHENG J B, LEVINE M A, BELL N H, et al.Genetic evidence that the human CYP2R1 enzyme is a key vitamin D 25-hydroxylase[J].PNAS, 2004, 101(20):7711-7715.
[12] LATIC N, ERBEN R G.FGF23 and vitamin D metabolism[J].JBMR Plus, 2021, 5(12):e10558.
[13] DEMAY M B, PITTAS A G, BIKLE D D, et al.Vitamin D for the prevention of disease:An endocrine society clinical practice guideline[J].The Journal of Clinical Endocrinology and Metabolism, 2024, 109(8):1907-1947.
[14] WANG K L, KONG L H, WEN X, et al.The positive effect of 6-gingerol on high-fat diet and streptozotocin-induced prediabetic mice:Potential pathways and underlying mechanisms[J].Nutrients, 2023, 15(4):824.
[15] SUN W L, SUN J, ZHANG B W, et al.Baicalein improves insulin resistance via regulating SOCS3 and enhances the effect of acarbose on diabetes prevention[J].Journal of Functional Foods, 2017, 37:339-353.
[16] SUN W L, ZHANG B W, YU X X, et al.Oroxin A from Oroxylum indicum prevents the progression from prediabetes to diabetes in streptozotocin and high-fat diet induced mice[J].Phytomedicine, 2018, 38:24-34.
[17] YANG S L, WANG J X, MA F E, et al.Comprehensive systematic review and meta-analysis on the therapeutic efficacy of curcumin in osteoporosis:Unveiling mechanisms and preclinical evidence[J].Frontiers in Nutrition, 2025, 12:1590256.
[18] BARBÁCHANO A, FERNÁNDEZ-BARRAL A, FERRER-MAYORGA G, et al.The endocrine vitamin D system in the gut[J].Molecular and Cellular Endocrinology, 2017, 453:79-87.
[19] DONLON C M, LEBOFF M S, CHOU S H, et al.Baseline characteristics of participants in the VITamin D and OmegA-3 TriaL (VITAL):Effects on bone structure and architecture[J].Contemporary Clinical Trials, 2018, 67:56-67.
[20] MANSON J E, COOK N R, LEE I M, et al.Vitamin D supplements and prevention of cancer and cardiovascular disease[J].The New England Journal of Medicine, 2019, 380(1):33-44.
[21] LEBOFF M S, CHOU S H, MURATA E M, et al.Effects of supplemental vitamin D on bone health outcomes in women and men in the VITamin D and OmegA-3 TriaL (VITAL)[J].Journal of Bone and Mineral Research, 2020, 35(5):883-893.
[22] LEBOFF M S, MURATA E M, COOK N R, et al.VITamin D and OmegA-3 TriaL (VITAL):Effects of vitamin D supplements on risk of falls in the US population[J].The Journal of Clinical Endocrinology and Metabolism, 2020, 105(9):2929-2938.
[23] CARLBERG C, SEUTER S, DE MELLO V D F, et al.Primary vitamin D target genes allow a categorization of possible benefits of vitamin D3 supplementation[J].PLoS One, 2013, 8(7):e71042.
[24] RYYNÄNEN J, NEME A, TUOMAINEN T P, et al.Changes in vitamin D target gene expression in adipose tissue monitor the vitamin D response of human individuals[J].Molecular Nutrition & Food Research, 2014, 58(10):2036-2045.
[25] VUKIĆ M, NEME A, SEUTER S, et al.Relevance of vitamin D receptor target genes for monitoring the vitamin D responsiveness of primary human cells[J].PLoS One, 2015, 10(4):e0124339.
[26] SAKSA N, NEME A, RYYNÄNEN J, et al.Dissecting high from low responders in a vitamin D3 intervention study[J].The Journal of Steroid Biochemistry and Molecular Biology, 2015, 148:275-282.
[27] HOLICK M F, BINKLEY N C, BISCHOFF-FERRARI H A, et al.Evaluation, treatment, and prevention of vitamin D deficiency:An Endocrine Society clinical practice guideline[J].The Journal of Clinical Endocrinology and Metabolism, 2011, 96(7):1911-1930.
[28] ORKABY A R, DJOUSSE L, MANSON J E.Vitamin D supplements and prevention of cardiovascular disease[J].Current Opinion in Cardiology, 2019, 34(6):700-705.
[29] PŁUDOWSKI P, KOS-KUDŁA B, WALCZAK M, et al.Guidelines for preventing and treating vitamin D deficiency:A 2023 update in Poland[J].Nutrients, 2023, 15(3):695.
[30] THOMAS R L, JIANG L J, ADAMS J S, et al.Vitamin D metabolites and the gut microbiome in older men[J].Nature Communications, 2020, 11:5997.
[31] HAUSSLER M R, JURUTKA P W, MIZWICKI M, et al.Vitamin D receptor (VDR)-mediated actions of 1α, 25(OH)2 vitamin D3:Genomic and non-genomic mechanisms[J].Best Practice & Research.Clinical Endocrinology & Metabolism, 2011, 25(4):543-559.
[32] TERPENING C M, HAUSSLER C A, JURUTKA P W, et al.The vitamin D-responsive element in the rat bone Gla protein gene is an imperfect direct repeat that cooperates with other cis-elements in 1, 25-dihydroxyvitamin D3- mediated transcriptional activation[J].Molecular Endocrinology, 1991, 5(3):373-385.
[33] ZEITELHOFER M, ADZEMOVIC M Z, GOMEZ-CABRERO D, et al.Functional genomics analysis of vitamin D effects on CD4+ T cells in vivo in experimental autoimmune encephalomyelitis[J].PNAS, 2017, 114(9):E1678-E1687.
[34] LIU P T, STENGER S, LI H Y, et al.Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response[J].Science, 2006, 311(5768):1770-1773.
[35] MISRA M, PACAUD D, PETRYK A, et al.Vitamin D deficiency in children and its management:Review of current knowledge and recommendations[J].Pediatrics, 2008, 122(2):398-417.
[36] ADAMS J S, HEWISON M.Update in vitamin D[J].The Journal of Clinical Endocrinology & Metabolism, 2010, 95(2):471-478.
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