Yadav Shivmurat, Porwal Konica, Sinha Rohit Anthony, Chattopadhyay Naibedya, Gupta Sushil Kumar
Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow -226014, India.
Division of Endocrinology and Centre for ASTHI, CSIR-Central Drug Research Institute, (CSIR-CDRI), BS-10/1, Sector 10, Jankipuram Extension, Sitapur Road, Lucknow 226031, India.
Biochem Biophys Rep. 2021 May 27;26:101033. doi: 10.1016/j.bbrep.2021.101033. eCollection 2021 Jul.
Adequate dietary calcium (Ca) intake is essential for bone accretion, peak bone mass (PBM) attainment, bone quality and strength during the mammalian growth period. Severe Ca deficiency during growing age results in secondary hyperparathyroidism (SHPT) and poor bone quality and strength. However, the impact of moderate Ca deficiency during rats early growth period on bone health and the reversibility with supplementing calcium later in adult life remains unclear. Female Sprague-Dawley (SD) rats (postnatal 28th day, P28) were initiated either with a moderate calcium-deficient diet (MCD, 0.25% w/w Ca) or a control diet (0.8% w/w Ca, control group) till P70. Thereafter, MCD rats were continued either with MCD diet or supplemented with calcium diet (0.8% w/w Ca, calcium supplemented group, CaS) till P150. Another group (control rats) were fed 0.8% w/w Ca containing diet from P28 till P150. MCD group, as compared to the control group, had significantly reduced serum ionized Ca and procollagen type 1 N-terminal propeptide (P1NP) at P70 while no significant change was observed in serum corrected Ca, inorganic phosphate (P), alkaline phosphatase (ALP), 25-hydroxy vitamin D [25(OH)D], intact parathyroid hormone (iPTH), and urinary C-terminal telopeptide of collagen 1 (CTX-1), Ca, and P. Femoral and tibial metaphysis in MCD rats had significantly reduced linear growth, cortical and trabecular volumetric BMD (vBMD), trabecular microarchitecture (BV/TV%, trabecular thickness, separation and number, structural model index and connectivity density), cortical thickness, and bone stiffness despite the absence of secondary hyperparathyroidism (SHPT). Continued MCD at P70-P150 results in persistence of compromised bone strength while calcium supplementation (CaS group) improved all the parameters related to bone strength and microarchitecture. Our results indicate that uncorrected moderate/subclinical calcium deficiency in growing rats can result in poor bone quality and strength despite the absence of SHPT. This finding could have relevance in children with poor calcium intake in childhood and adolescence.
充足的膳食钙摄入对于哺乳动物生长发育期的骨骼生长、达到峰值骨量（PBM）、骨骼质量和强度至关重要。生长年龄期间严重缺钙会导致继发性甲状旁腺功能亢进（SHPT）以及骨骼质量和强度不佳。然而，大鼠早期生长阶段中度缺钙对骨骼健康的影响以及成年后期补充钙后的可逆性仍不清楚。雌性斯普拉格-道利（SD）大鼠（出生后第28天，P28）开始要么给予中度缺钙饮食（MCD，0.25% w/w钙），要么给予对照饮食（0.8% w/w钙，对照组）直至P70。此后，MCD组大鼠继续给予MCD饮食或补充钙饮食（0.8% w/w钙，补钙组，CaS）直至P150。另一组（对照大鼠）从P28到P150喂食含0.8% w/w钙的饮食。与对照组相比，MCD组在P70时血清离子钙和1型前胶原N端前肽（P1NP）显著降低，而血清校正钙、无机磷（P）、碱性磷酸酶（ALP）、25-羟基维生素D [25(OH)D]、完整甲状旁腺激素（iPTH）以及尿1型胶原C端肽（CTX-1）、钙和磷未见显著变化。尽管没有继发性甲状旁腺功能亢进（SHPT），MCD组大鼠的股骨和胫骨干骺端线性生长、皮质和小梁体积骨密度（vBMD）、小梁微结构（骨体积分数%、小梁厚度、间距和数量、结构模型指数和连接密度）、皮质厚度和骨硬度均显著降低。在P70 - P150持续给予MCD会导致骨骼强度受损持续存在，而补钙（CaS组）改善了所有与骨骼强度和微结构相关的参数。我们的结果表明，生长中的大鼠未纠正的中度/亚临床缺钙尽管没有SHPT，也会导致骨骼质量和强度不佳。这一发现可能与儿童期和青春期钙摄入不足的儿童有关。
