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Low Calcium and High Fructose Diet Diminish the Quality of Circumferential Long-Bone Growth

机译:低钙和高果糖饮食减少了周向长骨生长的质量

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High fructose (HF) intake is a public health problem. However, little is known about effects on bone quality during growth. Greater data exists for low calcium (Ca~(2+)). Low-Ca (0.02%) or normal calcium and calorie-equivalent glucose or fructose diets (43%) were fed to male, 3-wk-old, B6 mice for 6 wks (4 groups; n=9/group). Weight and long-bone lengths were not affected. Low-Ca diet resulted in less stiff and strong (~40%; p<0.01) long bone and increased toughness (energy absorption) of long-bone mid-shaft, measured by 3-point bending; post-yield displacement was increased in low Ca by >65% (p<0.05). By histomorphometry, low Ca resulted in decreased (>20%, p<0.05) cortical width, partially explaining the bending results. Only the glucose-fed group exhibited compensation to maintain outside circumference and diameter by increased periosteal bone formation rate (p.BFR); 3-fold greater vs. each of the other 3 groups (p<0.05). One plausible mechanism for poor circumferential growth involves bone in a feedback loop and is suggested by decreased intestinal Ca transport and Ca transporter protein in mucosa. The fructose diet completely prevented both adaptive increases in Ca transport, and lahydroxylase-mediated synthesis of 1,25(OH)_2D_3 levels.
机译:高果糖(HF)摄入是一个公共卫生问题。然而,关于在生长期间对骨质的影响很少。低钙(CA〜(2+))存在更大的数据。低Ca(0.02%)或正常的钙和热量相同的葡萄糖或果糖饮食(43%)被加入6周(4组; N = 9 /组)。重量和长骨长度不受影响。低CA饮食导致较少且强(〜40%; P <0.01)长骨和长骨中轴的韧性(能量吸收),通过3点弯曲测量;产量后位移在低Ca中增加> 65%(P <0.05)。通过组织形态学,低Ca导致降低(> 20%,P <0.05)皮质宽度,部分地解释弯曲结果。只有葡萄糖喂养的组表现出补偿以通过增加骨膜骨形成率(p.BFR)来维持外周和直径; 3倍较大与其他3组中的每一个(P <0.05)。圆周生长差的一种合理机制涉及反馈回路中的骨骼,并通过粘膜中的肠道CA输送和CA转运蛋白减少而建议。果糖饮食完全防止了Ca输送的适应性增加,并且达羟羟基酶介导的合成1,25(OH)_2d_3水平。

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