Roux-en-Y gastric bypass surgery reduces bone mineral density and induces metabolic acidosis in rats
Roux-en-Y gastric bypass surgery reduces bone mineral density and induces metabolic acidosis in rats
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DOI：
10.1152/ajpregu.00038.2013
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发表时间：
2013-11-01
影响因子：
2.8
通讯作者：
Lutz, Thomas A.
中科院分区：
文献类型：
--
作者：
Abegg, Kathrin;Gehring, Nicole;Lutz, Thomas A.
Roux-en-Y胃旁路术（RYGB）手术导致人体骨质流失，这可能是由维生素D和钙吸收不良以及随后的继发性甲状旁腺功能亢进引起的。然而，由于这些情况经常发生在肥胖人群中，目前还不清楚它们是否是RYGB后骨质流失的主要原因。为了确定大鼠RYGB模型中钙和维生素D吸收不良对骨丢失的贡献，成年雄性Wistar大鼠随机进行RYGB手术、假手术-随意进食或假手术-体重匹配。术后14 wk在不同时间点评估骨密度、钙磷平衡、酸碱状态和骨转换标志物。RYGB后几周骨密度下降。术后早期肠钙吸收减少，但血浆钙和甲状旁腺激素水平正常。25-羟基维生素D水平降低，而活性1，25-二羟维生素D水平在手术后增加。RYGB大鼠在整个研究期间由于血浆乳酸水平升高和尿钙丢失增加而显示代谢性酸中毒。这些结果表明，初始钙吸收不良可能在大鼠RYGB后早期骨丢失中起关键作用，但其他因素，包括慢性代谢性酸中毒，导致肠道钙吸收正常化后骨恢复不足。继发性甲状旁腺功能亢进与术后骨丢失无关。上调的维生素D活化可以补偿任何维生素D吸收不良。
Roux-en-Y gastric bypass (RYGB) surgery leads to bone loss in humans, which may be caused by vitamin D and calcium malabsorption and subsequent secondary hyperparathyroidism. However, because these conditions occur frequently in obese people, it is unclear whether they are the primary causes of bone loss after RYGB. To determine the contribution of calcium and vitamin D malabsorption to bone loss in a rat RYGB model, adult male Wistar rats were randomized for RYGB surgery, sham-operation-ad libitum fed, or sham-operation-body weight-matched. Bone mineral density, calcium and phosphorus balance, acid-base status, and markers of bone turnover were assessed at different time points for 14 wk after surgery. Bone mineral density decreased for several weeks after RYGB. Intestinal calcium absorption was reduced early after surgery, but plasma calcium and parathyroid hormone levels were normal. 25-hydroxyvitamin D levels decreased, while levels of active 1,25-dihydroxyvitamin D increased after surgery. RYGB rats displayed metabolic acidosis due to increased plasma lactate levels and increased urinary calcium loss throughout the study. These results suggest that initial calcium malabsorption may play a key role in bone loss early after RYGB in rats, but other factors, including chronic metabolic acidosis, contribute to insufficient bone restoration after normalization of intestinal calcium absorption. Secondary hyperparathyroidism is not involved in postoperative bone loss. Upregulated vitamin D activation may compensate for any vitamin D malabsorption.