Oner G, Bhaumick B, Bala R M
Endocrinology. 1984 May;114(5):1860-3. doi: 10.1210/endo-114-5-1860.
We have studied potential mechanisms by which zinc deficiency (ZD) may result in growth impairment in young animals. Dietary-induced ZD in young rats resulted in diminished skeletal growth as measured by tibial epiphyseal width. Treatment with bovine GH (bGH) did not increase skeletal growth suggesting GH resistance rather than GH deficiency in zinc-deficient rats. Serum levels of basic somatomedin (SM) were lower in zinc-deficient rats than in control rats receiving a zinc adequate diet, either ad libitum or in pair matched amounts, and were restored to normal by zinc repletion but not by bGH treatment, suggesting that SM production is impaired by ZD. There was a high correlation between tibial epiphyseal widths and serum or femur zinc concentrations. These findings, along with observations that despite similar levels of serum basic SM the bGH-treated zinc-deficient rats had smaller tibial epiphyseal widths than pair fed control rats, additionally suggest that the action of SM on skeletal growth is impaired by ZD.
我们研究了锌缺乏(ZD)可能导致幼龄动物生长发育受损的潜在机制。通过饮食诱导幼鼠出现锌缺乏,结果显示,以胫骨骨骺宽度衡量,骨骼生长减缓。用牛生长激素(bGH)治疗并未促进骨骼生长,这表明缺锌大鼠存在生长激素抵抗而非生长激素缺乏。缺锌大鼠血清中碱性生长调节素(SM)水平低于随意进食或按配对量进食锌充足日粮的对照大鼠,补锌后血清SM水平恢复正常,但bGH治疗不能使其恢复正常,这表明锌缺乏会损害SM的产生。胫骨骨骺宽度与血清或股骨锌浓度之间存在高度相关性。这些发现,以及尽管血清碱性SM水平相似,但bGH治疗的缺锌大鼠胫骨骨骺宽度仍小于配对喂养的对照大鼠这一观察结果,进一步表明锌缺乏会损害SM对骨骼生长的作用。