Jolin T
Departamento de Endocrinología Experimental, Facultad de Medicina, Universidad Autónoma de Madrid, Spain.
Endocrinology. 1988 Jul;123(1):248-57. doi: 10.1210/endo-123-1-248.
Hepatic mitochondrial alpha-glycerophosphate dehydrogenase (alpha-GPD) and cytosolic malic enzyme (ME) response to a single injection of a receptor-saturating dose of T3 were measured 10, 20, and 30 days after diabetes induction, and compared with values in controls either fed ad libitum (C) or under a restricted diet (FR). An insulin-treated diabetic (D + I) group was also included. Basal enzyme levels as well as enzyme response to T3 injection were correlated with nuclear T3 content, maximal nuclear T3-binding capacity (MBC) and equilibrium association constant (Ka). Diabetes for 10, 20, and 30 days was associated with a progressive decrease in the MBC; the mean decrease was 17%, 50%, and 59%, respectively, from the corresponding C values. The MBC in FR animals did not change appreciably during the experimental period. Moreover, neither the decreased MBC in D groups nor MBC in C, FR, or D + I animals were influenced by T3 injection. The Ka values were comparable in all experimental groups. Specifically bound nuclear T3 was decreased within the experimental period between 33% and 73% in D rats and 6% and 39% in FR rats respect to C values. T3 injection raised the mean nuclear T3 content in all groups. However, at each time interval the mean values of the nuclear T3 in D groups was significantly lower than that in C, FR, or D + I groups after T3 injection. The basal alpha-GPD activity tended to be relatively stable during the experimental period in both D and FR rats, whereas ME activity in D and FR groups was decreased, respectively, 52-64% and 18-39% from C values. The response of both alpha-GPD and ME to T3 injection in FR rats was comparable to that of C groups. The alpha-GPD response to T3 in D rats was not different from that of C rats on days 10 and 20 of the experiment, but on day 30 it decreased by 26%. In contrast, the induction of ME by T3 was severely decreased (by 66-88% of C values) within the experimental diabetes period. Thus, the measurements made in FR rats excluded the possibility that the quantitative changes in the enzyme response to T3 in D rats were nutrition-dependent. The differences between the response of alpha-GPD and ME to T3 in D rats suggest that cellular factors play a role in inhibiting or increasing the response to a given concentration of the T3-receptor complex.
在糖尿病诱导后的第10、20和30天，测量肝脏线粒体α-甘油磷酸脱氢酶（α-GPD）和胞质苹果酸酶（ME）对单次注射受体饱和剂量T3的反应，并与自由进食对照组（C）或限食对照组（FR）的值进行比较。还纳入了胰岛素治疗的糖尿病组（D + I）。基础酶水平以及酶对T3注射的反应与核T3含量、最大核T3结合能力（MBC）和平衡缔合常数（Ka）相关。糖尿病10、20和30天与MBC的逐渐降低相关；与相应的C组值相比，平均降低分别为17%、50%和59%。FR组动物的MBC在实验期间没有明显变化。此外，D组降低的MBC以及C、FR或D + I组动物的MBC均不受T3注射的影响。所有实验组的Ka值相当。与C组值相比，在实验期间，D组大鼠特异性结合的核T3降低了33%至73%，FR组大鼠降低了6%至39%。T3注射提高了所有组的平均核T3含量。然而，在每个时间间隔，D组大鼠注射T3后的核T3平均值均显著低于C、FR或D + I组。在实验期间，D组和FR组大鼠的基础α-GPD活性均趋于相对稳定，而D组和FR组的ME活性分别比C组值降低了52 - 64%和18 - 39%。FR组大鼠的α-GPD和ME对T3注射的反应与C组相当。在实验的第10天和第20天，D组大鼠的α-GPD对T3的反应与C组大鼠没有差异，但在第30天，其降低了26%。相反，在实验性糖尿病期间，T3对ME的诱导作用严重降低（降至C组值的66 - 88%）。因此，在FR组大鼠中进行的测量排除了D组大鼠中酶对T3反应的定量变化依赖于营养的可能性。D组大鼠中α-GPD和ME对T3反应的差异表明，细胞因子在抑制或增强对给定浓度的T3-受体复合物的反应中起作用。
