Extracellular-superoxide dismutase (EC-SOD) is a secretory glycoprotein located in blood vessel walls at high levels and may be important in the antioxidant capability of vascular walls. The aim of this study was to assess plasma levels of EC-SOD and to evaluate the relationship of the EC-SOD level with insulin resistance in type 2 diabetic patients. We determined plasma EC-SOD in 122 patients and found for the first time that the EC-SOD level was strongly and positively related to adiponectin (r=0.503, P < 0.001), and significantly and inversely related to fasting plasma glucose (FPG) (r=-0.209, P=0.022), body-mass index (BMI) (r=-0.187, P=0.040) and homeostasis model assessment-insulin resistance index (HOMA-R) (r=-0.190, P=0.039). Stepwise-multiple regression analysis also showed a significant influence of adiponectin (F=33.27) on the EC-SOD level. Administration of pioglitazone to 19 diabetic patients significantly increased the plasma levels of EC-SOD (69.9+/-19.3 ng/ml to 97.4+/-25.9 ng/ml; P < 0.0001) and adiponectin, while it decreased tumor necrosis factor-alpha (TNF-alpha). The present observations suggest that factors related to the pathogenesis of insulin resistance play an important role in the regulation of the plasma EC-SOD concentration. It is possible that the increase in the EC-SOD level by pioglitazone administration in diabetic patients is due to a decline of TNF-alpha, which is known to suppress EC-SOD expression.
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T Adachi, M Inoue, H Hara, E Maehata, and S Suzuki
H. Kaneko, M. Yoshida, Y. Hara, K. Taya, K. Araki, G. Watanabe, S. Sasamoto, and Y. Hasegawa
To investigate the physiological importance of inhibin in the regulation of FSH secretion in prepubertal bulls, animals (6-month-old) were passively immunized against inhibin. Five animals were given an i.v. bolus injection of 50 ml inhibin antiserum raised against bovine 32 kDa inhibin in a castrated male goat, and four bulls were given the same amount of castrated male goat serum (control serum) as controls. Treatment with the inhibin antiserum resulted in a marked increase (P < 0·01) in plasma concentrations of FSH within 12 h compared with control animals, and FSH levels in immunized animals remained high until 168 h after the injection. Concentrations of plasma LH and testosterone in the immunized animals were not different from those in the control animals. The present findings provide strong evidence that inhibin plays an important role in the inhibitory regulation of FSH secretion in prepubertal bulls.
Journal of Endocrinology (1993) 137, 15–19
T Nagasawa, K Ichikawa, K Minemura, M Hara, H Yajima, A Sakurai, H Kobayashi, K Hiramatsu, S Shigematsu, and K Hashizume
Cellular and nuclear uptake of tri-iodothyronine (T3) and thyroxine (T4) was examined using the cultured cell line derived from rat liver, clone 9, and rat hepatoma, dRLH-84. The saturable cellular uptake of T3 and T4 was demonstrated in these cells. First we examined the cell cycle-dependent alteration of thyroid hormone uptake. Cellular T3 uptake was minimal in the early G1 phase and increased in the late G1 phase, reaching a maximal level in the S phase. Alterations in nuclear T3 uptake were in accordance with the changes in cellular T3 uptake. On the other hand, cellular and nuclear T4 uptake was unchanged throughout the cell cycle, suggesting the T3 specificity of the cell cycle-dependent alteration of cellular hormone transport. Next we examined the effect of sodium butyrate on the cellular transport of thyroid hormones. After treatment with 5 mm sodium butyrate, cellular and nuclear uptake of T3 was increased, reaching a maximal level (four- to sevenfold increase) after 48 h. When cells were incubated for 48 h with various concentrations of sodium butyrate, T3 uptake was enhanced by 1 mm sodium butyrate, reaching a maximal level with 5 mm. Although cellular T4 uptake was also increased after treatment with sodium butyrate, the degree and time-course of the increase were different from those of T3. The maximal increase in cellular T4 uptake (two- to threefold increase) was attained 20 h after treatment. Despite the increase in cellular T4 uptake, nuclear T4 uptake was decreased after treatment with sodium butyrate. For both T3 and T4, the enhanced cellular uptake was due to the increased Vmax without changes in the Michaelis–Menten constant. These data indicate that cellular transport of T4 is different from that of T3 in rat hepatic cells.
Journal of Endocrinology (1995) 147, 479–485