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甲状腺激素和糖尿病对脂肪组织脂蛋白脂肪酶的调节作用。低三碘甲状腺原氨酸状态的意义。

Modulation of adipose lipoprotein lipase by thyroid hormone and diabetes. The significance of the low T3 state.

作者信息

Gavin L A, McMahon F, Moeller M

出版信息

Diabetes. 1985 Dec;34(12):1266-71. doi: 10.2337/diab.34.12.1266.

Abstract

The present study was performed to assess the potential relationship between the low T3 syndrome and hypothyroidism. Comparative studies were performed on the relative effects of diabetes and insulin on heparin-releasable adipose lipoprotein lipase (LPL) in the intact and hypothyroid rat. Hypothyroidism for 10 days (Tx) significantly increased adipose LPL activity (5.8 +/- 0.2 mu eq/g/h) compared with the activity (3.6 +/- 0.4 mu eq/g/h) in the normal group. Diabetes for 72 h (streptozocin, STZ, 10 mg/100 g body wt, i.p.) significantly reduced (P less than 0.005) adipose LPL activity in the Tx model. However, despite the suppressant effect of diabetes (43 +/- 11%), the enzyme activity remained equivalent to the normal group. Insulin stimulated adipose LPL in the Tx-diabetic group. The enzyme demonstrated a synergistic response to insulin and hypothyroidism. Subsequent studies were performed in the intact diabetic rat, a low T3 state. Adipose LPL activity was reduced to a similar degree by diabetes (79 +/- 2%) irrespective of the serum T3 concentration. Furthermore, the magnitude of the adipose LPL stimulation by insulin was not modulated by the endogenous serum T3. However, co-treatment of the diabetic group with T3 and insulin blunted the adipose LPL response to insulin. These various modulations in adipose LPL activity were associated with significant but opposite changes in serum triglyceride levels in both the hypothyroid and intact rat. These studies demonstrate that hypothyroidism counteracts the suppressant effect of diabetes on heparin-releasable rat adipose LPL activity and magnifies the enzyme response to insulin.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本研究旨在评估低T3综合征与甲状腺功能减退之间的潜在关系。对糖尿病和胰岛素对完整及甲状腺功能减退大鼠体内肝素可释放脂肪脂蛋白脂肪酶(LPL)的相对作用进行了比较研究。与正常组活性(3.6±0.4μeq/g/h)相比,甲状腺功能减退10天(Tx)显著增加了脂肪LPL活性(5.8±0.2μeq/g/h)。糖尿病72小时(链脲佐菌素,STZ,10mg/100g体重,腹腔注射)显著降低(P<0.005)Tx模型中的脂肪LPL活性。然而,尽管糖尿病有抑制作用(43±11%),酶活性仍与正常组相当。胰岛素刺激Tx糖尿病组的脂肪LPL。该酶对胰岛素和甲状腺功能减退表现出协同反应。随后在完整的糖尿病大鼠(低T3状态)中进行了研究。无论血清T3浓度如何,糖尿病均使脂肪LPL活性降低至相似程度(79±2%)。此外,胰岛素对脂肪LPL的刺激程度不受内源性血清T3的调节。然而,糖尿病组联合T3和胰岛素治疗减弱了脂肪LPL对胰岛素的反应。甲状腺功能减退和完整大鼠中脂肪LPL活性的这些不同调节与血清甘油三酯水平的显著但相反变化相关。这些研究表明,甲状腺功能减退可抵消糖尿病对肝素可释放大鼠脂肪LPL活性的抑制作用,并放大该酶对胰岛素的反应。(摘要截断于250字)

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