Thajchayapong P, Queener S F, McClintock R, Allen D O, Bell N H
Horm Metab Res. 1976 May;8(3):190-5. doi: 10.1055/s-0028-1093658.
Studies were carried out with rat epididymal fat pads first to compare the effects of the synthetic N-terminal 1-34 peptide of bovine parathyroid hormone and of the native hormone to determine whether this portion of the molecule is responsible for the lipolytic action of the hormone and second to determine whether this biologic action of parathyroid hormone is mediated by cyclic adenosine 3',5'-monophosphate. The N-terminal polypeptide was as effective as the native hormone in stimulating lipolysis in the concentration range between 10(-8) M and 10(-6) M. Parathyroid hormone stimulated lipolysis by isolated fat cells. The concentration of cyclic adenosine 3',5'-monophosphate in the fat pads was significantly increased by the hormone (10(-6)M). Lipolytic stimulation by parathyroid hormone (10(-6)M) was diminished by insulin (100 muU/ml) and prostaglandin E1 (1 mug/ml), both of which are known inhibitors of lipolysis. The findings indicate that the amino-terminal 1-34 peptide portion of parathyroid hormone is responsible for the lipolytic action and that this effect is mediated through cyclic adenosine 3',5'-monophosphate.
首先用大鼠附睾脂肪垫进行研究，比较牛甲状旁腺激素的合成N端1 - 34肽与天然激素的作用，以确定该分子的这一部分是否负责激素的脂解作用；其次确定甲状旁腺激素的这种生物学作用是否由环磷酸腺苷介导。在10(-8)M至10(-6)M的浓度范围内，N端多肽在刺激脂解方面与天然激素一样有效。甲状旁腺激素可刺激分离的脂肪细胞进行脂解。激素（10(-6)M）可使脂肪垫中环磷酸腺苷的浓度显著增加。胰岛素（100微单位/毫升）和前列腺素E1（1微克/毫升）可减弱甲状旁腺激素（10(-6)M）的脂解刺激作用，这两种物质均为已知的脂解抑制剂。这些发现表明，甲状旁腺激素的氨基端1 - 34肽部分负责脂解作用，且这种作用是通过环磷酸腺苷介导的。
