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将肉鸡脂肪细胞在体外长时间暴露于生长抑素会增强脂肪分解,并诱导抗脂肪分解作用的脱敏。

Prolonged in vitro exposure of broiler adipocytes to somatostatin enhances lipolysis and induces desensitization of antilipolysis.

作者信息

Oscar T P

机构信息

Agricultural Research Service, USDA, Princess Anne, Maryland 21853, USA.

出版信息

Poult Sci. 1996 Mar;75(3):393-401. doi: 10.3382/ps.0750393.

Abstract

Adipocytes isolated from abdominal fat of female broilers and maintained in primary culture were used to characterize acute and chronic effects of somatostatin (SRIF) on lipolysis and antilipolysis and to determine whether desensitization and cross-regulation phenomena are involved in the regulation of adipocyte metabolism by SRIF and glucagon. Acute exposure of adipocytes to SRIF resulted in a dose-dependent inhibition of basal and glucagon-stimulated lipolysis. The potency and extent of lipolysis inhibition by SRIF were inversely related to the dose of glucagon used to stimulate lipolysis. Preincubation of adipocytes with SRIF induced a dose-response and time-dependent increase in the set-point of lipolysis. Adipocyte sensitivity to glucagon was not altered by SRIF pretreatment. In contrast, preincubation with SRIF reduced adipocyte sensitivity and maximal responsiveness to SRIF. The pattern and extent of antilipolysis attenuation were dependent on the dose and time of preincubation with SRIF as well as on the concentration of glucagon used to acutely stimulate lipolysis. In two experiments, the attenuation of antilipolysis induced by SRIF pretreatment was observed in the absence of enhanced lipolysis, whereas in one experiment enhanced lipolysis was observed in the absence of attenuated antilipolysis. These results indicated that persistent activation of antilipolysis by SRIF increased the set-point of lipolysis by sensitizing (i.e., cross-regulating) lipolysis and by desensitizing antilipolysis.

摘要

从雌性肉鸡腹部脂肪中分离并维持在原代培养中的脂肪细胞,用于表征生长抑素(SRIF)对脂肪分解和抗脂肪分解的急性和慢性影响,并确定脱敏和交叉调节现象是否参与SRIF和胰高血糖素对脂肪细胞代谢的调节。脂肪细胞急性暴露于SRIF会导致基础和胰高血糖素刺激的脂肪分解呈剂量依赖性抑制。SRIF对脂肪分解的抑制效力和程度与用于刺激脂肪分解的胰高血糖素剂量呈负相关。脂肪细胞与SRIF预孵育会导致脂肪分解设定点呈剂量反应和时间依赖性增加。SRIF预处理不会改变脂肪细胞对胰高血糖素的敏感性。相反,与SRIF预孵育会降低脂肪细胞对SRIF的敏感性和最大反应性。抗脂肪分解减弱的模式和程度取决于与SRIF预孵育的剂量和时间以及用于急性刺激脂肪分解的胰高血糖素浓度。在两个实验中,在没有增强脂肪分解的情况下观察到SRIF预处理诱导的抗脂肪分解减弱,而在一个实验中,在没有抗脂肪分解减弱的情况下观察到增强的脂肪分解。这些结果表明,SRIF对抗脂肪分解的持续激活通过使脂肪分解敏感化(即交叉调节)和使抗脂肪分解脱敏来增加脂肪分解的设定点。

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