Bairras C, Mauriege P, Bukowiecki L, Atgie C
Département Universitaire des Sciences d'Agen (DUSA), Université Bordeaux 1, Ave Michel Serres, 47 000 Agen, France.
J Physiol Biochem. 2007 Dec;63(4):287-96. doi: 10.1007/BF03165760.
Obese Zucker rat is often used as a model of genetic obesity to understand the mechanism of the development of obesity. In the present work, in order to better understand the regulation of lipolysis in the Zucker rat, the lipolytic activities of adipocytes isolated from different adipose depots of lean and obese Zucker rats, in the basal state or after catecholamine stimulation have been measured. The obese Zucker rat presents hyperinsulinemia without hyperglycemia and with elevated plasma free fatty acids, suggesting a dyslipidemia. Morphological studies of three adipose deposits show a marked hypertrophic and hyperplastic type of obesity, much pronounced in the subcutaneous depot. In the current study we show that the basal lipolytic rate is higher in adipocytes from each deposit of obese rats (when results are corrected for cell surface area). This finding, associated with the increase of all deposits, could contribute to the elevated plasma FFA observed. Investigation of the responsiveness of dibutyril cAMP (DBcAMP) points out that the defect in the NE responsiveness is essentially located at post-receptor level. Nevertheless, a receptor defect could not be excluded as suggested by a decrease of the beta-ARs observed in all deposits. Our study points out that the lipolytic resistance to catecholamines in adipose tissue of obese Zucker rats appears to counteract the increase in the lipolytic rate, in order to moderate the increase in plasma FFA levels that may contribute to the hyperinsulinemia observed, characteristic of an insulino-resistant state.
肥胖 Zucker 大鼠常被用作遗传性肥胖模型，以了解肥胖发生发展的机制。在本研究中，为了更好地理解 Zucker 大鼠脂肪分解的调节机制，我们测定了从瘦 Zucker 大鼠和肥胖 Zucker 大鼠不同脂肪库分离的脂肪细胞在基础状态或儿茶酚胺刺激后的脂肪分解活性。肥胖 Zucker 大鼠表现为高胰岛素血症但无高血糖，且血浆游离脂肪酸升高，提示存在血脂异常。对三种脂肪沉积的形态学研究显示出明显的肥大性和增生性肥胖类型，在皮下脂肪库中更为明显。在本研究中，我们发现肥胖大鼠各脂肪库的脂肪细胞基础脂肪分解率更高（当结果校正细胞表面积时）。这一发现与所有脂肪库的增加相关，可能导致观察到的血浆游离脂肪酸升高。对二丁酰环磷腺苷（DBcAMP）反应性的研究指出，去甲肾上腺素反应性缺陷主要位于受体后水平。然而，正如在所有脂肪库中观察到的β-肾上腺素能受体减少所提示的，不能排除受体缺陷。我们的研究指出，肥胖 Zucker 大鼠脂肪组织对儿茶酚胺的脂肪分解抵抗似乎抵消了脂肪分解率的增加，以缓和可能导致观察到的高胰岛素血症的血浆游离脂肪酸水平的升高，这是胰岛素抵抗状态的特征。
