ABSTRACT
Obese Zucker rat is often used as a model of genetic obesity to understand themechanism of the development of obesity. In the present work, in order to betterunderstand the regulation of lipolysis in the Zucker rat, the lipolytic activities ofadipocytes isolated from different adipose depots of lean and obese Zucker rats, inthe basal state or after catecholamine stimulation have been measured. The obeseZucker rat presents hyperinsulinemia without hyperglycemia and with elevated plasmafree fatty acids, suggesting a dyslipidemia. Morphological studies of three adiposedeposits show a marked hypertrophic and hyperplastic type of obesity, much pronouncedin the subcutaneous depot. In the current study we show that the basallipolytic rate is higher in adipocytes from each deposit of obese rats (when results arecorrected for cell surface area). This finding, associated with the increase of alldeposits, could contribute to the elevated plasma FFA observed. Investigation of theresponsiveness of dibutyril cAMP (DBcAMP) points out that the defect in the NEresponsiveness is essentially located at post-receptor level. Nevertheless, a receptordefect could not be excluded as suggested by a decrease of the â-ARs observed in alldeposits. Our study points out that the lipolytic resistance to catecholamines in adiposetissue of obese Zucker rats appears to counteract the increase in the lipolyticrate, in order to moderate the increase in plasma FFA levels that may contribute tothe hyperinsulinemia observed, characteristic of an insulino-resistant state (AU)
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