Dubuc P U
Am J Physiol. 1976 Jun;230(6):1474-9. doi: 10.1152/ajplegacy.1976.230.6.1474.
In ob/ob mice a 12-wk period of food restriction led to a reduced rate of somatic growth and a decreased lean body mass, along with small but reliable reductions in systemic immunoreactive insulin levels and evidence of increased insulin sensitivity. However, no effects of limited access to food were noted on the basal hyperglycemia, the elevated percent carcass lipid, or on the significantly higher levels of serum corticoids that occur in obese animals. These data indicate that hyperphagia alone is not responsible for the maintenance of many of the commonly reported characteristics of the obese-hyperglycemic syndrome, but do not exclude the contribution of factors secondary to the quantity of ingested food. Additionally, the present data lend support to recent work suggesting that chronic hyperinsulinemia or an elevated set point of total carcass lipid may be instrumental in the development of this syndrome.
在ob/ob小鼠中，为期12周的食物限制导致躯体生长速率降低和去脂体重减少，同时全身免疫反应性胰岛素水平有小幅但可靠的下降，并有胰岛素敏感性增加的证据。然而，食物获取受限对基础高血糖、胴体脂质百分比升高或肥胖动物中显著更高的血清皮质激素水平并无影响。这些数据表明，单纯的摄食过多并非导致肥胖 - 高血糖综合征许多常见特征持续存在的原因，但并不排除摄入食物量继发因素的作用。此外，目前的数据支持了最近的研究工作，即慢性高胰岛素血症或总胴体脂质设定点升高可能在该综合征的发展中起作用。
