Thio Liu Lin, Erbayat-Altay Ebru, Rensing Nicholas, Yamada Kelvin A
Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Pediatr Res. 2006 Oct;60(4):413-7. doi: 10.1203/01.pdr.0000238244.54610.27. Epub 2006 Aug 28.
The ketogenic diet (KD) is an efficacious therapy for medically refractory childhood epilepsy that also slows weight gain. We tested the hypothesis that the KD slows weight gain via neurohormones involved in energy homeostasis. We found that juvenile rodents fed a KD had slower weight gain than those fed a standard diet (SD). Rats fed a KD had higher serum leptin levels and lower insulin levels compared with those fed an SD. We investigated the increase in leptin further because this change was the only one consistent with slower weight gain. Although rats fed the SD experienced slower weight gain when calorie restricted, they had serum leptin levels similar to those fed the SD ad libitum. Furthermore, leptin deficient (ob/ob) and leptin receptor deficient (db/db) mice did not show slower weight gain on the KD. All animals on the KD had elevated serum beta-hydroxybutyrate (betaHB) levels. Thus, ketosis is insufficient and a functioning leptin signaling system appears necessary for the KD to slow weight gain. The increase in leptin may contribute to the anticonvulsant effects of the KD.
生酮饮食（KD）是治疗药物难治性儿童癫痫的一种有效疗法，它还能减缓体重增加。我们检验了这样一个假设，即KD通过参与能量平衡的神经激素来减缓体重增加。我们发现，喂食KD的幼年啮齿动物比喂食标准饮食（SD）的动物体重增加更慢。与喂食SD的大鼠相比，喂食KD的大鼠血清瘦素水平更高，胰岛素水平更低。我们进一步研究了瘦素的增加，因为这种变化是唯一与体重增加减缓相一致的。尽管限制热量摄入时喂食SD的大鼠体重增加较慢，但它们的血清瘦素水平与自由进食SD的大鼠相似。此外，瘦素缺乏（ob/ob）和瘦素受体缺乏（db/db）的小鼠在KD饮食下体重增加并未减缓。所有采用KD饮食的动物血清β-羟基丁酸（βHB）水平均升高。因此，酮症并不充分，而一个正常运作的瘦素信号系统似乎是KD减缓体重增加所必需的。瘦素的增加可能有助于KD的抗惊厥作用。
