Plagemann A, Rittel F, Waas T, Harder T, Rohde W
Institute of Experimental Endocrinology, Humboldt University Medical School (Charité), Berlin, Germany.
Regul Pept. 1999 Dec 23;85(2-3):109-13. doi: 10.1016/s0167-0115(99)00085-3.
Perinatal malnutrition and growth retardation at birth are suggested to be important risk factors for the development of overweight and syndrome X in later life. Underlying mechanisms are unknown. Body weight and food intake are regulated, e.g. by hypothalamic neuropeptidergic systems which are thought to be highly vulnerable to persisting malorganization due to perinatal malnutrition. To investigate possible consequences for hypothalamic cholecystokinin-8S (CCK-8S) in the offspring, pregnant Wistar rats were fed an 8% protein diet during pregnancy and lactation (low-protein group; LP) while control mothers (CO) received a 17% protein isocaloric standard diet. LP offspring displayed underweight at birth (P < 0.05) and during suckling (P < 0.001), while leptin levels were not altered. At weaning, under basal conditions CCK-8S was decreased in LP offspring in the paraventricular hypothalamic nucleus and arcuate hypothalamic nucleus (P < 0.05), as well as in the dorsomedial hypothalamic nucleus, lateral hypothalamic area and ventromedial hypothalamic nucleus (P < 0.01). In summary, these data indicate (1) an inhibition of the satiety peptide CCK-8S in main regulators of body weight and food intake in low-protein malnourished newborn rats; (2) no direct relationship of hypothalamic CCK-8S to circulating leptin at this age; and (3) no neurochemical signs of hypothalamic CCKergic dysregulation in this animal model at the age of weaning.
围产期营养不良和出生时生长发育迟缓被认为是日后超重和X综合征发生的重要危险因素。其潜在机制尚不清楚。体重和食物摄入量受例如下丘脑神经肽能系统的调节，该系统被认为因围产期营养不良而极易受到持续的结构紊乱影响。为了研究对后代下丘脑胆囊收缩素8S（CCK - 8S）可能产生的影响，将怀孕的Wistar大鼠在妊娠和哺乳期喂食8%蛋白质饮食（低蛋白组；LP），而对照母鼠（CO）接受17%蛋白质的等热量标准饮食。LP组后代出生时（P < 0.05）和哺乳期间（P < 0.001）体重不足，而瘦素水平未改变。断奶时，在基础条件下，LP组后代下丘脑室旁核、弓状核中的CCK - 8S减少（P < 0.05），在背内侧下丘脑核、外侧下丘脑区和腹内侧下丘脑核中也减少（P < 0.01）。总之，这些数据表明：（1）低蛋白营养不良新生大鼠体重和食物摄入的主要调节因子中饱足肽CCK - 8S受到抑制；（2）这个年龄段下丘脑CCK - 8S与循环瘦素无直接关系；（3）在断奶时这个动物模型中没有下丘脑CCK能失调的神经化学迹象。
