Crace C J, Swenne I, Hill D J, Milner R D
Department of Paediatrics, University of Sheffield, UK.
Ups J Med Sci. 1991;96(1):17-22. doi: 10.3109/03009739109179255.
Rats subjected to temporary protein-energy malnutrition and subsequent nutritional rehabilitation remain smaller than adequately fed animals, have a subnormal insulin secretion and persisting cellular hypoplasia in several tissues. This investigation studies whether impaired production of insulin-like growth factor I (IGF I) is another persisting consequence of malnutrition. Rats were subjected to severe protein-energy malnutrition between 3 and 6 weeks of age and subsequently fed adequate diet up to 12 weeks of age. Serum and tissue samples for analysis of IGF I were obtained at 12 weeks of age. IGF I concentrations were similar in serum, heart, liver and lung of previously malnourished and control rats. In the kidneys of previously-malnourished rats the IGF I concentration was twice that of control rats. Results suggest that during protein-energy malnutrition and subsequent nutritional rehabilitation IGF I tissue concentrations are primarily regulated by the prevailing plane of nutrition. It is speculated that the temporary protein-energy malnutrition blunts the cellular capacity for IGF I production and, except in the kidney, prevents increased IGF I tissue concentrations and associated compensatory growth.
经历过短期蛋白质 - 能量营养不良并随后进行营养康复的大鼠,其体型仍比正常喂养的动物小,胰岛素分泌低于正常水平,且多个组织中存在持续性细胞发育不全。本研究旨在探究胰岛素样生长因子I(IGF - I)生成受损是否是营养不良的另一个持续性后果。大鼠在3至6周龄时遭受严重蛋白质 - 能量营养不良,随后在12周龄前给予充足饮食。在12周龄时获取血清和组织样本以分析IGF - I。先前营养不良的大鼠与对照大鼠的血清、心脏、肝脏和肺中的IGF - I浓度相似。先前营养不良的大鼠肾脏中的IGF - I浓度是对照大鼠的两倍。结果表明,在蛋白质 - 能量营养不良及随后的营养康复过程中,IGF - I组织浓度主要受当前营养水平调控。据推测,短期蛋白质 - 能量营养不良会削弱细胞产生IGF - I的能力,并且除肾脏外,会阻止IGF - I组织浓度升高及相关的代偿性生长。