Huang Ting-ting, Qiu Xiao-shan, Shen Zhen-yu, Ke Zhi-yong, Lai Feng
Pediatric Department, the First Affiliated Hospital of Sun Yet-Sen University, Guangzhou 510080, China.
Zhonghua Yu Fang Yi Xue Za Zhi. 2004 May;38(3):182-5.
To investigate the effects of pregnancy malnutrition on the occurrence of insulin resistance (IR) in rat offspring during adult stage and to find out the relationship between TNF-alpha and IR; and to find out a reasonable early nutritional intervention measure for the prevention of IR, through giving different diets to offspring.
An IUGR model was built by maternal nutrition restriction. 80 newborn IUGR female pups were randomly divided into 4 groups, the mother rats were given the following diet respectively for 3 weeks after delivery, pups were fed by mother milk: (1) The IUGR (intrauterine growth retardation) rat model was used and the animals were divided into: IUGR control group (group S/N) fed with normal diet, (2) IUGR high-caloric diet group (group A), (3) IUGR high-protein and high-caloric diet group (group B) and (4) IUGR high-protein isocaloric diet group (group C). Each group had 20 pups and another 20 normal female pups were fed with normal diet as the normal control group (group C/N). All pups were weaned at the 4th week of age and fed with normal diet till the end of the experiment. At the 12th week (adulthood) and 48th week (senility) of life, body weight and length, the fasting blood glucose, insulin concentration, TNF-alpha of adipose tissue and body weight were measured. Body mass index (BMI), ISI (insulin sensitive index), IRI (insulin resistant index) and HBCI (beta cell insulin excretion index) and their correlation to TNF-alpha were calculated.
At 12th week and 48th week of life, the insulin sensitivity of IUGR model group was significantly lower than group C/N, although there was no significant difference of body weight between these two groups. TNF-alpha was negatively correlated with ISI, positively correlated with IRI and no relation to HBCI. Group A and B was fatter and developed more severe IR. There were no significant differences in ISI, IRI, HBCI and TNF-alpha between group C and group C/N.
IUGR offspring of pregnancy malnutrition mother rats showed IR at the age of 12th week. TNF-alpha was closely related to the occurrence of IR in IUGR pups. IUGR pups fed with high caloric diet or high protein and caloric diet at the early postnatal period amplified the metabolic abnormality. The high protein isocaloric diet is effective early nutritional intervention measure for the prevention of occurrence of IR at adulthood.
探讨孕期营养不良对大鼠成年子代胰岛素抵抗(IR)发生的影响,明确肿瘤坏死因子-α(TNF-α)与IR之间的关系;通过给予子代不同饮食,探寻预防IR的合理早期营养干预措施。
采用母体营养限制构建宫内生长受限(IUGR)模型。80只新生IUGR雌性幼鼠随机分为4组,产后母鼠分别给予以下饮食3周,幼鼠母乳喂养:(1)采用IUGR(宫内生长迟缓)大鼠模型,动物分为:IUGR对照组(S/N组),喂以正常饮食;(2)IUGR高热量饮食组(A组);(3)IUGR高蛋白高热量饮食组(B组);(4)IUGR高蛋白等热量饮食组(C组)。每组20只幼鼠,另取20只正常雌性幼鼠喂以正常饮食作为正常对照组(C/N组)。所有幼鼠在4周龄时断奶,之后喂以正常饮食直至实验结束。在生命的第12周(成年期)和第48周(衰老期),测量体重、体长、空腹血糖、胰岛素浓度、脂肪组织TNF-α及体重。计算体重指数(BMI)、胰岛素敏感指数(ISI)、胰岛素抵抗指数(IRI)和β细胞胰岛素分泌指数(HBCI)及其与TNF-α的相关性。
在生命的第12周和第48周,IUGR模型组的胰岛素敏感性显著低于C/N组,尽管两组体重无显著差异。TNF-α与ISI呈负相关,与IRI呈正相关,与HBCI无关。A组和B组更胖,发生的IR更严重。C组与C/N组在ISI、IRI、HBCI和TNF-α方面无显著差异。
孕期营养不良母鼠的IUGR子代在12周龄时出现IR。TNF-α与IUGR幼鼠IR的发生密切相关。出生后早期喂以高热量饮食或高蛋白高热量饮食的IUGR幼鼠代谢异常加剧。高蛋白等热量饮食是预防成年期IR发生的有效早期营养干预措施。