Hugi D, Bruckmaier R M, Blum J W
Division of Nutrition Pathology, University, Berne, Switzerland.
J Anim Sci. 1997 Feb;75(2):469-82. doi: 10.2527/1997.752469x.
Calves intensively fed milk replacers frequently develop postprandial insulin resistance, characterized by excessively elevated plasma insulin concentrations, hyperglycemia, and glucosuria. To test the hypothesis that insulin secretion and insulin-dependent dependent glucose metabolism are modified by age and carbohydrate intake, 20 male calves (Simmental x Red Holstein) were fed a milk replacer containing 290 and 423 g lactose/kg DM from 60-70 to 190-200 kg BW. Responses of insulin and glucose to milk replacer intake and orally administered glucose and pre- and postprandial glucose responses to i.v. infused glucose and i.v. injected insulin were tested at 75-105 and 160-200 kg BW. Urine was collected during 24h to determine glucose, galactose, dopamine, noradrenaline, and creatinine excretion. Insulin resistance, hyperinsulinemia, hyperglycemia, glucosuria, and galactosuria developed with increasing age and occurred primarily postprandially. High lactose intake enhanced postprandial hyperglycemia but did not significantly increase glucosuria, galactosuria, and hyperinsulinemia. Based on urinary excretion of dopamine and noradrenaline there was a marked age-dependent increase in the activity of the sympathetic nervous system, which was not modified by lactose intake. high feeding intensity and lactose intake, excessive hyperinsulinemia per se and enhanced activity of the sympathetic nervous system possibly contributed to the development of insulin resistance. Glucose-dependent insulinotropic polypeptide, growth hormone and cortisol concentrations, and iron intake were low and comparable in both groups and therefore were etiologically not involved in the development of insulin resistance. Increasing circulating concentrations of insulin-like growth factor I during growth may have in part allowed high growth rates in the presence of insulin resistance.
人工代乳粉集中喂养的犊牛经常出现餐后胰岛素抵抗，其特征为血浆胰岛素浓度过度升高、高血糖和糖尿。为了验证胰岛素分泌和胰岛素依赖性葡萄糖代谢受年龄和碳水化合物摄入量影响这一假设，选取20头雄性犊牛（西门塔尔牛×红荷斯坦牛），在体重从60 - 70千克增长到190 - 200千克期间，给它们喂食每千克干物质含290克和423克乳糖的人工代乳粉。在体重75 - 105千克和160 - 200千克时，测试胰岛素和葡萄糖对人工代乳粉摄入、口服葡萄糖的反应，以及静脉输注葡萄糖和静脉注射胰岛素前后的餐后葡萄糖反应。收集24小时尿液以测定葡萄糖、半乳糖、多巴胺、去甲肾上腺素和肌酐排泄量。胰岛素抵抗、高胰岛素血症、高血糖、糖尿和半乳糖尿随着年龄增长而出现，且主要发生在餐后。高乳糖摄入量会加剧餐后高血糖，但不会显著增加糖尿、半乳糖尿和高胰岛素血症。基于多巴胺和去甲肾上腺素的尿排泄量，交感神经系统的活性有明显的年龄依赖性增加，且不受乳糖摄入量影响。高饲养强度和乳糖摄入量、胰岛素血症本身过高以及交感神经系统活性增强可能导致了胰岛素抵抗的发生。两组的葡萄糖依赖性促胰岛素多肽、生长激素和皮质醇浓度以及铁摄入量均较低且相当，因此在病因学上与胰岛素抵抗的发生无关。生长过程中循环胰岛素样生长因子I浓度的增加可能在一定程度上使得在存在胰岛素抵抗的情况下仍能实现高生长率。
