Early appearance of the metabolic syndrome in socially reared bonnet macaques
Early appearance of the metabolic syndrome in socially reared bonnet macaques
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DOI：
10.1210/jc.2004-0452
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发表时间：
2005-01-01
影响因子：
5.8
通讯作者：
Rosenblum, LA
中科院分区：
文献类型：
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作者：
Kaufman, D;Smith, ELP;Rosenblum, LA
在250只实验室出生的帽子猕猴中，生活在社会群体中并以商业猴食为食，我们测量了体重、顶臀长、腹矢径（SAD）以及空腹血清胰岛素、葡萄糖、甘油三酯、高密度脂蛋白、低密度脂蛋白和总胆固醇。测量体重指数（BMI =体重/顶臀长（2））和通过胰岛素/葡萄糖比率（IGR）和稳态模型评估确定的胰岛素抵抗。我们使用基于形态测量、胰岛素抵抗和血脂水平的综合评分来定义代谢综合征，类似于临床标准。BMI升高与SAD、胰岛素、IGR、稳态模型评估和甘油三酯显著增加相关。在120只5-17岁的成年猴中，雄性（n = 48）的BMI、SAD、胰岛素和IGR水平高于雌性，与年龄无关。113只成年猴中的16只和36只青春期受试者中的5只，年龄3-4岁（14%），符合我们的代谢综合征标准，12只猴中的4只，年龄20-28岁。代谢综合征的标志物在我们的群体中存在于3-4岁的年龄，并且在没有常规肥胖干预的情况下在整个生命周期中观察到。社会饲养和圈养的帽子猕猴可能为研究代谢综合征的发病机制，预防和治疗提供了一个有用的模型。
Among 250 laboratory-born bonnet macaques living in social groups and maintained on commercial monkey chow, we measured weight, crown-rump length, sagittal abdominal diameter (SAD), and fasting serum insulin, glucose, triglycerides, high-density lipoproteins, low-density lipoproteins, and total cholesterol. Body mass index (BMI = weight/crown-rump length(2)), and insulin resistance determined by the insulin/glucose ratio (IGR) and homeostasis model assessment, were measured. We defined the metabolic syndrome using a composite score based on morphometry, insulin resistance, and serum lipid levels, analogous to clinical criteria. Elevated BMI was associated with significantly greater SAD, insulin, IGR, homeostasis model assessment, and triglycerides. Among 120 adult monkeys aged 5-17 yr, males (n = 48) had higher BMI, SAD, insulin, and IGR levels than females, independent of age. Sixteen of 113 adult monkeys and five of 36 peripubertal subjects, aged 3-4 yr (14%), met our criteria for the metabolic syndrome, as did four of 12 monkeys, aged 20-28 yr. Markers of the metabolic syndrome are present by 3-4 yr of age in our colony and are observed across the life span in the absence of conventional obesifying interventions. Socially reared and housed bonnet macaques may provide a useful model for studying the pathogenesis, prevention, and treatment of the metabolic syndrome.