Paternal metabolic and cardiovascular risk factors for fetal growth restriction: a case-control study.
Paternal metabolic and cardiovascular risk factors for fetal growth restriction: a case-control study.
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DOI：
10.2337/dc12-1280
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发表时间：
2013-06
期刊：
影响因子：
16.2
通讯作者：
Williams DJ
中科院分区：
文献类型：
--
作者：
Hillman S;Peebles DM;Williams DJ
低出生体重后代的父亲更有可能在以后的生活中患2型糖尿病和心血管疾病。我们调查了在胎儿生长受限的后代出生时，父亲的胰岛素抵抗和心血管危险因素是否明显。我们进行了一项病例对照研究，在没有公认的胎儿疾病的情况下，与生育正常出生体重后代的男性（n = 77）相比，生育受胎儿生长受限影响的妊娠的男性（n = 42）。所有母亲均健康、不吸烟，年龄、BMI、种族和产次相似。在后代出生的4周内，所有父亲都测量了胰岛素抵抗（HOMA指数）、血压、腰围、内皮功能（血流介导的扩张）、血脂、体重和吸烟习惯。采用多变量逻辑回归分析进行比较。胎儿生长受限后代的父亲[平均值（SD）1.8th（2.2）定制出生百分位数]与正常生长后代的父亲相比，更可能患有胰岛素抵抗、高血压、中枢性肥胖和内皮功能障碍以及吸烟。多变量分析后，父亲的胰岛素抵抗和吸烟仍然是不同的组。与正常发育后代的父亲相比，受胎儿生长受限影响的妊娠男性的HOMA-IR值高1个单位的OR为7.68（95%CI 2.63-22.40; P < 0.0001），吸烟者为3.39（1.26-9.16; P = 0.016）。最近生育了生长受限后代的男性有胰岛素抵抗综合征的临床前证据，并且比正常生长后代的父亲更有可能吸烟。父亲的生活方式可能影响对胎儿生长重要的遗传因素。
Fathers of low–birth weight offspring are more likely to have type 2 diabetes and cardiovascular disease in later life. We investigated whether paternal insulin resistance and cardiovascular risk factors were evident at the time that fetal growth–restricted offspring were born. We carried out a case-control study of men who fathered pregnancies affected by fetal growth restriction, in the absence of recognized fetal disease (n = 42), compared with men who fathered normal–birth weight offspring (n = 77). All mothers were healthy, nonsmoking, and similar in age, BMI, ethnicity, and parity. Within 4 weeks of offspring birth, all fathers had measures of insulin resistance (HOMA index), blood pressure, waist circumference, endothelial function (flow-mediated dilatation), lipid profile, weight, and smoking habit. Comparison was made using multivariable logistical regression analysis. Fathers of fetal growth–restricted offspring [mean (SD) 1.8th (2.2) customized birth centile] were more likely to have insulin resistance, hypertension, central adiposity, and endothelial dysfunction and to smoke cigarettes compared with fathers of normal grown offspring. After multivariable analysis, paternal insulin resistance and smoking remained different between the groups. Compared with fathers of normal grown offspring, men who fathered pregnancies affected by fetal growth restriction had an OR 7.68 (95% CI 2.63–22.40; P < 0.0001) of having a 1-unit higher log HOMA-IR value and 3.39 (1.26–9.16; P = 0.016) of being a smoker. Men who recently fathered growth-restricted offspring have preclinical evidence of the insulin resistance syndrome and are more likely to smoke than fathers of normal grown offspring. Paternal lifestyle may influence heritable factors important for fetal growth.
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