Low birth weight leads to obesity, diabetes and increased leptin levels in adults: the CoLaus study.
Low birth weight leads to obesity, diabetes and increased leptin levels in adults: the CoLaus study.
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DOI：
10.1186/s12933-016-0389-2
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发表时间：
2016-05-03
影响因子：
9.3
通讯作者：
Marques-Vidal P
中科院分区：
文献类型：
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作者：
Jornayvaz FR;Vollenweider P;Bochud M;Mooser V;Waeber G;Marques-Vidal P
低出生体重与肥胖、胰岛素抵抗和2型糖尿病的发病率增加有关，但这种联系的确切机制仍不清楚。我们的目的是评估出生体重和葡萄糖稳态标志物或成人肥胖之间的关系。对居住在瑞士洛桑的年龄在35-75岁之间的1458名女性和1088名男性进行的横断面人群研究。出生体重是自我报告的，并分为≤2.5、2.6-3.5、3.6-4.0和>4.0 kg。通过生物阻抗评估身体组成。用ELISA法测定瘦素和脂联素水平。低出生体重（≤2.5 kg）的女性空腹血糖、胰岛素、HOMA、糖尿病和代谢综合征水平较高;男性中未观察到显著相似的趋势。在两种性别中，身高随着出生体重的增加而增加，而出生体重与体重指数、腰围和体脂百分比之间存在U形关联。在调整年龄，吸烟状况，体力活动和脂肪量后，瘦素和出生体重类别之间存在负相关：出生体重类别≤2.5、2.6-3.5、3.6-4.0和>4.0 kg的校正平均值±标准误分别为17.3 ± 0.7、16.2 ± 0.3、15.6 ± 0.5和14.0 ± 0.8 ng/dL，女性分别为9.8 ± 0.8、9.1 ± 0.3、7.8 ± 0.4和7.7 ± 0.5 ng/dL（p < 0.05）。报告的出生体重与瘦素/脂肪质量比之间也存在负相关：女性的平均值±标准误为0.77 ± 0.04，0.73 ± 0.02，0.69 ± 0.03和0.62 ± 0.04男性为0.46 ± 0.05，0.45 ± 0.02，0.39 ± 0.02，0.38 ± 0.03（p < 0.05）。出生体重组之间的脂联素水平没有差异。出生体重低的中年人比出生体重正常的成年人有更高的糖尿病和肥胖患病率，也有更高的瘦素水平和瘦素与脂肪质量比。出生体重低的成年人中较高的瘦素水平和瘦素与脂肪质量比可能与儿童期的营养因素或瘦素抵抗的发展和/或体脂单位产生的较高瘦素有关。出生时体重较低的受试者应接受有关发生糖尿病和/或心血管疾病风险的咨询。本文的在线版本（doi：10.1186/s12933-016-0389-2）包含补充材料，可供授权用户使用。
Low birth weight is associated with increased rates of obesity, insulin resistance and type 2 diabetes, but the precise mechanisms for this association remain unclear. We aimed to assess the relationships between birth weight and markers of glucose homeostasis or obesity in adults. Cross-sectional population-based study on 1458 women and 1088 men aged 35–75 years living in Lausanne, Switzerland. Birth weight was self-reported and categorized into ≤2.5, 2.6–3.5, 3.6–4.0 and >4.0 kg. Body composition was assessed by bioimpedance. Leptin and adiponectin levels were measured by ELISA. Women with low birth weight (≤2.5 kg) had higher levels of fasting plasma glucose, insulin, HOMA, diabetes and metabolic syndrome; a non significant similar trend was seen in men. In both genders, height increased with birth weight, whereas a U-shaped association was found between birth weight and body mass index, waist circumference and body fat percentage. After adjusting for age, smoking status, physical activity and fat mass, an inverse association was found between leptin and birth weight categories: adjusted mean ± standard error 17.3 ± 0.7, 16.2 ± 0.3, 15.6 ± 0.5 and 14.0 ± 0.8 ng/dL for birth weight categories ≤2.5, 2.6–3.5, 3.6–4.0 and >4.0 kg, respectively, in women (p < 0.05) and 9.8 ± 0.8, 9.1 ± 03, 7.8 ± 0.4 and 7.7 ± 0.5 ng/dL in men (p < 0.05). An inverse association was also found between reported birth weight and leptin to fat mass ratio: mean ± standard error 0.77 ± 0.04, 0.73 ± 0.02, 0.69 ± 0.03 and 0.62 ± 0.04 in women (p < 0.05); 0.46 ± 0.05, 0.45 ± 0.02, 0.39 ± 0.02 and 0.38 ± 0.03 in men (p < 0.05). No differences in adiponectin levels were found between birth weight groups. Middle-aged adults born with a low weight present a higher prevalence of diabetes and obesity and also higher leptin levels and leptin to fat mass ratio than adults born with a normal weight. The higher leptin levels and leptin to fat mass ratio among adults born with a low weight might be related to nutritional factors during childhood or to the development of leptin resistance and/or higher leptin production by body fat unit. Subjects born with a low weight should be counselled regarding the risks of developing diabetes and/or cardiovascular disease. The online version of this article (doi:10.1186/s12933-016-0389-2) contains supplementary material, which is available to authorized users.