Finken M J J, Keijzer-Veen M G, Dekker F W, Frölich M, Hille E T M, Romijn J A, Wit J M
Department of Pediatrics, Leiden University Medical Center, P.O. Box 9600, 2300, RC Leiden, The Netherlands.
Diabetologia. 2006 Mar;49(3):478-85. doi: 10.1007/s00125-005-0118-y. Epub 2006 Feb 1.
AIMS/HYPOTHESIS: An increased risk of type 2 diabetes mellitus is associated with low birthweight after full-term gestation, including amplification of this risk by weight gain during infancy and adult body composition. Premature birth is also associated with insulin resistance, but studies conducted so far have not provided follow-up into adulthood. We studied the effects of (1) lower birthweight (as standard deviation score [SDS]) and infancy weight gain on insulin resistance in 19-year-olds born before 32 weeks of gestation, and (2) the interaction between lower birthweight SDS and infancy weight gain, as well as between lower birthweight and adult body composition, on insulin resistance.
This was a prospective follow-up study in 346 subjects from the Project on Preterm and Small-for-gestational-age infants cohort, in whom fasting glucose, insulin and C-peptide levels were measured at 19 years. Insulin resistance was calculated with homeostatic modelling (homeostatic model assessment for insulin resistance index [HOMA-IR]).
Birthweight SDS was unrelated to the outcomes. Rapid infancy weight gain until 3 months post-term was weakly associated with higher insulin level (p=0.05). Adult fatness was positively associated with insulin and C-peptide levels and HOMA-IR (all p<0.001). On these parameters, there was a statistical interaction between birthweight SDS and adult fat mass (p=0.002 to 0.03).
CONCLUSIONS/INTERPRETATION: In subjects born very preterm, rapid infancy weight gain until 3 months predicted higher insulin levels at 19 years, but the association was weak. Adult obesity strongly predicted higher insulin and C-peptide levels as well as HOMA-IR. The effect of adult fat mass on these parameters was dependent on its interaction with birthweight SDS.
目的/假设:足月妊娠后低出生体重与2型糖尿病风险增加相关,包括婴儿期体重增加和成年人体成分对这种风险的放大作用。早产也与胰岛素抵抗有关,但迄今为止的研究尚未对成年期进行随访。我们研究了以下因素的影响:(1)出生体重较低(以标准差评分[SDS]表示)和婴儿期体重增加对妊娠32周前出生的19岁人群胰岛素抵抗的影响;(2)出生体重较低的SDS与婴儿期体重增加之间的相互作用,以及出生体重较低与成年人体成分之间的相互作用对胰岛素抵抗的影响。
这是一项对来自早产和小于胎龄儿队列研究项目的346名受试者进行的前瞻性随访研究,在他们19岁时测量空腹血糖、胰岛素和C肽水平。采用稳态模型计算胰岛素抵抗(胰岛素抵抗指数的稳态模型评估[HOMA-IR])。
出生体重SDS与研究结果无关。直到足月后3个月婴儿期体重快速增加与较高的胰岛素水平弱相关(p=0.05)。成年肥胖与胰岛素、C肽水平和HOMA-IR呈正相关(所有p<0.001)。在这些参数上,出生体重SDS与成年脂肪量之间存在统计学相互作用(p=0.002至0.03)。
结论/解读:在极早产出生的受试者中,直到3个月时婴儿期体重快速增加预示着19岁时胰岛素水平较高,但这种关联较弱。成年肥胖强烈预示着较高的胰岛素和C肽水平以及HOMA-IR。成年脂肪量对这些参数的影响取决于其与出生体重SDS的相互作用。