Premature birth and later insulin resistance

被引:438
作者
Hofman, PL
Regan, F
Jackson, WE
Jefferies, C
Knight, DB
Robinson, EM
Cutfield, WS
机构
[1] Univ Auckland, Fac Med & Hlth Sci, Liggins Inst, Auckland 1, New Zealand
[2] Univ Auckland, Dept Community Hlth, Hlth Res Council Biostat Unit, Auckland 1, New Zealand
[3] Natl Womens Hosp Neonatal Unit, Auckland, New Zealand
关键词
D O I
10.1056/NEJMoa042275
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Term infants who are small for gestational age appear prone to the development of insulin resistance during childhood. We hypothesized that insulin resistance, a marker of type 2 diabetes mellitus, would be prevalent among children who had been born prematurely, irrespective of whether they were appropriate for gestational age or small for gestational age. Methods: Seventy-two healthy prepubertal children 4 to 10 years of age were studied: 50 who had been born prematurely (32 weeks' gestation or less), including 38 with a birth weight that was appropriate for gestational age (above the 10th percentile) and 12 with a birth weight that was low (i.e., who were small) for gestational age, and 22 control subjects (at least 37 weeks' gestation, with a birth weight above the 10th percentile). Insulin sensitivity was measured with the use of paired insulin and glucose data obtained by frequent measurements during intravenous glucose-tolerance tests. Results: Children who had been born prematurely, whether their weight was appropriate or low for gestational age, had an isolated reduction in insulin sensitivity as compared with controls (appropriate-for-gestational-age group, 14.2 x 10(-4) per minute per milliunit per liter [95 percent confidence interval, 11.5 to 16.2]; small-for-gestational-age group, 12.9 x 10(-4) per minute per milliunit per liter [95 percent confidence interval, 9.7 to 17.4]; and control group, 21.6 x 10(-4) per minute per milliunit per liter [95 percent confidence interval, 17.1 to 27.4]; P=0.002). There were no significant differences in insulin sensitivity between the two premature groups (P=0.80). As compared with controls, both groups of premature children had a compensatory increase in acute insulin release (appropriate-for-gestational-age group, 2002 pmol per liter [95 percent confidence interval, 2153 to 2432]; small-for-gestational-age group, 2253 pmol per liter [95 percent confidence interval, 1622 to 3128]; and control group, 1148 pmol per liter [95 percent confidence interval, 875 to 1500]; P<0.001). Conclusions: Like children who were born at term but who were small for gestational age, children who were born prematurely have an isolated reduction in insulin sensitivity, which may be a risk factor for type 2 diabetes mellitus.
引用
收藏
页码:2179 / 2186
页数:8
相关论文
共 32 条
[1]  
*AUCKL DISTR HLTH, 2004, NEWB SERV NAT WOM AN
[2]   TYPE 2 (NON-INSULIN-DEPENDENT) DIABETES-MELLITUS, HYPERTENSION AND HYPERLIPEMIA (SYNDROME-X) - RELATION TO REDUCED FETAL GROWTH [J].
BARKER, DJP ;
HALES, CN ;
FALL, CHD ;
OSMOND, C ;
PHIPPS, K ;
CLARK, PMS .
DIABETOLOGIA, 1993, 36 (01) :62-67
[3]  
BARKER DJP, 1989, LANCET, V2, P577
[4]   THE FETAL AND INFANT ORIGINS OF ADULT DISEASE [J].
BARKER, DJP .
BRITISH MEDICAL JOURNAL, 1990, 301 (6761) :1111-1111
[5]   GROWTH INUTERO, BLOOD-PRESSURE IN CHILDHOOD AND ADULT LIFE, AND MORTALITY FROM CARDIOVASCULAR-DISEASE [J].
BARKER, DJP ;
OSMOND, C ;
GOLDING, J ;
KUH, D ;
WADSWORTH, MEJ .
BRITISH MEDICAL JOURNAL, 1989, 298 (6673) :564-567
[6]   The long-term outcome of retarded fetal growth [J].
Barker, DJP .
CLINICAL OBSTETRICS AND GYNECOLOGY, 1997, 40 (04) :853-863
[7]   Fetal origins of adult disease:: strength of effects and biological basis [J].
Barker, DJP ;
Eriksson, JG ;
Forsén, T ;
Osmond, C .
INTERNATIONAL JOURNAL OF EPIDEMIOLOGY, 2002, 31 (06) :1235-1239
[8]   FETAL GROWTH AND ADULT DISEASE [J].
BARKER, DJP .
BRITISH JOURNAL OF OBSTETRICS AND GYNAECOLOGY, 1992, 99 (04) :275-276
[9]   In utero programming of chronic disease [J].
Barker, DJP .
CLINICAL SCIENCE, 1998, 95 (02) :115-128
[10]   Determinants of insulin sensitivity and secretion in very-low-birth-weight children [J].
Bazaes, RA ;
Alegría, A ;
Pittaluga, E ;
Avila, A ;
Iñiguez, G ;
Mericq, V .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2004, 89 (03) :1267-1272