ORIGINAL COMMUNICATION Shortness at birth is associated with insulin resistance in pre-pubertal Jamaican children F Bennett 1 , C Watson-Brown 1 , M Thame 1 , R Wilks 1 , C Osmond 2 , N Hales 3 , D Barker 3 and T Forrester 1 * 1 Tropical Metabolism Research Unit, University of the West Indies, Kingston, Jamaica, West Indies; 2 MRC Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, UK; and 3 Department of Clinical Biochemistry, University of Cambridge, Cambridge, UK Aim: To investigate the relationship between anthropometry at birth and glucose=insulin metabolism in childhood using the response to an oral glucose challenge. Method: Four hundred mother=child pairs on whom gestational and birth data were available were studied. After an overnight fast, anthropometric measurements were made on the children and an oral glucose tolerance test performed. The plasma concentrations of insulin, pro-insulin and 32 – 33 split pro-insulin were also measured. Skinfold thicknesses were used to calculate percentage body fat and fat mass was derived from the percentage fat and absolute weight. Results: The mean age of the children was 8 y (range 7.5 – 10.5), and six exhibited impaired glucose tolerance based on WHO criteria. Insulin concentration 120 min after the oral glucose load (a measure of insulin resistance) was inversely related to length at birth (P<0.005). The children who were in the shortest quartile at birth and were heaviest at 8 y old had the highest insulin concentration. Conclusion: Shortness at birth is related to insulin resistance. Such insensitivity to the action of insulin is greater in heavier children. European Journal of Clinical Nutrition (2002) 56, 506 – 511. doi:10.1038=sj.ejcn.1601339 Keywords: type 2 diabetes mellitus; crown – heel length; insulin resistance Introduction In Jamaica, diabetes mellitus is an important disease with a prevalence of 13.4% (Cooper et al, 1997) and it accounts for 10% of total mortality. (The Statistical Institute of Jamaica, 1996). These rates are higher than those reported for West Africa (Cooper et al, 1997). Data on the role of genetic factors in the aetiology and pathogenesis of diabetes in these popu- lations are not available, but the gradient in prevalence across these populations of African origin is partly attribu- table to increasing body mass index (BMI; Cooper et al, 1997). Fetal programming of glucose intolerance might also make a significant contribution to the genesis of type 2 diabetes mellitus (Hales et al, 1991; Forrester et al, 1996; Phipps et al, 1993; Leger et al, 1997). Recent studies have shown that impaired glucose tolerance and frank diabetes in adult life are related to growth restraint during fetal life (Hales et al, 1991; Barker, 1994). Abnormal glucose tolerance has been described in relation to lower birth weight, pond- eral index and growth in early childhood (Hales et al, 1991; Barker, 1994). In Jamaica, the informative phenotype appears to be shortness at birth (Forrester et al, 1996) rather than thinness as in the UK (Law et al, 1995). *Correspondence: T Forrester, Tropical Metabolism Research Unit, University of the West Indies, Mona, Kingston 7, Jamaica, West Indies. E-mail: tmru@infochan.com Guarantor: T Forrester. Contributors: FB contributed to the design of the study and the collection, analysis and presentation of data. He was principally responsible for the blood glucose assays. CNH performed the insulin assays. CW-B assisted with logistical coordination of the study, the making of all measurements and collection of blood. She also contributed to data analysis and manuscript preparation. MT assisted in logistics, measurement, data analysis and manuscript preparation. CO assisted with study design and took the lead in data analysis. He also contributed to manuscript preparation. DB and NH both participated in study design and manuscript preparation. TF conceived the study, was lead author for the grant to fund the study and supervised all aspects of the study including logistics, data collection, data analysis and manuscript preparation. Received 11 December 2000; revised 5 September 2001; accepted 6 September 2001 European Journal of Clinical Nutrition (2002) 56, 506–511 ß 2002 Nature Publishing Group All rights reserved 0954–3007/02 $25.00 www.nature.com/ejcn