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Obesity and the insulin resistance syndrome
  1. D B Dunger
  1. Correspondence to:
    Prof. D B Dunger
    Addenbrooke’s Hospital, Cambridge CB2 2QQ, UK; dbd25cam.ac.uk

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Commentary on the paper by Viner et al (see 10)

The increasing prevalence of obesity during childhood in the UK has been highlighted by several recent publications1,2 and has become the subject of considerable debate, not only in the media but also through the establishment of a select committee at the House of Commons and a working group of our own Royal College. The alarm bells have been ringing on the other side of the Atlantic for several years where the prevalence of obesity and type 2 diabetes during childhood has been increasing dramatically.3 A paper from the Yale group published in 2002 reported the presence of impaired glucose tolerance in 20–25% of obese children and adolescents and a further 4% had undiagnosed type 2 diabetes.4 Other reports from the Bogalusa cohort in the USA suggested that as many as 50% of overweight youngsters will have features of syndrome X (the insulin resistance syndrome5). Thus, the report from Viner et al is both timely and relevant as it assesses the prevalence of these risk factors in obese UK children and adolescents.6

The authors report both prospective and retrospective data on 103 obese children and adolescents aged 2–18 years. They report that one third of these children had features of the insulin resistance syndrome. The occurrence of impaired glucose tolerance in this cohort despite, in many cases extreme obesity, was only around 11% and none of the subjects had previously undiagnosed type 2 diabetes. This is perhaps encouraging given the high rates of impaired glucose tolerance reported in obese children from the USA and Far East. Nevertheless, overall the data should give us cause for concern as population studies indicate that these adverse features will track into adult life and, although it remains relatively rare, the first reports of type 2 diabetes occurring during childhood in the UK are now emerging.

Viner et al report data from a very selected population attending an obesity clinic at Great Ormond Street Hospital6 and, although their findings are similar to those reported by others who have set up similar clinics over the last five years, the data are not population based. We urgently need more epidemiological data from well constructed cohorts such as the Avon Longitudinal Study of Parents and Children. We also need to address the question as to what normative data are appropriate during childhood and adolescence. Normative data used in the present study are derived from multiple sources and do not necessarily take into account variation in insulin and lipid assays. There are no direct measures of insulin sensitivity, and the extent to which high insulin levels in obese children may reflect earlier maturation, increased statural growth, and increased lean body mass has not really been determined. In the present study, the authors were not able to detect any differences between ethnic groups, or between males and females, although such differences have been reported in many other studies during childhood and adolescence. Thus we cannot be certain that these data are representative of the general overweight obese population in the UK.

The data reported by Viner et al also highlight another intriguing observation. Some children, despite extreme obesity, do not appear to develop any features of the insulin resistance syndrome, nor do they appear to be at immediate risk of the development of type 2 diabetes. This may reflect the cross-sectional nature of the study and perhaps, as has been shown in studies from the USA, the greatest risk may be at puberty when gender and ethnic differences may become more evident. Certainly other data from paediatric and adult populations in the UK indicate that the risk of insulin resistance syndrome and type 2 diabetes may be greatest in children of South Asian descent.7,8 Cardiovascular disease risk is also greater in US blacks compared to white children. Such variation in disease risk may have its origins in pre-natal and early post-natal rates of weight gain or so called “thrifty genes”.9 We must encourage debate on how we might change exercise patterns and improve the diets of children in order to reduce the overall burden of obesity. In addition, we need to identify factors which predispose to visceral fat deposition, insulin resistance syndrome, and impaired glucose tolerance, as such high risk subjects may need more targeted intervention.

Commentary on the paper by Viner et al (see 10)

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