Physiology of obesity in childhood and adolescence

SummaryBody weight is regulated by a feedback loop in which peripheral signals report nutritional information to an integratory centre in the brain [Friedman JM. Obesity in the new millenium. Nature 2000;404:632–4] The cloning of the ob gene is consistent with this concept and suggests that body fat content in adult rodents is regulated by a negative feedback loop centred in the hypothalamus. In recent years a large number of additional signalling molecules secreted by adipose tissue have been discovered [1, Kiess W, Galler A, Reich A, Müller G, Kapellen T, Deutscher J, et al. Clinical aspects of obesity in childhood and adolescence. Obes Rev 2001;2:29–36]. These factors, named adipocytokines, include resistin, adiponectin and visfatin [Zhang Y, Proenca R, Maffei M, et al. Positional cloning of the mouse obese gene and its human homologue. Nature 1994;372:425–32; Kershaw EE, Flier JS. Adipose tissue as an endocrine organ. J Clin Endocrinol Metab 2004;89:2548–56; Shuldiner AR, Yang R, Gong DW. Resistin, obesity and insulin resistance—the emerging role of the adipocyte as an endocrine organ. N Engl J Med 2001;345:1345–6; Steppan CM, Bailey ST, Bhat S, et al. The hormone resistin links obesity to diabetes. Nature 2001;409:307–12]. Among the adipocytokines, adiponectin is perhaps the most interesting compound for the clinician as low adiponectin serum levels have been found in obese patients, and in particular, insulin-resistant patients [Hu E, Liang P, Spiegelman BM. AdipoQ is a novel adipose-specific gene dysregulated in obesity. J Biol Chem 1996;271:10697–10703; Trujillo ME, Scherer PE. Adiponectin—journey from an adipocyte secretory protein to biomarker of the metabolic syndrome. J Intern Med 2005;257:167–75; Böttner A, Wabitsch M, Kratzsch J, Seidel B, Berthold A, Blüher M, et al. Adiponectin expression is dependent on differentiation of adipocytes. Biochem Biophys Res Commun 2005, in press; Matsuzawa Y, Funahashi T, Kihara S, et al. Adiponectin and metabolic syndrome. Arterioscler Thromb Vasc Biol 2004;24:29–33; Böttner A, Kratzsch J, Müller G, et al. Gender differences of adiponectin levels develop during the progression of puberty and are related to serum androgen levels. J Clin Endocrinol Metab 2004;89:4053–4061; Spranger J, Kroke A, Mohlig M, et al. Adiponectin and protection against type 2 diabetes mellitus. Lancet 2003;361:226–228; Vasseur F, Lepretre F, Lacquemant C, et al. The genetics of adiponectin. Curr Diabetes Rep 2003;3:151–8] It is now well known that obesity is the most common chronic disorder in the industrialized societies. In some countries, the prevalence of obesity in childhood and adolescence has reached epidemic dimensions. Childhood obesity is associated with substantial co-morbidity. Although diagnostic strategies are clear and straightforward, treatment remains difficult and frustrating both for the patient, family and the multidisciplinary team caring for children with obesity. In our opinion, much more attention should be paid to the development of preventive strategies at all ages. Prevention should in any case start early in life. New drugs are being developed that promise to be useful for treatment and secondary prevention. However, no sufficient data are available for the use of such agents in childhood and adolescence. Finally, public awareness of the increasing health burden and economic dimension of the childhood obesity epidemic has to be considered by the public and by policy decision-makers.