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Extra info for Overweight and the Metabolic Syndrome - From Bench to Bedside

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39] Okosun IS, Chandra KM, Boev A, et al. S. adults: Prevalence and trends, 1960–2000. Prev Med 2004;39:197–206. [40] Malina RM, Bouchard C. Subcutaneous fat distribution during growth. In: Fat Distribution During Growth and Later Health Outcomes. New York: Wiley–Liss, 1988;68. [41] Brambilla P, Manzoni P, Sironi S. Peripheral and abdominal adiposity in childhood obesity. Int J Obes Relat Metab Disord 1994;18:795–800. [42] Roche AF, Siervogel RM, Chumlea WC, et al. Grading of body fatness from limited anthropometric data.

Consumption of a fat-rich diet activates a proinflammatory response and induces insulin resistance in the hypothalamus. Endocrinology 2005. [130] Levin BE, Dunn-Meynell AA. Reduced central leptin sensitivity in rats with diet-induced obesity. Am J Physiol Regul Integr Comp Physiol 2002;283(4):R941–R948. [131] Levin BE, Dunn-Meynell AA, Banks WA. Obesity-prone rats have normal blood–brain barrier transport but defective central leptin signaling before obesity onset. Am J Physiol Regul Integr Comp Physiol 2004;286(1):R143–150.

For most children until they are postpuberty, DXA is the method of choice. This provides an estimate of the amount of fat, lean, and bony tissues, all of which should be monitored along with any change in weight during treatment. For older obese children and adults, the easiest measure to monitor is body weight. This can be combined with a measure of abdominal circumference and BMI to track progress. As fat tissue is reduced and weight is lost, it is important that there is not a greater loss of lean tissue, which can have significant health risks.

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Overweight and the Metabolic Syndrome - From Bench to Bedside by G. Bray, D. Ryan


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