Letters to the Editor
To the Editor: In a recent issue of the Journal, dePiano et al (1) drew attention to the need for a multidisciplinary approach to the treatment of nonalcoholic steatohepatitis (NAFLD). The concept is not new (2,3), but the difficulties involved in this type of management must be taken into consideration. The adherence to the experimental protocol was poor, probably due to the fact that the program was excessively time consuming. Adolescents were asked to spend 5 hours/week engaging in physical activity, attending nutritional classes, and attending physiological orientation groups. Nine patients dropped out of the follow-up and 11 adolescents did not fill out the 3-day diary recall. Thus, between-group statistical analyses were performed on only 18 simple obese and 5 NAFLD adolescents. Therefore, the power, title, and conclusions of the study may be debatable and misleading. The limited number of NAFLD patients makes this study an investigation of simple obesity rather than of obesity-related fatty liver disease. Sample size may also account for the lack of significant difference in baseline consumption of lipid. The determination of amount and quality of lipids intake should be of great interest in the understanding of the disease. High lipids (mostly saturated) intake contributes to reduced insulin sensitivity (4) and mitochondrial lipid oxidation (5), increased levels of leptin (6) independent of body weight (7), and, as stated by the authors, increased fat deposition in the hepatocytes (1).
Finally, we would also point out that the increased ratio between visceral and subcutaneous fat may be more detrimental than body mass index per se in terms of NAFLD development, this being associated with reduced levels of adiponectin (8). The evidence that 7% of NAFLD children are of normal weight supports these data (3).
In conclusion, we agree with the therapeutic approach suggested by the authors, but we believe strongly that it should be tailored to individual patient need. As far as dietary intake of lipids in the pathogenesis of NAFLD is concerned, it should be carefully evaluated in a larger cohort of adolescents.
1. de Piano A, Prado WL, Caranti DA, et al
. Metabolic and nutritional profile of obese adolescents with nonalcoholic fatty liver disease. J Pediatr Gastroenterol Nutr 2007; 44:446–452.
2. Nobili V, Marcellini M, Devito R, et al
. NAFLD in children: a prospective clinical-pathological study and effect of lifestyle advice. Hepatology 2006; 44:458–465.
3. Nobili V, Manco M, Raponi M, et al
. Case Management applied in a multispecialist paediatric outpatients clinic for patients affected by non alcoholic fatty liver disease (NAFLD). J Paediatr Child Health 2007; 43:427.
4. Manco M, Calvani M, Mingrone G. Effects of dietary fatty acids on insulin sensitivity and secretion. Obes Diabetes Metab 2004; 6:402–413.
5. Ciapaite J, Bakker SJ, Van Eikenhorst G, et al
. Functioning of oxidative phosphorylation in liver mitochondria of high-fat diet fed rats. Biochim Biophys Acta 2007; 1772:307–316.
6. Leibowitz SF, Chang GQ, Dourmashkin JT, et al
. Leptin secretion after a high-fat meal in normal-weight rats: strong predictor of long-term body fat accrual on a high-fat diet. Am J Physiol Endocrinol Metab 2006; 290:E258–E267.
7. Nobili V, Manco M, Ciampalini P, et al
. Leptin, free leptin index, insulin resistance and liver fibrosis in children with non-alcoholic fatty liver disease. Eur J Endocrinol 2006; 155:735–743.
8. Pagano C, Soardo G, Esposito W, et al
. Plasma adiponectin is decreased in nonalcoholic fatty liver disease. Eur J Endocrinol 2005; 152:113–118.