A B Dzwonek1, V Novelli, A Schwenk. 1. Infectious Diseases and Microbiology Unit, University College London Institute of Child Health, and Clinical Infectious Diseases Unit, Great Ormond Street Children's Hospital NHS Trust, London, UK.
Abstract
OBJECTIVES: HIV-related lipodystrophy is a syndrome of adipose tissue redistribution, dyslipidaemia and insulin resistance. Combination antiretroviral therapy (CART) is a key risk factor. We hypothesized that fat redistribution in HIV-infected children is related to altered endocrine function of adipose tissue, namely leptin secretion. METHODS: Serum leptin and fat redistribution were measured in 104 HIV-infected children in a prospective observational study from 2003 to 2004. Fat redistribution was defined by clinical observation. Body fatness was estimated using body mass index and four skinfold measurements. Serum leptin was determined using an enzyme-linked immunosorbent assay (Quantikine; R&D Systems, Abingdon, UK). Linear analogue models were used to adjust the leptin concentration for body fatness. RESULTS: There was no significant difference in serum leptin among children treated with protease inhibitors (PIs), children on non-PI CART and children not treated with CART (P>0.05). When leptin concentrations were adjusted for body fatness, there was again no difference among PI-treated, non-PI-treated and untreated children. Categorization of CART exposure as never, current or past did not change these results. CONCLUSIONS: There is no evidence that leptin plays any role in lipodystrophy other than reflecting body fatness.
OBJECTIVES: HIV-related lipodystrophy is a syndrome of adipose tissue redistribution, dyslipidaemia and insulin resistance. Combination antiretroviral therapy (CART) is a key risk factor. We hypothesized that fat redistribution in HIV-infectedchildren is related to altered endocrine function of adipose tissue, namely leptin secretion. METHODS: Serum leptin and fat redistribution were measured in 104 HIV-infectedchildren in a prospective observational study from 2003 to 2004. Fat redistribution was defined by clinical observation. Body fatness was estimated using body mass index and four skinfold measurements. Serum leptin was determined using an enzyme-linked immunosorbent assay (Quantikine; R&D Systems, Abingdon, UK). Linear analogue models were used to adjust the leptin concentration for body fatness. RESULTS: There was no significant difference in serum leptin among children treated with protease inhibitors (PIs), children on non-PI CART and children not treated with CART (P>0.05). When leptin concentrations were adjusted for body fatness, there was again no difference among PI-treated, non-PI-treated and untreated children. Categorization of CART exposure as never, current or past did not change these results. CONCLUSIONS: There is no evidence that leptin plays any role in lipodystrophy other than reflecting body fatness.
Authors: David Dimock; Vijaya Thomas; Anna Cushing; Julia B Purdy; Carol Worrell; Jeffrey B Kopp; Rohan Hazra; Colleen Hadigan Journal: Metabolism Date: 2010-10-13 Impact factor: 8.694