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      Quantitative and qualitative differences in subcutaneous adipose tissue stores across lipodystrophy types shown by magnetic resonance imaging

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          Lipodystrophies are characterized by redistributed subcutaneous fat stores. We previously quantified subcutaneous fat by magnetic resonance imaging (MRI) in the legs of two patients with familial partial lipodystrophy subtypes 2 and 3 (FPLD2 and FPLD3, respectively). We now extend the MRI analysis across the whole body of patients with different forms of lipodystrophy.


          We studied five subcutaneous fat stores (supraclavicular, abdominal, gluteal, thigh and calf) and the abdominal visceral fat stores in 10, 2, 1, 1 and 2 female subjects with, respectively, FPLD2, FPLD3, HIV-related partial lipodystrophy (HIVPL), acquired partial lipodystrophy (APL), congenital generalized lipodystrophy (CGL) and in six normal control subjects.


          Compared with normal controls, FPLD2 subjects had significantly increased supraclavicular fat, with decreased abdominal, gluteal, thigh and calf subcutaneous fat. FPLD3 subjects had increased supraclavicular and abdominal subcutaneous fat, with less severe reductions in gluteal, thigh and calf fat compared to FPLD2 subjects. The repartitioning of fat in the HIVPL subject closely resembled that of FPLD3 subjects. APL and CGL subjects had reduced upper body, gluteal and thigh subcutaneous fat; the APL subject had increased, while CGL subjects had decreased subcutaneous calf fat. Visceral fat was markedly increased in FPLD2 and APL subjects.


          Semi-automated MRI-based adipose tissue quantification indicates differences between various lipodystrophy types in these studied clinical cases and is a potentially useful tool for extended quantitative phenomic analysis of genetic metabolic disorders. Further studies with a larger sample size are essential for confirming these preliminary findings.

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          Most cited references 27

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          Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III)

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            Nuclear lamin A/C R482Q mutation in canadian kindreds with Dunnigan-type familial partial lipodystrophy.

             R Hegele,  H-Z Cao (2000)
            Patients with Dunnigan-type familial partial lipodystrophy (FPLD) are born with normal fat distribution, but after puberty experience regional and progressive adipocyte degeneration, often associated with profound insulin resistance and diabetes. Recently, the FPLD gene was mapped to chromosome 1q21-22, which harbours the LMNA gene encoding nuclear lamins A and C. Mutations in LMNA were shown to underlie autosomal dominant Emery-Dreifuss muscular dystrophy (EDMD-AD), which is characterized by regional and progressive skeletal muscle wasting and cardiac effects. We hypothesized that the analogy between the regional muscle wasting in EDMD-AD and the regional adipocyte degeneration in FPLD, in addition to its chromosomal localization, made LMNA a good candidate gene for FPLD. DNA sequencing of LMNA in five Canadian FPLD probands indicated that each had a novel missense mutation, R482Q, which co-segregated with the FPLD phenotype and was absent from 2000 normal alleles ( P = 1.1 x 10(-13)). This is the first report of a mutation underlying a degenerative disorder of adipose tissue and suggests that LMNA mutations could underlie other diseases characterized by tissue type- and anatomical site-specific cellular degeneration.
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              Standardized assessment of whole body adipose tissue topography by MRI.

              To assess standardized whole body adipose tissue topography in a cohort of subjects at an increased risk for type 2 diabetes and to compare fat distribution in subgroups regarding anthropometric (age, body mass index [BMI]) and metabolic parameters (insulin sensitivity). A total of 80 volunteers (40 females, 40 males) underwent T1-weighted MR imaging of the entire body. Standardized adipose tissue (AT) profiles were calculated considering the different body structure of the participants. The measured data were interpolated to a defined number of sampling points enabling a direct comparison of the profiles independent on body structure. Resulting mean profiles and region-dependent standard deviations of four age groups and three BMI-groups were compared for females and males. Correlations between insulin sensitivity and body fat distribution were analyzed. Reliable adipose tissue profiles could be obtained from all volunteers. In BMI-matched subgroups, females show significant higher AT and subcutaneous abdominal AT (P < 0.05 both), but lower visceral AT (P < 0.01) compared to the males. Furthermore, visceral AT increases with age, as shown in the matched age groups. In both gender groups, insulin-resistant subjects are characterized by higher visceral adipose tissue (VAT) compared to insulin-sensitive subjects. In addition, profiles of insulin-resistant subjects show more AT in the shoulder/neck region but less AT in the upper extremities. Standardized assessment of whole body AT profiles based on T1-weighted MRI provides a reliable basis for interindividual comparison of the body fat distribution and allows a fast and reliable quantification of total body adipose tissue and the distribution of different AT components as subcutaneous and visceral fat in different body regions. Differences in standardized profiles might enable an early identification of people at risk of metabolic disorders, as not only the amount but also the distribution of AT is expected to play an essential role in the pathogenesis of metabolic diseases. Copyright 2005 Wiley-Liss, Inc.

                Author and article information

                BMC Med Imaging
                BMC Medical Imaging
                BioMed Central (London )
                12 March 2007
                : 7
                : 3
                [1 ]Vascular Biology Research Group, Robarts Research Institute, London, Ontario, N6A 5K8, Canada
                [2 ]Imaging Research Laboratories, Robarts Research Institute, London, Ontario, N6A 5K8, Canada
                [3 ]Department of Medicine, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, N6A 5A5, Canada
                [4 ]Blackburn Cardiovascular Genetics Laboratory, Robarts Research Institute, 100 Perth Drive, Room 406, London, Ontario, N6A 5K8, Canada
                Copyright © 2007 Al-Attar et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Research Article

                Radiology & Imaging


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