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Previous Volume 353:2088 November 10, 2005 Number 19 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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To the Editor: The excellent review of nuclear receptors by Shulman and Mangelsdorf (Aug. 11 issue)¹ mentioned that the study of patients with mutations in PPAR, the gene encoding peroxisome-proliferator–activated receptor (PPAR), which is rare, can yield corroborating and new insights into the metabolic syndrome. However, it is important to acknowledge that all reported cases of the metabolic syndrome involving heterozygous germ-line loss-of-function PPAR mutations^2,3,4,5 concurrently have familial partial lipodystrophy type 3 (FPLD3). Given the role of PPAR in adipogenesis, it seems reasonable that adipose tissue is repartitioned from peripheral to central stores in patients with such mutations. . . . [Full Text of this Article]

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