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Characterization of adiposity and metabolism in Lmna-deficient mice

  1. Author:
    Cutler, D. A.
    Sullivan, T.
    Marcus-Samuels, B.
    Stewart, C. L.
    Reitman, M. L.

  2. Author Address

    NIDDKD, Diabet Branch, NIH, Bldg 10, Room 8N-250, 10 Ctr Dr, Bethesda, MD 20892 USA. NIDDKD, Diabet Branch, NIH, Bethesda, MD 20892 USA. NCI, Lab Canc & Dev Biol, NIH, Frederick, MD 21702 USA. George Washington Univ, Grad Program Genet, Washington, DC 20052 USA. Reitman ML NIDDKD, Diabet Branch, NIH, Bldg 10, Room 8N-250, 10 Ctr Dr, Bethesda, MD 20892 USA.
    1. Year: 2002
  2. Journal: Biochemical and Biophysical Research Communications
    1. 291
    2. 3
    3. Pages: 522-527
  4. Type of Article: Article
  1. Abstract:

    Dunnigan's Familial Partial Lipodystrophy (FPLD) is an autosomal dominant disease characterized by regional fat loss and insulin resistance. FPLD is caused by mutations in the LMNA gene, which encodes intermediate filaments of the nuclear lamina. Different LMNA mutations cause Emery-Dreifuss muscular dystrophy and/or a dilated cardiomyopathy. It is not known how LMNA mutations cause any of the disease phenotypes. Here we measure physical and metabolic characteristics of Lmna-/- and +/- mice to determine their usefulness as models for FPLD. Lmna-/- mice, which die prematurely of muscular dystrophy, have little fat, but do not show the insulin resistance characteristic of FPLD. Lmna+/- mice, despite treatment with a high fat diet, do not have decreased fat stores or metabolic features of FPLD. We also show, in mice, that Lmna transcripts are expressed at high levels in muscle and adipose tissue, but do not vary by body region or sex. In conclusion, Lmna+/- and - /- mice do not mimic Dunnigan's FPLD, and differential expression of lamins A and C does not appear to contribute to sex- or tissue-specific LMNA phenotypes.

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