In vivo modulation of Hmgic reduces obesity (original) (raw)

Nature Genetics volume 24, pages 377–380 (2000)Cite this article

Abstract

The HMGI family of proteins consists of three members1,2, HMGIC, HMGI and HMGI(Y), that function as architectural factors3,4,5 and are essential components of the enhancesome6,7. HMGIC is predominantly expressed in proliferating, undifferentiated mesenchymal cells and is not detected in adult tissues8,9. It is disrupted and misexpressed in a number of mesenchymal tumour cell types10,11,12, including fat-cell tumours12 (lipomas). In addition Hmgic –/– mice have a deficiency in fat tissue13. To study its role in adipogenesis and obesity, we examined Hmgic expression in the adipose tissue of adult, obese mice. Mice with a partial or complete deficiency of Hmgic resisted diet-induced obesity. Disruption of Hmgic caused a reduction in the obesity induced by leptin deficiency (Lep ob /Lep ob) in a gene-dose–dependent manner. Our studies implicate a role for HMGIC in fat-cell proliferation, indicating that it may be an adipose-specific target for the treatment of obesity.

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Acknowledgements

We thank J. D'Armiento, HMGene, Inc. and members of the laboratory for a critical reading of the manuscript. K.C. is supported by National Institutes of Health grant CA77929 and NJ Commission on Science and Technology.

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Authors and Affiliations

  1. Department of Biochemistry, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway, New Jersey, USA
    Ashim Anand & Kiran Chada

Authors

  1. Ashim Anand
  2. Kiran Chada

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Correspondence toKiran Chada.

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Anand, A., Chada, K. In vivo modulation of Hmgic reduces obesity.Nat Genet 24, 377–380 (2000). https://doi.org/10.1038/74207

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