Nature Genetics
24, 377 - 380 (2000)
doi:10.1038/74207
In vivo modulation of Hmgic reduces obesityAshim Anand
& Kiran Chada
Department of Biochemistry, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway, New Jersey, USA.
Correspondence should be addressed to Kiran Chada Chada@umdnj.eduThe 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 (Lepob/Lepob) 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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