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In vivo modulation of Hmgic reduces obesity
1Department of Biochemistry, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway, NJ, USA.
Nature Genetics
|March 31, 2000
Summary
High mobility group I-C (HMGIC) protein is crucial for fat cell proliferation. Deficiency in HMGIC reduces obesity in mice, suggesting it as a potential target for obesity treatments.
Area of Science:
- Molecular Biology
- Genetics
- Endocrinology
Background:
- The High Mobility Group I (HMG I) protein family includes HMGIC, HMGI, and HMGI(Y), acting as architectural factors in gene regulation.
- HMGIC is primarily found in proliferating mesenchymal cells and is absent in adult tissues, but is altered in mesenchymal tumors like lipomas.
- Hmgic knockout mice exhibit reduced fat tissue, hinting at its role in adipogenesis.
Purpose of the Study:
- To investigate the role of HMGIC in adipogenesis and obesity.
- To examine HMGIC expression in the adipose tissue of obese mice.
- To determine if HMGIC is a potential therapeutic target for obesity.
Main Methods:
- Examined Hmgic expression in adult obese mice adipose tissue.
- Studied the effects of partial or complete Hmgic deficiency on diet-induced obesity.
- Assessed the impact of Hmgic disruption on leptin-deficient (Lepob/Lepob) induced obesity.
Main Results:
- Mice with partial or complete Hmgic deficiency showed resistance to diet-induced obesity.
- Hmgic disruption reduced obesity in Lepob/Lepob mice in a gene-dose-dependent manner.
- These findings indicate HMGIC's involvement in fat cell proliferation.
Conclusions:
- HMGIC plays a significant role in fat cell proliferation.
- HMGIC is implicated in the development of obesity.
- HMGIC represents a potential adipose-specific target for novel obesity treatments.