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Insulin regulates Bbs4 during adipogenesis
Netta Nahum1,2, Efrat Forti1, Olga Aksanov1
1Department of Biotechnology and Epidemiology, Ben-Gurion University, Beer-Sheva, Israel.
IUBMB Life
|April 4, 2017
Summary
Insulin directly regulates Bardet-Biedl syndrome (BBS) genes involved in adipogenesis. This hormonal control suggests a metabolic link between BBS genes, obesity, and metabolic syndrome.
Area of Science:
- Genetics
- Metabolic Disorders
- Cell Biology
Background:
- Bardet-Biedl syndrome (BBS) is linked to obesity and type 2 diabetes.
- The direct relationship between BBS and diabetes remains unclear.
- Insulin and IGF-1 regulate adipogenesis and adipocyte function.
Purpose of the Study:
- To investigate the role of insulin in Bardet-Biedl syndrome.
- To explore the regulation of BBS genes by insulin during adipogenesis.
Main Methods:
- In vitro studies using adipocytes with silenced (SiBbs4) or overexpressed (OEBbs4) Bbs4.
- Analysis of BBS gene transcription and protein expression.
- Glucose uptake assays.
- Investigation of the PI3K pathway.
Main Results:
- Insulin and IGF-1 dose- and time-dependently decreased BBS gene transcription and protein levels during adipogenesis.
- Silencing Bbs4 impaired glucose uptake, while overexpression reversed this effect.
- PI3K inhibition upregulated Bbs transcripts, indicating PI3K pathway involvement.
Conclusions:
- Insulin directly regulates BBS genes (Bbs1, 2, 4, 6).
- Hormonal regulation of BBS genes suggests a metabolic link to obesity and metabolic syndrome.