SRC-3 deficient mice developed fat redistribution under high-fat diet

Area of Science:

• Metabolic research
• Obesity research
• Endocrinology

Background:

• Aberrant body fat distribution is linked to metabolic abnormalities.
• Steroid receptor coactivator-3 (SRC-3) deficiency protects against diet-induced obesity.
• Little is known about visceral (VAT) and subcutaneous adipose tissue (SCAT) distribution in SRC-3 deficient mice.

Purpose of the Study:

• To investigate the differential distribution of VAT and SCAT in SRC-3 deficient mice compared to wild-type mice under high-fat diet (HFD) conditions.
• To explore the underlying molecular mechanisms of fat redistribution in SRC-3 deficient mice.

Main Methods:

• Comparison of VAT/SCAT weight ratios in SRC-3(-/-) and SRC-3(+/+) mice under normal diet (ND) and HFD.
• Analysis of serological changes in SRC-3(-/-) mice.
• Gene expression assays to assess adipogenesis, thermogenesis, and lipolysis in VAT and SCAT of SRC-3(-/-) mice.

Main Results:

• Under HFD, SRC-3(-/-) mice exhibited significant fat redistribution with an elevated VAT/SCAT ratio compared to ND.
• SRC-3(+/+) mice showed no significant change in VAT/SCAT ratio between ND and HFD.
• Gene expression analysis revealed increased adipogenesis in VAT and enhanced thermogenesis/lipolysis in SCAT of SRC-3(-/-) mice, explaining preferential VAT accumulation.

Conclusions:

• SRC-3 deficiency leads to fat redistribution under HFD in mice.
• Altered fat distribution in SRC-3 deficient mice is associated with specific changes in adipogenesis, thermogenesis, and lipolysis.
• These findings provide insights into the pathogenesis of fat redistribution and its link to metabolic abnormalities.