MafB deficiency accelerates the development of obesity in mice
Mai Thi Nhu Tran1, Michito Hamada2, Megumi Nakamura1
1Department of Anatomy and Embryology Faculty of Medicine University of Tsukuba Ibaraki Japan.
Abstract:
MafB, a transcription factor expressed selectively in macrophages, has important roles in some macrophage-related diseases, especially in atherosclerosis. In this study, we investigated the mechanism by which hematopoietic-specific MafB deficiency induces the development of obesity. Wild-type and hematopoietic cell-specific Mafb-deficient mice were fed a high-fat diet for 10 weeks. The Mafb-deficient mice exhibited higher body weights and faster rates of body weight increase than control mice. The Mafb-deficient mice also had a higher percentage of body fat than the wild-type mice, due to increased adipocyte size and serum cholesterol levels. Reverse transcription-PCR analysis showed a reduction in apoptosis inhibitor of macrophage (AIM) in Mafb-deficient adipose tissue. AIM is known as an inhibitor of lipogenesis in adipocytes and is expressed in adipose tissue macrophages. Collectively, our data suggest that Mafb deficiency in hematopoietic cells accelerates the development of obesity.
Insights
MafB deficiency in hematopoietic cells accelerates obesity development. This occurs due to reduced apoptosis inhibitor of macrophage (AIM), leading to increased adipocyte size and cholesterol.
Area of Science:
- Immunology
- Metabolic Diseases
- Molecular Biology
Background:
- MafB is a transcription factor selectively expressed in macrophages.
- MafB plays a role in macrophage-related diseases like atherosclerosis.
- The specific role of MafB in obesity development is not well understood.
Purpose of the Study:
- To investigate the mechanism by which hematopoietic-specific MafB deficiency induces obesity.
- To determine the impact of MafB deficiency on body weight, body fat percentage, adipocyte size, and serum cholesterol levels.
- To explore the relationship between MafB deficiency, apoptosis inhibitor of macrophage (AIM) expression, and lipogenesis in adipose tissue.
Main Methods:
- Hematopoietic cell-specific Mafb-deficient mice and wild-type littermates were fed a high-fat diet for 10 weeks.
- Body weight, body fat percentage, adipocyte size, and serum cholesterol levels were measured.
- Reverse transcription-PCR was used to analyze apoptosis inhibitor of macrophage (AIM) expression in adipose tissue.
Main Results:
- Mafb-deficient mice showed significantly higher body weights and accelerated weight gain compared to controls.
- A higher percentage of body fat was observed in Mafb-deficient mice, attributed to increased adipocyte size and elevated serum cholesterol.
- Reduced expression of apoptosis inhibitor of macrophage (AIM) was detected in the adipose tissue of Mafb-deficient mice.
Conclusions:
- MafB deficiency in hematopoietic cells accelerates obesity development.
- Reduced AIM expression in adipose tissue macrophages may contribute to increased lipogenesis and adipocyte hypertrophy.
- These findings highlight MafB's critical role in regulating metabolic homeostasis and preventing obesity.
