MafB deficiency accelerates the development of obesity in mice
Journal
FEBS Open Bio
Journal Volume
6
Journal Issue
6
Pages
540-547
Date Issued
2016
Author(s)
Tran, M.T.N.
Hamada, M.
Nakamura, M.
Jeon, H.
Kamei, R.
Tsunakawa, Y.
Kulathunga, K.
Fujisawa, K.
Kudo, T.
Takahashi, S.
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. We investigated whether hematopoietic cell-specific Mafb deficiency induces obesity. Mafb-deficient mice exhibited higher weights and higher body fat percentages with larger adipocytes, and higher levels of serum cholesterol. In Mafb-deficient adipose tissue macrophages, the expression of AIM, the inhibitor for lipogenesis in adipocytes, was decreased. ? 2016 Federation of European Biochemical Societies.
Subjects
Adipose tissue macrophages; Apoptosis inhibitor of macrophage; MafB; Obesity
SDGs
Other Subjects
transcription factor MafB; adipocyte; animal experiment; animal model; animal tissue; apoptosis; Article; body fat; body weight; controlled study; lipid diet; macrophage; mouse; nonhuman; obesity; priority journal; reverse transcription polymerase chain reaction; weight gain
Type
journal article