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学術論文

Increased apoptosis and browning of TAK1-deficient adipocytes protects against obesity

MPS-Authors
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Sassmann,  Antonia
Pharmacology, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Singh,  Pratibha
Pharmacology, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Tang,  Cong
Pharmacology, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Wietelmann,  Astrid
Small Animal Magnetic Resonance Imaging, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Wettschureck,  Nina
Pharmacology, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Offermanns,  Stefan
Pharmacology, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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引用

Sassmann, A., Singh, P., Tang, C., Wietelmann, A., Wettschureck, N., & Offermanns, S. (2016). Increased apoptosis and browning of TAK1-deficient adipocytes protects against obesity. JCI INSIGHT, 1(7):. doi:10.1172/jci.insight.81175.


引用: https://hdl.handle.net/21.11116/0000-0001-C113-F
要旨
Obesity is an increasing health problem worldwide, and nonsurgical strategies to treat obesity have remained rather inefficient. We here show that acute loss of TGF-beta-activated kinase 1 (TAK1) in adipocytes results in an increased rate of apoptotic adipocyte death and increased numbers of M2 macrophages in white adipose tissue. Mice with adipocyte-specific TAK1 deficiency have reduced adipocyte numbers and are resistant to obesity induced by a high-fat diet or leptin deficiency. In addition, adipocyte-specific TAK1-deficient mice under a high-fat diet showed increased energy expenditure, which was accompanied by enhanced expression of the uncoupling protein UCP1. Interestingly, acute induction of adipocyte-specific TAK1 deficiency in mice already under a high-fat diet was able to stop further weight gain and improved glucose tolerance. Thus, loss of TAK1 in adipocytes reduces the total number of adipocytes, increases browning of white adipose tissue, and may be an attractive strategy to treat obesity, obesity-dependent diabetes, and other associated complications.