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

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): e81175. doi:10.1172/jci.insight.81175.

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 Creators:
Sassmann, Antonia1, Author              
Singh, Pratibha1, Author              
Tang, Cong1, Author              
Wietelmann, Astrid2, Author              
Wettschureck, Nina1, Author              
Offermanns, Stefan1, Author              
Affiliations:
1Pharmacology, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591696              
2Small Animal Magnetic Resonance Imaging, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591708              

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Free keywords: ADIPOSE-TISSUE CELLULARITY; NF-KAPPA-B; INSULIN-RESISTANCE; BEIGE FAT; ADAPTIVE THERMOGENESIS; METABOLIC DISEASE; SIGNALING PATHWAY; INNATE IMMUNITY; KINASE TAK1; INFLAMMATIONResearch & Experimental Medicine;
 Abstract: 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.

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Language(s): eng - English
 Dates: 2016
 Publication Status: Published online
 Pages: 17
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: ISI: 000387111800001
DOI: 10.1172/jci.insight.81175
 Degree: -

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Title: JCI INSIGHT
Source Genre: Journal
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Publ. Info: 2015 MANCHESTER RD, ANN ARBOR, MI 48104 USA : AMER SOC CLINICAL INVESTIGATION INC
Pages: - Volume / Issue: 1 (7) Sequence Number: e81175 Start / End Page: - Identifier: ISSN: 2379-3708