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Reduced oxygen consumption by fat cells improves metabolic defects

Low oxygen levels are a hallmark of expanding fat tissue in obesity, and can lead to type 2 diabetes. In addition to a lack of adequate blood supply, increased oxygen demand in fat cells now emerges as being key to this harmful state.
  1. Nolwenn Joffin

    1. Nolwenn Joffin is in the Touchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.

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  2. Philipp E. Scherer

    1. Philipp E. Scherer is in the Touchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.

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A major cause of type 2 diabetes is obesity, in which fat cells expand rapidly, in both size and number, and their oxygen demand outstrips supply. This low-oxygen state, known as hypoxia, leads to upregulation of the anti-hypoxic protein HIF-1α, which in turn causes tissue inflammation and prevents fat cells (adipocytes) from responding normally to insulin1,2. Hypoxia in expanding fat is often thought of mainly as a problem of supply, caused by the inability of blood vessels that deliver oxygen to grow as fast as the surrounding tissue3,4. Writing in Nature Metabolism, Seo et al.5 highlight a pathway by which excessive oxygen consumption in adipocytes can also contribute to hypoxia in expanding fat tissue. This pathway involves the enhanced activity of the enzyme adenine nucleotide translocase 2 (ANT2) in energy-generating organelles called mitochondria.

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Nature 564, 47-48 (2018)

doi: https://doi.org/10.1038/d41586-018-07248-6

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